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alevel biology ocr > chapter 14- hormones > Flashcards

chapter 14- hormones Flashcards

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1
Q

what is the endocrine system

A

it works alongside the neuronal system to react to changes in the body or environment and bring about the most appropriate response

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2
Q

what are endocrine glands

A

they make up the endocrine system

a group of specialised cells that secrete hormones

they secrete them directly into the blood and have no ducts

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3
Q

describe what is meant by an endocrine gland (2 marks)

A

a group of cells that secretes/release/produces hormones directly into the bloodstream

allow doesnt have ducts

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4
Q

what is a hormone

A

is any member of a class of signaling molecules produced by glands in multicellular organisms that are transported by the circulatory system to target distant organs to regulate physiology and behaviour

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5
Q

the pancreas contains endocrine glands such as the islets of langerhans, it also contains cells that produce digestive enzymes

suggest why the cells that produce digestive enzymes are describe as exocrine rather than endocrine (1)

A

because digestive enzymes are released into ducts/not released directly into the blood

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6
Q

what are the 2 types of hormone

A

steroid and non steroid (amino acid based) hormones

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7
Q

which type of hormone can go through the phospholipid bilayer

A

steroid

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8
Q

what are non steroid hormones made out of and why is that beneficial

A

they are made out of proteins/amino acids that have a specific 3D shape with R groups that

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9
Q

hormones are released directly into the blood plasma and could be under ….. or …….. control

A

nervous or hormonal control

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10
Q

amino acid/non steroid hormones could also be made out of

A

glycoproteins eg FSH
polypeptides eg ADH
proteins eg insulin
amines eg nor/adrenaline
tyrosine derivatives eg thyroxine from tyrosine

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11
Q

how can amines make non steroid hormones

A

the breakdown of amino acids releases amines

eg decaying fish smells of trimethylamine

many neurotransmitters are also amines inc adrenaline and noradrenaline

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12
Q

what does thyroxine control

A

metabolic rate can be ana/catabolic

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13
Q

what are steroid hormones based on +egs

A

cholesterol
sex hormones oestrogen and testosterone and the antiimflammatory drug dexamethasone

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14
Q

how do steroid hormones work

A

they are lipid soluble so dissolve through cell surface membrane

they enter the cell

bind to receptor protein in the nucleus

mRNA synthesis (first step of protein synthesis)

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15
Q

how do non steroid based hormones work

A

they are water soluble so cannot pass through cell surface membrane

they bind to receptors on SSM

cell signaling pathway using second messengers

transcription factors being activated d in the nucleus and protein synthesis beginning (and translation)

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16
Q

compare hormonal and neuronal communication

A

hormones are not released directly into their target cells so the process is slower and more general

hormones are not broken down as quickly my neurotransmitters so there is a longer lasting effect

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17
Q

hCG is produced by the placenta and affects many tissues, the susceptible cells have glycoprotein receptors on their scm, these are complementary to the shape of the hCG molecules

what can be concluded from this info (3)

A

hCG is not a lipid based hormone/it is a peptide hormone
hCG binds to cells surface receptor
cell signalling is involved in the action of hCG
hCG uses cAMP/second messenger to bring about response in the cell

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18
Q

name the organ responsible for the secretion of FSH and LH

A

(anterior) pituitary gland

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19
Q

oestrogen is a steroid hormone others like FSH and LH are glycoproteins

oestrogen receptors are found in the cytoplasm of target cells
FSH and LH receptors are found on the CSM of target cells

suggest why (2)

A

LH cannot pass cross the SCM, oestrogen can co the cross membrane/phospholipid bilayer

oestrogen is lipid soluble, FSH and LH are not lipid soluble

bilayer is hydrophobic

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20
Q

which molecule does oestrogen interact with when it changes cell activity

A

DNA

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21
Q
A
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22
Q

where are the adrenal glands located

A

at the top of each kidney covered by a capsule

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23
Q

what is the outside layer of the adrenal gland called

A

adrenal cortex

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24
Q

what is the middle layer (inside) layer of the adrenal gland called

A

the adrenal medulla

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25
Q

what type of hormones does the adrenal cortex produce

A

steroid based hormones that are vital for life

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26
Q

what is the adrenal cortex under the control of

A

hormones produced by the pituitary gland

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27
Q

What are the two main hormones produced by the adrenal cortex?

