5.1.1 Communication and Homeostasis Flashcards

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1
Q

ectotherms

what is their core body temp dependent on

A

their surroundings

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2
Q

give some examples of ectotherms

A

fish, invertebrates, amphibians and reptiles (most animals)

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3
Q

why do ectotherms that live in water not need to regulate body temp?

A

-Due to higher heat capacity of water, the temperature of the environment doesn’t change much

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4
Q

why is it important ectotherms on land regulate temp?

A
  • drastic seasonal and daily changes in temp (these can increase or reduce radiation they absorb from sun)
  • need to warm up to carry out metabolic reactions that happen fast enough to be active.
    eg) lizard in sun warm up to catch prey fast
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5
Q

How do ectotherms increase body temp by conduction

A

press body against warm ground

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6
Q

give an example of how ectotherms use exothermic metabolic reactions to warm up

A

Galapagos lizards contract muscles and vibrate which increases cell metabolism to raise body temps
-butterflies and moths also do this

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7
Q

how do ectotherms cool down and why

A

opposite to warming up processes

  • must cool down to prevent core body temp being too high resulting in denaturation of enzymes
  • shelter from sun in cracks in rocks, digging
  • press body against cool earth, stones or nearby water and mud
  • orientate to minimise surface area in sun
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8
Q

What physiological adaptations do ectotherms have

A
  • dark colours absorb more radiation (lizards in cold are darker vice versa)
  • alter heart rate to increase/decrease metabolism and effect of warming and cooling on their surface
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9
Q

are ectotherms or endotherms more vulnerable to changes in environment

A

ectotherms- adapted for conditions

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10
Q

why do ectotherms need less food

A

they use less energy regulating body temps, therefore can survive in places food is in short supply eg deserts

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11
Q

What factors are effecting the external environment of an organism

A

temperature, pH, light intensity
water availability, oxygen availability
threats, sounds, pain

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12
Q

What factors are effecting the internal environment of an organism

A

blood glucose, internal temp, waste products like urea, hormone levels, osmoregulation, pH

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13
Q

what are the two communication systems in the body

A

nervous system- cells and neurones

endocrine system- hormones

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14
Q

which communication system is slow acting

A

endocrine is slower acting but lasts longer

nervous is very fast acting but doesn’t last long

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15
Q

In the endocrine system, where do hormones come from and where do they go

A

from a gland to a target organ, through blood

  • receptors on target organ have specific 3D shape (glycoproteins)
  • sometimes a 2nd messenger will become active when hormone arrives at cell and this brings about response
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16
Q

do steroid need a receptor?

A

no they can go straight through phospholipid bilayeras they are lipid soluble so dont need a second messenger

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17
Q

what is a gland

A

group of cells that release one of more substances through secretion. endocrine glands contain secretory cells which pass secreted substances into bloodstream.

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18
Q

what is the difference between endocrine and exocrine glands

A

endocrine means secreting inside so into blood capillaries inside gland.
exocrine eg saliva gland, secrete to outside, they secrete into tube or duct which are not hormones. usually enzymes eg lipases to the duodenum/ gut

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19
Q

what are the 3 hormone catagories

A
  • proteins- eg insulin , peptides
  • amines eg adrenaline come from amino acids
  • steroids- eg testosterone from cholesterol
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20
Q

what are paracrine and autocrine hormone secreting cells

A

paracrine- secrete hormones which effect adjacent cells eg gastric pits
autocrine-regulate their own activity, eg testosterone

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21
Q

how is a target cell regulated

A

only by the hormones it has receptors for not by other hormones.

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22
Q

different cells may respond differently to the same hormone. why?

A

the transduction machinery of different target cell types reads the hormone signal in different ways.

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23
Q

how are blood hormone concentrations usually controlled?

A

NEGATIVE FEEDBACK- a reduction in concentration stimulates additional secretion and an increase in concentration inhibits further secretion.

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24
Q

how quickly are hormones degraded

A

after hormone binds to receptor they are usually degraded rapidly.
-this rapid recovery system means that target cells can be sensitive to changing levels of the hormones that regulate their activities.

