chapter 14- hormonal communication Flashcards
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
2
Q
what are endocrine glands? a group of ….
and what is their role? they secrete …
secrete where? ducts or no ducts?
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, the hormones travel to target cells and trigger a cell response eg production of proteins
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
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
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
6
Q
what are the 2 types of hormone
A
steroid and non steroid (amino acid based) hormones
7
Q
which type of hormone can go through the phospholipid bilayer
A
steroid
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
9
Q
hormones are released directly into the blood plasma and could be under ….. or …….. control
A
nervous or hormonal control
10
Q
How does the lipid solubility of hormones affect the location of their receptors?
A
the receptors for lipid soluble hormones are inside the cell
for non lipid soluble they are on the cell surface membrane outside the cell
11
Q
amino acid/non steroid hormones could also be made out of
inc egs
A
glycoproteins eg FSH
polypeptides eg ADH
proteins eg insulin
amines eg nor/adrenaline
tyrosine derivatives eg thyroxine from tyrosine
12
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
13
Q
what does thyroxine control
A
metabolic rate can be ana/catabolic
14
Q
what are steroid hormones based on +egs
A
cholesterol
sex hormones oestrogen and testosterone and the antiimflammatory drug dexamethasone
15
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)
16
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 CSM
cell signaling pathway using second messengers
transcription factors being activated in the nucleus and protein synthesis beginning (and translation)
17
Q
compare hormonal and neuronal communication
2 reasons and exp why
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
18
Q
hCG is produced by the placenta and affects many tissues, the susceptible cells have glycoprotein receptors on their csm, 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
19
Q
name the organ responsible for the secretion of FSH and LH
A
(anterior) pituitary gland
20
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
21
Q
which molecule does oestrogen interact with when it changes cell activity
A
DNA
22
Q
A
23
Q
where are the adrenal glands located
A
at the top of each kidney covered by a capsule
24
Q
what is the outside layer of the adrenal gland called
A
adrenal cortex
25
what is the middle layer (inside) layer of the adrenal gland called
the adrenal medulla
26
what type of hormones does the adrenal cortex produce
| s/ns
steroid based hormones that are vital for life
27
what is the adrenal cortex under the control of
hormones produced by the pituitary gland
28
What are the two main hormones produced by the adrenal cortex?
cortisol (a glucocorticoid), aldosterone (a mineralocorticoid), androgens (a group of sex hormones)
29
what three groups of hormones does the adrenal cortex release
glucocorticords
mineralocorticoirds
androgens
30
what do glucocorticoids do
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
ms: regulation of metabolism
31
what are mineralcorticoids
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 (Na+ K+ reabsorption in kidneys)
MS: control bp, water reabsorption, Na+/K+ ion reabsorption in the kidneys
32
what are androgens/what do they do
small amounts of sex hormones that have a small impact (compared to oestrogen which is in large amounts)
important for women after menopause
ms: regulation of sexual characteristics and cell growth
33
Which adrenal hormone is released in response to stress and helps regulate metabolism?
cortisol
34
Which adrenal hormone helps regulate blood pressure by controlling sodium and potassium concentration in the blood?
aldosterone
35
what type of hormones does the adrenal medulla release
| essential or non?
what based?
non essential amine based hormones
36
Which two adrenal hormones increase heart rate, increase blood pressure and widen/dilate pupils?
adrenaline and noradrenaline
37
when does the adrenal medulla release hormones
when the body is under stress
38
what is the adrenal medulla under the control of
| which ns?