A

cortisol, aldosterone

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28
Q

what three groups of hormones does the adrenal cortex release

A

glucocorticords
mineralocorticoirds
androgens

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29
Q

what do glucocorticoids do

A

like cortisol
they regulate metabolism and coordinate how fats, carbs and proteins are converted to energy and regulate bp and cv function in response to stress

like corticosterone + cortisol is linked with the immune response and decreasing inflammation

the release is controlled by the hypothalamus

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30
Q

what are mineralcorticoids

A

mediated by signals triggered by the kidney

eg aldosterone
controls bp, maintain and balance conc of water and salt in the blood and body fluid, electrolyte balance
MS: control bp, water reabsorption, Na+/K+ ion reabsorption in the kidneys

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31
Q

what are androgens

A

small amounts of sex hormones that have a small impact (compared to oestrogen which is in large amounts)

important for women after menopause

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32
Q

Which adrenal hormone is released in response to stress and helps regulate metabolism?

A

cortisol

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33
Q

Which adrenal hormone helps regulate blood pressure by controlling sodium and potassium concentration in the blood?

A

aldosterone

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34
Q

what type of hormones does the adrenal medulla release

A

non essential amine based hormones

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35
Q

Which two adrenal hormones increase heart rate, increase blood pressure and widen pupils?

A

adrenaline and noradrenaline

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36
Q

when does the adrenal medulla release hormones

A

when the body is under stress

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37
Q

what is the adrenal medulla under the control of

A

the sympathetic nervous system

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38
Q

which homones does the adrenal medulla release

A

adrenaline and noradrenaline

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39
Q

in adrenalines response what acts as the 1st mesenger

A

adrenaline

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40
Q

in adrenalines response what acts as the 2nd mesenger

A

the g protein

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41
Q

in adrenalines response what activates the adeyl cyclase

A

the g protein

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42
Q

in adrenalines response what does the adeyl cyclase do

A

convert atp in camp

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43
Q

what is camp

A

cyclic adenosine monophosphate

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44
Q

what does camp do

A

activates the enzyme that hydrolyses glycogen into glucose and opens the channel proteins that allow glucose out of the liver cell

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45
Q

hr can be increased by the hormone adrenaline
which binds to cardiac cells

describe how adrenaline binds to cardiac cells (2)

A

binds to receptor in csm (1)
which is a glycoprotein (1)

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46
Q

what effect does adrenaline have on the heart

A

interacts with beta adrenergic receptors to accelerate heart rate and increase force of myocardial contraction

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47
Q

what effect does adrenaline have on blood vessels

A

vasoconstriction in skin and gastrointestinal tract, vasodilation in the musculature, coronary and hepatic circulation

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48
Q

what is hepatic circulation

A

liver circulation

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49
Q

what effect does adrenaline have on respiratory tract

A

increased respiratory rate and bronchodilation (like an epi pen)

smooth muscle in bronchioles relaxes which makes bronchioles dilate and allow more oxygen to reach the blood

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50
Q

what affect does adrenaline have on the san

A

increases rate of firing impulses so that heart rate increases circulating blood more quickly

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51
Q

what affect does adrenaline have on a liver cell

A

increase in glycogenolysis (not breakdown of gly to glu thats too simple)
which makes glucose available for respiration

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52
Q

what affect does adrenaline have on erector muscles in the skin

A

contraction of muscle causes hairs to be raises and so makes animal look larger and more aggressive