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25
Q

give examples of endotherms

A

mammals and birds

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26
Q

how do endotherms produce heat

A

internally so is independent from external temperature.

-rely on metabollic processes to warm up and maintain a very stable core. (can even survive in hot or cold environments)

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27
Q

why do endotherms eat more

A

-metabolic rate 5x higher than ectotherms so eat more to meet needs

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28
Q

what detects temperature change in endotherms and how is skin effected by changes in external condititions.

A

the hypothalamus- detects temp of blood. acts as a thermostat
(the temperature of the skin is highly effected by environmental conditions than temperature of hypothalamus)
endotherms are HIGHLY SENSITIVE and respond to changes in temperature

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29
Q

How does vasodilation allow endotherms to COOL down

A

arterioles near surface of skin dilate as external temperature rises. vessels that connect arterioles and venules constrict which forces blood through capillary network close to the skin surface.
-skin flushes due to increased radiation then cools
»»the cooling by conduction is due to skin being pressed against cool surfaces.

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30
Q

how does increased sweating cool endotherms

A

as core temp increases the body sweats more. there are sweat glands all over the body of mammals and sweat evaporates= heat is lost
(hairy animals such as dogs have sweat glands in less hairy places like paws but they also pant to release heat)

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31
Q

how does reducing the insulating effect of hairs and feathers cool endotherms

A

as temp rises»> the erector pili muscles relax so feathers and hair lie flat to the skin to avoid insulation.
Not much effect in humans

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32
Q

what are the ways endotherms cool down

A
  • vasodilation
  • increased sweating and panting
  • reducing insulating effect of feathers and hair
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33
Q

what anatomic adaptation of endotherms can help to cool down

A

endotherms in climates such as hot deserts- can have relatively large SA:V ratio to maximise cooling such as large ears or pale fur to reflect radiation

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34
Q

how do endotherms warm up through vasoconstriction

A

arterioles near skin surface constrict and arteriovenous shunt vessels dilate so LESS blood flows through capillary network near skin surface.

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35
Q

how do endotherms warm up through decreased sweating

A

rate of sweating decreases and sweat production will stop entirely when body temperature falls.
-reduces chance of cooling by process of evaporation on skin surface
(evaporation from lungs still occurs)

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36
Q

how does raising body hairs/ feathers help to warm up endotherms

A

erector pili muscles contract-
makes hair/feathers erect, trapping layer of air so insulates skin. effective way to reduce heat loss in most mammals but has little effect in humans

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37
Q

name ways endotherms can warm up

A

vasoconstriction
decreased sweating
raising body hairs or feathers
shivering

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38
Q

how does shivering warm up endotherms

also how does metabollic heat warm up endotherms?

A
  • organism may shiver when temp drops due to involuntary muscle contractions and relaxations of large voluntary muscles in body.
  • metabolic heat can also warm up endotherms through exothermic reactions but is less effective
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39
Q

describe possible anatomical adaptations of endotherms living in cold climates

A
  • may have additional anatomical adaptations like small ears which reduces sa:v ratio so less cooling can occur.
  • insulating fat like whales
  • hibernate(build up fat stores for winter and lowering metabolic rate for sleep)
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40
Q

how do neurotransmitters get across a synapse

A
  • eg acetycholine (chemical)
  • leaves sensory neurone by exocytosis by fusing to the membrane.
  • diffuse over synapse and binds to receptor on relay neurone made from glycoproteins with specific 3D shape, and glycolipids.
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41
Q

where is adrenaline released

A

adrenal glands above the kidney

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42
Q

how much adrenaline is needed in fight or flight response

what triggers release

A

very little amount- has big and fast effect

  • fight or flight triggers impulses from neurones reaching adrenal gland
  • spinal chord can also trigger large amounts of adrenaline
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43
Q

are endocrine glands duct-less

A

yes

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44
Q

how are hormones secreted by cell

A

by exocytosis

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45
Q

what hormone chemical group does adrenaline belong in

A

catecholemine hormone chemical group this is sympathomimetic

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46
Q

describe the structure of the adrenal cortex and where is it found
endocrine gland