the sympathetic nervous system
39
which homones does the adrenal medulla release
adrenaline and noradrenaline
40
in adrenalines response what acts as the 1st messenger
adrenaline
41
in adrenalines response what acts as the 2nd messenger
the g protein
42
in adrenalines response what activates the adeyl cyclase
the g protein
43
in adrenalines response what does the adeyl cyclase do
convert atp in camp
44
what is camp
cyclic adenosine monophosphate
45
what does camp do in the context of adrenaline
activates the enzyme that hydrolyses glycogen into glucose and opens the channel proteins that allow glucose out of the liver cell
when glucagon binds to its receptor it stimulates the conversion of atp to camp
46
hr can be increased by the hormone adrenaline
which binds to cardiac cells
describe how adrenaline binds to cardiac cells (2)
binds to receptor in csm (1)
which is a glycoprotein (1)
47
what effect does adrenaline have on the heart
interacts with beta adrenergic receptors to accelerate heart rate and increase force of myocardial contraction
48
what effect does adrenaline have on blood vessels
vasoconstriction in skin and gastrointestinal tract, vasodilation in the musculature, coronary and hepatic circulation
49
what is hepatic circulation
liver circulation
50
what effect does adrenaline have on respiratory tract
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
51
what affect does adrenaline have on the san
increases rate of firing impulses so that heart rate increases circulating blood more quickly
52
what affect does adrenaline have on a liver cell
increase in glycogenolysis (not breakdown of gly to glu thats too simple)
which makes glucose available for respiration
53
what affect does adrenaline have on erector muscles in the skin and why could this be beneficial
contraction of muscle causes hairs to be raises and so makes animal look larger and more aggressive
54
what effect does adrenaline have on gastrointestinal tract and liver
reduced gut mobility (less peristalsis) reduced blood flow to the gastrointestinal tract, reduced digestion, increased breakdown of glycogen to glucose in the liver
55
what effect does adrenaline have on central nervous system
activation of the sympathetic branch of the autonomic nervous system (fight/flight responses)
56
main functions of adrenaline
increases:
hr
bgc
blood flow to muscles
glycogenolysis
bp
air flow to alveoli
br
decreases blood flow to gut
pupil dilation
dilation of bronchioles
57
what effect does noradrenaline have on the brain
increases arousal, vigilance, formation and retrieval of memory, focuses attention, increases restlessness and anxiety
58
what effect does noradrenaline have on the eyes
increase in tear production, making the eyes more moist, pupil dilation through contraction of the iris
59
what effect does noradrenaline have on the heart
increase in the amount of blood pumped (same as adrenaline) so hr increases
60
what effect does noradrenaline have on adipose tissue
increase in calories consumed/respiration of lipids to provide body heat (non shivering thermogenesis)
61
what effect does noradrenaline have on blood vessels
vasoconstriction of blood vessels in particular area (gut) to bring an increase in blood pressure (same as adrenaline)
62
what effect does noradrenaline have on the kidneys
release of renin and retention of sodium in the bloodstream and causes a rise in blood pressure
63
what types of gland are there in the pancreas
exocrine and endocrine
64
what are exocrine glands and what do they do in the pancreas
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
65
what are pancreatic juices
an alkaline fluid that neutralises the acidic pH from the stomach to make it optimum for the enzymes in the pancreas (amylase, proteases, lipase)
66
what are endocrine glands and what do they do in the pancreas
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
67
what is the duodenum
small intestine
68
what type of hormone is insulin
protein based/non steroid
69
is insulin an anabolic or catabolic hormone
anabolic
70
what does insulin do
regulates the metabolism of carbohydrates by promoting the absorption of glucose (into glycogen) from the blood into liver cells and skeletal muscle
71
what type of hormone is glucagon
a polypeptide based hormone
72
what does glucagon do
works to raise the concentration of glucose in the blood
73
is glucagon a catabolic or anabolic hormone
catabolic
74
what builds glucose into glycogen
insulin
75
what breaks glycogen into glucose
glucagon
76
what is pancreatic acini
exocrine tissue
a berry-like collection of cells that drain digestive enzymes into a duct to small intestine
77
through a microscope what do acini look like
usually darker
78
what other glands are acini found in
the stomach
sebaceous glands of the scalp (oil)
salivary glands of the tongue
mammary glands of the breasts
79
what are the islets of langerhans
endocrine tissue
spherical cluster of cells
usually lighter stained
they produce and secrete hormones
80
Where in the body are the Islets of Langerhans found?
pancreas
81
what 2 types of cells make up islets of langerhan
alpha and beta
82
what are the alpha cells of IOL (4)
they produce and secrete glucagon
they are larger and more numerous than beta cells
often stained pink in differential staining
83
what are beta cells of IOL (4)
produce and secrete insulin
smaller and less numerous than alpha
often stained blue in differential staining
84
what is the homeostatic norm of blood glucose concentration
90mg per 100cm-3 blood or 90mg dL-1
85
what are the 3 processes that increase blood glucose concentration
diet/eating
increase in glycogenolysis
increase in gluconeogenesis
86
how can diet increase blood glucose conc
eating and digesting carbohydrates ie polysaccharides (slow release), disaccharides or monosaccharides (glucose straight into blood stream)
87
how can an increase in glycogenolysis increase blood glucose concentration/what is it
breaking down glycogen into the glucose in the liver and muscle cells
releasing that glucose into the blood incr the conc
88
how can an increase in gluconeogenesis increase blood glucose concentration and what is it
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)
89
when is gluconeogenesis used
in extreme circumstances
90
why is glycogen branched
for faster breakdown as there is multiple locations for glucogenesis
91
what are the 2 processes to decrease blood glucose concentration
respiration and glycogenesis
92
how does respiration decrease blood glucose concentration
glucose in the blood is used for cellular respiration to produce atp
demand for atp increases then drain on blood glucose increases
93
what is glycogenesis and how does it decrease blood glucose concentration
it is the production of glycogen
blood glucose is converted into glycogen and stored in liver and muscle cells
94
what is the enzyme thats responsible for all the condensation reactions that build glycogen making the 1,4 and 1,6 glycosidic bonds
glycogen synthase
95
what does glycogenesis follow on from in the cori cycle
glycolysis it takes the 2 lactate and the 2 pyruvate and 6 atp to make glucose
96
what happens when blood glucose concentrations get too high
the responses to insulin
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
97
explain why there is a delay in the increase of insulin concentration following the increase in blood glucose concentration (2)
increase in blood sugar is detected by beta cells
it takes time for depolarisation in beta cells to occur.