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53
Q

what effect does adrenaline have on gastrointestinal tract and liver

A

reduced gut mobility (less peristalsis) reduced blood flow to the gastrointestinal tract, reduced digestion, increased breakdown of glycogen to glucose in the liver

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54
Q

what effect does adrenaline have on central nervous system

A

activation of the sympathetic branch of the autonomic nervous system (fight/flight responses)

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55
Q

what effect does noradrenaline have on the brain

A

increases arousal, vigilance, formation and retrieval of memory, focuses attention, increases restlessness and anxiety

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56
Q

what effect does noradrenaline have on the eyes

A

increase in tear production, making the eyes more moist, pupil dilation through contraction of the iris

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57
Q

what effect does noradrenaline have on the heart

A

increase in the amount of blood pumped (same as adrenaline)

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58
Q

what effect does noradrenaline have on adipose tissue

A

increase in calories consumed/respiration of lipids to provide body heat (non shivering thermogenesis)

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59
Q

what effect does noradrenaline have on blood vessels

A

vasoconstriction of blood vessels in particular area (gut) to bring an increase in blood pressure (same as adrenaline)

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60
Q

what effect does noradrenaline have on the kidneys

A

release of renin and retention of sodium in the bloodstream and causes a rise in blood pressure

61
Q

what types of gland are there in the pancreas

A

exocrine and endocrine

62
Q

what are exocrine glands and what do they do in the pancreas

A

they HAVE DUCTS
produce digestive enzymes for the small intestine (amylase, proteases, lipase)

production of pancreatic juices

the enzymes of PJs are secreted into a branching pattern of ducts that drain into the main pancreatic duct which drains into the duodenum

63
Q

what are pancreatic juices

A

an alkaline fluid that neutralises the acidic pH from the stomach to make it optimum for the enzymes in the pancreas (amylase, proteases, lipase)

64
Q

what are endocrine glands and what do they do in the pancreas

A

produce the hormones insulin and glucagon (they have an antagonistic effect), they are released directly into the blood stream into blood vessels going directly through the pancreas

NO DUCTS

65
Q

what is the duodenum

A

small intestine

66
Q

what type of hormone is insulin

A

protein based/non steroid

67
Q

is insulin an anabolic or catabolic hormone

A

anabolic

68
Q

what does insulin do

A

regulates the metabolism of carbohydrates by promoting the absorption of glucose (into glycogen) from the blood into liver cells and skeletal muscle

69
Q

what type of hormone is glucagon

A

a polypeptide based hormone

70
Q

what does glucagon do

A

works to raise the concentration of glucose in the blood

71
Q

is glucagon a catabolic or anabolic hormone

A

catabolic

72
Q

what builds glucose into glycogen

A

insulin

73
Q

what breaks glycogen into glucose

A

glucagon

74
Q

what is pancreatic acini

A

exocrine tissue
a berry-like collection of cells that drain digestive enzymes into a duct to small intestine

75
Q

through a microscope what do acini look like

A

usually darker

76
Q

what other glands are acini found in

A

the stomach
sebaceous glands of the scalp (oil)
salivary glands of the tongue
mammary glands of the breasts

77
Q

what are the islets of langerhans

A

endocrine tissue
spherical cluster of cells
usually lighter stained

they produce and secrete hormones

78
Q

Where in the body are the Islets of Langerhans found?