A

-has capsule around outside,
-cortex in outer middle which is where hormones are secreted and medulla
-innermost is the medulla
»»>capillaries running through to take hormone
Found along perimeter of adrenal gland

47
Q

which hormone is secreted by adrenal cortex and what does it stimulate

A

cortisol- into immune system

stimulates hypothalamus to secrete CRH

48
Q

what does CRH stand for

A

corticotropin releasing hormone

49
Q

what does CRH do

A

stimulates pituitary gland to rekease ACTH

AdrenoCorticoTropin Hormone

50
Q

what does ACTH do

A

stimulates adrenal cortex to release cortisol

51
Q

what is function of cortisol

A
  • steroid hormone that helps regulate immune responses, metabolism and response to stress
52
Q

what does adrenaline bind to and what effect does this have

A

acts as a 1st messenger by binding to cell surface membrane of target cells which activates the inactive 2nd messenger adenyl cyclase (in liver cell muscle)

53
Q

what does adenyl cyclase do

A

Adenylyl cyclase converts ATP to 2nd messenger called cyclic AMP (adenosine monophosphate)

54
Q

what does cyclic AMP activate in a stress response situation and what does this lead to

A

activates protein kinases which changes glycogen > glucose from polysacc. to monosacc.
-therefore blood glucose concentration increases from cell to blood

55
Q

What is the whole process of the fight or flight response called

A

cascade amplification

56
Q

what is homeostasis

A

maintaining a constant internal environment

(maintainance of equillibrium optimal for functioning of as organism for reactions.

57
Q

what factors can effect homeostasis

A

temperature, pH, blood glucose, ion concentration with regard to nervous system (eg sodium and potassium ions)

58
Q

what regulations are usually involved in negative feedback systems

A

temperature and blood glucose

59
Q

what regulations are usually involved in positive feedback systems

A

fewer examples- blood clotting in childbirth and stimunlating of contractions

60
Q

briefly outline a negative feedback system

A

increase detected- responses lower levels= ideal conditions

decrease detected- responss raise levels = ideal conditions

61
Q

briefly outline a positive feedback system

A

change in conditions > responses reinforces change > conditions change > change in conditions again (amplifies)
eg) oxytocin in childbirth stimulates pituitary gland to stimulate contractions during birth which get more frequent.

62
Q

where are islets of langerhans found when looking through microscope?

A

among the enzyme secreting cells acini

typical section of pancreas seen will have around 6

63
Q

what do the blood vessels look like in the pancreas under microscope?

A

circular area within acini

64
Q

what do the branch of pancreatic ducts look like under microscope?

A

circular area within acini

65
Q

describe the distribution in the islets of langerhans

A

alpha around outside
beta more middle
capillaries where hormones taken

66
Q

what regulates the concentrations of hormones of the pancreas

A

negative feedback

67
Q

Describe what happens when there is an increase in blood glucose concentration in a NEGATIVE FEEDBACK

A
  • Beta cells secrete insulin»»
  • decreased glycogenesis (amino acids to glucose) decreased glycogenolysis,
  • increased lipogenesis in adipose cells particularly, increased uptake of glucose from blood
  • glycogenesis in liver and muscle (glucose»(phosphorylase)»Glycogen
  • lowers blood glucose
68
Q

Describe what happens when there is an decrease in blood glucose concentration in a NEGATIVE FEEDBACK

A

alpha cells secrete GLUCAGON

  • increase release of glucose from liver to blood
  • increased GLUCONEOgenesis
  • increased glycogenOLYSIS
  • decreased glycoGENESIS
  • raised concentration and reduces initial stimulus
69
Q

describe the classic homeostasis principle

A

stimulus is detected and regulation system controls effectors which produce response to cancel out stimulus

70
Q

typical blood glucose conc.