A

pancreas

79
Q

what 2 types of cells make up islets of langerhan

A

alpha and beta

80
Q

what are the alpha cells of IOL (4)

A

they produce and secrete glucagon
they are larger and more numerous than beta cells

often stained pink in differential staining

81
Q

what are beta cells of IOL (4)

A

produce and secrete insulin
smaller and less numerous than alpha
often stained blue in differential staining

82
Q

what is the homeostatic norm of blood glucose concentration

A

90mg per 100cm-3 blood or 90mg dL-1

83
Q

what are the 3 processes that increase blood glucose concentration

A

diet/eating
increase in glycogenolysis
increase in gluconeogenesis

84
Q

how can diet increase blood glucose conc

A

eating and digesting carbohydrates ie polysaccharides (slow release), disaccharides or monosaccharides (glucose straight into blood stream)

85
Q

how can an increase in glycogenolysis increase blood glucose concentration/what is it

A

breaking down glycogen into the glucose in the liver and muscle cells

releasing that glucose into the blood incr the conc

86
Q

how can an increase in gluconeogenesis increase blood glucose concentration and what is it

A

production of new glucose from non carb sources eg in the liver making glucose from glycerol (from fats digested or adipose tissue) and amino acids (that can be made)

87
Q

when is gluconeogenesis used

A

in extreme circumstances

88
Q

why is glycogen branched

A

for faster breakdown as there is multiple locations for glucogenesis

89
Q

what are the 2 processes to decrease blood glucose concentration

A

respiration and glycogenesis

90
Q

how does respiration decrease blood glucose concentration

A

glucose in the blood is used for cellular respiration to produce atp
demand for atp increases then drain on blood glucose increases

91
Q

what is glycogenesis and how does it decrease blood glucose concentration

A

it is the production of glycogen
blood glucose is converted into glycogen and stored in liver and muscle cells

92
Q

what is the enzyme thats responsible for all the condensation reactions that build glycogen making the 1,4 and 1,6 glycosidic bonds

A

glycogen synthase

93
Q

what does glycogenesis follow on from in the cori cycle

A

glycolysis it takes the 2 lactate and the 2 pyruvate and 6 atp to make glucose

94
Q

what happens when blood glucose concentrations get too high

the responses to insulin

A

beta cells in the islets of langherans detect a change and release insulin into the blood stream (endocrine)

glucose transport channel proteins open and glucose enters the cells by facilitated diffusion and blood glucose conc is lowered

insulin going into the receptor stimulates the vesicle for the glucose to travel towards the scm to get the glucose

increase respiratory rate
increase rate of glycogenesis in liver cells
increase rate of glucose conversion to fat by adipose tissue
inhibiting the release of glucagon by the alpha cells in the islets of langerhans

95
Q

virtually all cells have insulin receptors on in their cell surface membrane but the main response comes from

A

liver cells and skeletal muscle cells

96
Q

what is bad about cells having too much glucose

A

it will make water diffuse out of the cell where there is a lower conc of glucose
the cell will become crenated

97
Q

what happens if glucose is too low

A

alpha cells detect the change and release glucagon into the bloodstream

in liver cells: glucogenesis increases in rate and the glucose is released into the blood

increase in rate of gluconeogenesis and glucose is released into the blood

inhibits absorption of glucose from the blood by liver cells

inhibiting glycolysis in the liver

glucagon also decreases fatty acid synthesis in adipose tissue and the liver and promotes lipolysis causing them to release fatty acids into the blood where they can be catabolised to release energy in tissues such as skeletal muscle when required.

98
Q

what cells have glucagon receptors in their csm

A

liver, fat/adipose tissue cells

99
Q

which 2 hormones have the same cell surface receptor (intrinsic protein in liver cells) and what does this mean

A

glucagon and adrenaline

means they have similar shapes

100
Q

how does glucose leave the cell

A

via facilitated diffusion and goes into the blood to eg myocytes

101
Q

what is the stimulus for the control of insulin secretion in a resting state eg fasting

A

low glucose (detected beta cells)

102
Q

when controlling insulin secretion a resting state what happens so the levels of adp and atp

A

atp increases so adp increases as there is less cellular respiration to generate atp

103
Q

when controlling insulin secretion a resting state what happens to the potassium ion channels and what does this cause

A

they open so K+ leave making the inside more negative relative to the outside, this makes the membrane become hyperpolarised

104
Q

when controlling insulin secretion a resting state, the membrane becomes hyperpolarised causing .

A

the voltage gated Ca2+ channels to close

105
Q

when controlling insulin secretion a resting state, the voltage gated Ca2+ channels to close which means that

A

the vesicles containing insulin are not stimulated to move towards/fuse with the scm so no insulin doesnt exit the beta cell

106
Q

what is the stimulus for controlling insulin at not a resting state

A

high glucose=glucose stimulated state

107
Q

when controlling insulin secretion a glucose-stimulated state what happens so the levels of adp and atp

A

adp increases as atp increase because the glucose is respired

108
Q

when controlling insulin secretion a glucose-stimulated state what happens to the potassium ion channels and what does this cause

A

they close so inside cant be polarised so the membrane becomes depolarised

109
Q

when controlling insulin secretion at a glucose-stimulated state the membrane becomes depolarised meaning

A

the voltage gated Ca2+ channels open and Ca2+ enter

110
Q

when controlling insulin secretion at a glucose-stimulated state, the Ca2+ cause..

A

the vesicles containing insulin to move to and fuse with the csm and insulin is released into the blood in exocytosis

111
Q

diabetes mellitus is a group of …….. disorders in which there are high blood …. levels over a ……. period

A

metabolic
glucose
prolonged

112
Q

symptoms of high blood glucose levels

A

frequent urination, increased thirst, increased hunger

113
Q

serious long term complication of high glucose levels/diabetes

A

cvd, stroke, chronic kidney disease, foot ulcers, damage to the eyes

114
Q

acute complications of high glucose levels/diabetes

A

diabetes ketoacidoisis, Hyperosmolar hyperglycemic state , death

115
Q

what is type 1 diabetes

A

an inability of the beta cells to produce insulin

116
Q

when is type 1 diabetes usually developed/noticed

A

early onset in childhood (juvienile onset diabetes)

117
Q

what is the cause of type 1 diabetes

A

unknown but could be autoimmune response, attacking beta cells, receptors seen as foreign

118
Q

what is type 2 diabetes

A

an inability to use insulin to control blood glucose effectively

beta cells do not produce enough insulin or body cells do not respond to insulin properly (glycoprotein insulin receptor on csm doesnt work properly) so dont take up glucose so it is left in the blood stream

often insulin receptors on target cells do not produce the correct response in the cells metabolism

often diagnosed after the onset of the disease
used to be late onset (40+) but now occurs in children

119
Q

risk factors of type 2 diabetes

A

excess body mass, lack of exercise, overeating of refined carbohydrates

120
Q

what are the 2 ways insulin have been produced

A

isolation of pig/cow insulin
genetically engineered human insulin

121
Q

what is wrong with isolated pig/cow insulin

A

it is a difficult, expensive process, caused allergic reactions in some diabetics

122
Q

what was genetically engineered human insulin first come from

A

E.coli and then it was biosynthetic

123
Q

transplant and injections for diabetes

A

pancreas transplants are 80% successful in eliminating the symptoms of diabetes but there are never enough donors

injection of harvested beta cells have an 8% success rate and the immunosuppressant drugs used in the cell transplant eventually stops the cells producing insulin

124
Q

what is the potential use of stem cells in diabetes treatment

A

stem cells could be used to make beta cells for type 1 diabetes, likely to come from human embryos or umbilical cord stem cells, each group of stem cells could treat many patients

125
Q

advantages of using stem cells in diabetes treatment

A

overcomes donor organ problem
reduced cell transplant rejection
insulin injections become redundant

126
Q

disadvantages of using stem cells in diabetes treatment

A

destruction of human embryos (problematic)
injected stem cells could become cancerous tumors

127
Q

which type of diabetes is insulin depended diabetes and why

A

type 1 as they need insulin injections

128
Q

the risk for which type of diabetes increases with age

A

type 2

129
Q

the control of heart rate is under which nervous system

A

the autonomic nervous system

130
Q

what part of the ans/brain is responsible for controlling hr and what exactly is it