A

90-100mg 100cm^3

71
Q

EXTRA INFO just read through :)
Detail of what happens when there is an increase in blood glucose

secretion of insulin

A
  • glucose enters cell through channel protein and glucokinase phosphoralizes glucose to glucose-6-phosphate to pyruvate which makes mitochondria make loads of ATP/ADP
  • rise in ATP closes K+channel so more positive outside than inside. This depolarisation opens voltage gated Ca2+ channel over time becomes less negative to outside. positive inside and cAMP make vesicles fuse with membrane and leave via excytosis.
72
Q

what hormones does the pancreas secrete

A

insulin and glucagon into bloodstream

73
Q

where are alpha and beta cells found

A

islets of langerhans -exocrine secrete (duct) with many capillaries in the duct which allow exchange of oxygen for cells too as well as hormones

74
Q

what are acini

A

enzyme secreting cells

75
Q

what is the role of capillaries in ducts in islets of langerhans

A

capillaries in the duct which allow exchange of oxygen for cells too as well as hormones

76
Q

what is the role of the ribosomes in pancreas cells

A

translation of mRNA to synthesise proteins like insulin

77
Q

where is the only part of the body where the coding for insulin gene in a cell is “switched on”?

A

pancreas

210 bases

78
Q

how does insulin lower blood glucose concentration

A
  • inc. rate of absorption of glucose by cells (muscle+skeletal)
  • inc. respiration
  • inc rate of glycoGENOSIS stimulates liver to remove glucose»> glycogen
  • inc. glucose to fat conversion
  • inhibits release of glucagon
79
Q

which cells have insulin receptors on

A

virtualy all but red blood cells

80
Q

what bonds are formed when glucose to glycogen

A

condensation reaction&raquo_space;> glycosidic bonds

81
Q

briefly describe what happens when insulin binds to plasma membrane

A
  • binding changes 3D tert. structure of glucose transport protein channels
  • causes to open
  • sends intracellular chemical signal
  • signal triggers fusion of carrier containing vesicles on cell membrane (exocytosis)
  • also activates cells to convert glucose to glycogen+fat
82
Q

briefly describe what happens when glucagon binds to plasma membrane

A

-glucagon binds to receptor
-many ATP and G protein with adenyl cyclase form many molecules of cyclic AMP cAMP
-this phosphorylises inactive phosphorylase to active
-this makes glycogen hydrolyse to glucose and glucose is released into bloodstream
(similar to way ADRENALINE WORKS)

83
Q

which cells have glucagon receptors

A

liver and fat cells»> so are the only cells that respond to glucagon

84
Q

when glucose concentration returns to normal after being too low it is detected by____ when rises above level______….

A

alpha cells of pancreas

-alpha cells reduce secretion of glucagon (negative feedback)

85
Q

which cells secrete glucagon

A

alpha cells

-when blood glucose too low they detect

86
Q

what processes does glucagon causes

A
  • glycogenoLYSIS- liver breaks down glycogen
  • reduces amount of glucose absorbed by liver
  • increases gluconeogenesis- amino acids to glycerol into glucose in liver
87
Q

what is glycogenlysis

A

breakdown of glycogen

88
Q

what is glycolysis

A

breakdown of glucose for respiration (1st step of aerobic)

89
Q

what is glycogenesis

A

formation of glycogen

90
Q

what is glyconeogenesis

A

formation of glucose

91
Q

if body stopped eating what is metabolised instead of glucose?

A

metabolism of fat and eventually metabolises amino acids by breaking bonds to get energy

92
Q

what are the other names of type 1 diabetes

A
  • diabetes mellitus
  • juvenile onset diabetes
  • insulin dependent diabetes
93
Q

what could cause type 1

A

-autoimmune disease could attack Beta cells

but cause unknown for most

94
Q

symptoms of type 1

A
  • high blood glucose -glucose in urine
  • need to wee alot -excessive thirst
  • constant hunger -blurred vision
  • weight loss -tiredness
95
Q

how do you treat type 1

A

must regularly test blood sugar levels by pricking finger, drop of blood analysed by machine

  • based on this they work out how much insulin to inject
  • this causes glycogenesis so blood glucose levels decrease.
96
Q

what happens if you dont inject enough/ too much insulin

A

not enough insulin- hyperglycemia high blood glucose, unconscious/ death
too much insulin- hypoglycemia - low glucose level unconscious

97
Q

what is type 2 diabetes

and what causes the glucose to not be taken up

A

cannot effectively use insulin to lower blood glucose levels. Beta cells dont produce enough insulin OR persons body doesnt respond to insulin as insulin glycoprotein receptors so worn out from high sugar and lose responsiveness to insulin.