A

medulla oblongata, a cone shaped neuronal mass responsible for autonomic (involuntary) functions eg vomiting and sneezing

131
Q

where is the medulla oblongata located and what does it connect

A

in the brainstem connecting the higher levels of the brain to the spinal cord

132
Q

what control centres does the medulla oblongata contain and so which autonomic functions does it control

A

cardiac, respiratory, vomiting, vasomotor centres and so deal with the autonomic functions of breathing, hr and bp

133
Q

what is normal bp and what does this mean

A

120/80 mmHg
120 is systolic pressure from the ventricles so is larger
80 is diastolic pressure and so is lower

134
Q

what is the name of the control centre which increases heart rate and how does it work

A

cardio acceleratory centre
increases hr through sympathetic NS using the accelerator nerve connected to the SAN

135
Q

which control centre decreases hr and how does it work

A

decreases hr through the parasympathetic NS using the vagus nerve connected to the SAN

136
Q

normal resting hr is approx 70bpm. cutting the parasympathetic nerve to heart increases this to approx 100bpm, suggest 2 concs that could be made from this obs about the control of resting hr in normal humans

A

heart rate is controlled by the autonomic nervous system

parasympathetic/vagus nerve reduces heart rate

heart rate reduces by 30bpm approx

137
Q

what are the 2 sets of receptors in blood vessels

A

baroreceptors and chemoreceptors

138
Q

what do baroreceptors detect and where are they located

A

detect changes in blood pressure, located in aorta, vena cava, carotid arteries

139
Q

what do chemoreceptors detect and where are they located

A

located in aorta, carotid arteries, medulla oblongata, detect changes in blood CO2 conc by measuring blood pH

CO2 travels as carbonic acid and H+ are released decreasing the pH

140
Q

what happens when blood pressure is too high

and too low

A

baroreceptors detect it is too high
nervous impulses sent to MO
MO sends nervous impulses along parasympathetic neurones to the SAN
heart responds by decreasing heart rate
bp is reduced

too low=opposite

141
Q

what happens when blood co2 is too high and what is it caused by

and too low

A

caused by increased muscular/metabolic activity so more co2 produced by tissues from increased resp

blood pH is lowered

SAN increases hr

increased blood flow removed co2 faster

co2 level returns to normal

too low=opposite

142
Q

what hormones influence/control hr by affecting the SAN directly and what affect is it

A

adrenaline- increases hr
noradrenaline- increases hr

143
Q

which glands have one of the largest blood supplies and what is it

A

one of the biggest blood supply rates per gram of tissue of any organ, up to 60 small arteries may enter each gland

144
Q

in the f+f r what is a “threat” detected by and what does this cause communication between

A

detected by ANS
hypothalamus communicated with SNS and adrenal-cortical system

145
Q

what is the difference in sns and a-c s and what do they work together for

A

sympathetic ns: uses neuronal pathways to initiate body reactions
adrenal-cortical s: hormones in the bloodstream

the combined effort of the 2 systems results in the fight or flight response

146
Q

what does the sns do in the f/f r

A

sends nervous impulses to glands and smooth muscles and tells the adrenal medulla to release adrenaline and noradrenaline into the bloodstream these increase hr for eg

147
Q

suggest long term adverse effects of continued exposure to stress on body function

A

prolonged high bp can lead to cv problems

prolonged high bgl can lead to problems with bgl regulation/diabetes

suppression of the immune system can lead to susceptibility to disease or infection

148
Q

gestational diabetes is a medical condition that affects pregnant women, it results in high levels of glucose in the blood even tho the woman produces normal levels of insulin. what type of diabetes is it similar to ? (2)

A

type 2

insulin still produced/b cells still working

liver cells no longer respond to insulin, fewer or damaged receptors

if type 1 then would not produce normal levels of insulin

149
Q
A

alevel biology ocr (27 decks)

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