98
Q

what are the causes of type 2

A

excessive body fat, physical inactivity, excessive overeating of carbohydrates

99
Q

symptoms of type 2

A

similar to type 1 but less severe and develop SLOWLY over time as a result complications have already arisen before diagnosis

100
Q

how do you treat type 2 diabetes

A
  • regulate carb intake in diet -improve
  • exercise
  • encouraged to lose weight if overweight
  • sometimes drugs must be used that slow rate glucose is absorbed from intestine
101
Q

what is type 2 aka

A

non-insulin dependent diabetes

102
Q

what can type 2 diabetes lead to

A

heart disease, strokes, vision loss, kidney failure, non-traumatic lower limb amputations….u saw those feet :0

103
Q

where did insulin that was injected used to come from and why was this stopped

A

pigs and cows

  • difficult and expensive to extract
  • inethical
  • can cause allergic reactions
  • slightly different 3D shape
104
Q

where is insulin now sourced from and why is this better

A

genetically modified bacteria

  • in pure form so less likely allergic reaction
  • produced in higher quantities
  • comes from 1 clone
  • production cheaper and more ethical
105
Q

what will stem cell treatments for diabetes involve

A

could replace faulty beta cells in pancreatic islets as 1000 people receive pancreas transplants each year, but since demand higher than availability and bodies could reject transplant
-however only has less than 8% success rate.

106
Q

why is diabetes perfect candidate for stem cell research

A
  • as type 1 resulted from loss of single cell type and evidence shows relatively small islet cells can restore insulin production.
  • totipotent cells (from embryo or preserved umbilical chord cells) have potential to differentiate into any cell type.
107
Q

what are the advantages of potential stem cell therapy

A
  • doner availability no longer problem, stem cells would produce unlimited source of Beta cells
  • reduced liklihood of rejection problems as embryonic stem cells not rejected usually. SC can be made from somatic cell nuclear transfer
  • no longer need to inject
108
Q

what are the concerns of stem cells treatment for diabetes

A

-we still have limited control of growth and differentiation of stem cells so worries a precursor or stem-like cells transplanted could cause tumours

109
Q

what risk factors are associated with causing type 2

A

diet high in saturated fat and simple carbs
low dietary fibre
obesity

110
Q

what is insulin resistance

what does it lead to

A

when pancreas produces insulin but it isnt used effectively by body. muscle, fat and liver cells don’t respond to insulin.
-pancreas releases more insulin as if it is able to overcome insulin resistance, the pancreas stays within normal range. overtime pancreas cant keep up with insulin demand and blood glucose stays high

111
Q

why is high body mass associated with insulin resistance

A

fat deposited around internal organs, visceral fat, which secretes group of hormones called adipokines which could play role in development of insulin resistance

112
Q

why else could beta cells not produce insulin other than worn out (type 2)

A

could be genetic. 20 genes are responsible for type 2. one allele on 10th chromosome can reduce insulin secretion

113
Q

how do alpha glucose inhibitors treatment help with type 2

A

alpha glucodisase enzymes found on cell surface membranes of microvilli in ileum

  • they hydrolyse disaccarides to form monosaccharides such as glucose which is absorbed into blood
  • alpha glucosidase inhibitors are competitive and prevent disaccharides from entering the active site of enzyme. therefore less glucose is formed and blood gluocose conc. rises slowly after meals.
114
Q

how is insulin secretion controlled

A

1) at normal blood glucose lvls K+ channels in plasma membrane of Beta cells are open and K+ ions can diffuse out of the cell
2) when blood gluc rises it enters cell by a GLUCOSE TRANSPORTER
3) glucose metabolised in mitochondria to make ATP
4) ATP binds to K+ channels causing them to close becuase the channels are ATP sensitive K+ channels
5) K+ ions can no longer diffuse out of cell which makes potential difference of cell decrease to -30mV and depolarisation occurs
6) depolarisation causes voltage gated CALCIUM ion channels to open
7) Ca2+ ions enter cell and cause secretory vesicles to release insulin by exocytosis!!!