time is needed for the beta cells to produce and release insulin
98
virtually all cells have insulin receptors on in their cell surface membrane but the main response comes from
liver cells and skeletal muscle cells
99
on a graph of blood glucose conc/insulin levels before during and after a meal (straight low > high peak >low drop > straight low)
the straight line bits are over simplified , describe and explain how these concentration should be represented on the graph accurately (4)
line should not be straight/should fluctuate (1)
glucose and insulin levels fluctuate (1)
insulin levels should rise and fall after glucose (1)
glucose level maintained around a set point/return to normal
ref to negative feeback/homeostasis
100
what is bad about cells having too much glucose
it will make water diffuse out of the cell where there is a lower conc of glucose
the cell will become crenated
101
what happens if glucose is too low
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.
102
what cells have glucagon receptors in their csm
liver, fat/adipose tissue cells
103
which 2 hormones have the same cell surface receptor (intrinsic protein in liver cells) and what does this mean
glucagon and adrenaline
means they have similar shapes
104
how does glucose leave the cell
via facilitated diffusion and goes into the blood to eg myocytes
105
what is the stimulus for the control of insulin secretion in a resting state eg fasting
low glucose (detected beta cells)
106
when controlling insulin secretion a resting state what happens so the levels of adp and atp
atp increases so adp increases as there is less cellular respiration to generate atp
107
when controlling insulin secretion a resting state what happens to the potassium ion channels and what does this cause
they open so K+ leave making the inside more negative relative to the outside, this makes the membrane become hyperpolarised
108
when controlling insulin secretion a resting state, the membrane becomes hyperpolarised causing .
the voltage gated Ca2+ channels to close
109
when controlling insulin secretion a resting state, the voltage gated Ca2+ channels to close which means that
the vesicles containing insulin are not stimulated to move towards/fuse with the scm so no insulin doesnt exit the beta cell
110
what is the stimulus for controlling insulin at not a resting state
high glucose=glucose stimulated state
111
when controlling insulin secretion a glucose-stimulated state what happens so the levels of adp and atp
adp increases as atp increase because the glucose is respired
112
when controlling insulin secretion a glucose-stimulated state what happens to the potassium ion channels and what does this cause
they close so inside cant be polarised so the membrane becomes depolarised
113
when controlling insulin secretion at a glucose-stimulated state the membrane becomes depolarised meaning
the voltage gated Ca2+ channels open and Ca2+ enter
114
when controlling insulin secretion at a glucose-stimulated state, the Ca2+ cause..
the vesicles containing insulin to move to and fuse with the csm and insulin is released into the blood in exocytosis
115
after the initial release of insulin from the beta cell insulin secretion continues even when there is no further glucose intake
suggest and explain why the cell continues to secrete insulin (2)
still secreted as long as bgc remains high/er than normal
atp still present so K+ channels remain closed
still triggered by Ca2+
116
diabetes mellitus is a group of ........ disorders in which there are high blood .... levels over a ....... period
metabolic
glucose
prolonged
117
symptoms of high blood glucose levels
frequent urination, increased thirst, increased hunger
118
serious long term complication of high glucose levels/diabetes
cvd, stroke, chronic kidney disease, foot ulcers, damage to the eyes
119
acute complications of high glucose levels/diabetes
diabetes ketoacidoisis, Hyperosmolar hyperglycemic state , death
120
what is type 1 diabetes
an inability of the beta cells to produce insulin
121
when is type 1 diabetes usually developed/noticed
early onset in childhood (juvienile onset diabetes)
122
In addition to a controlled diet, how is Type 1 diabetes typically treated?
insulin injection
123
Type 1 diabetes is treated with insulin injections. Where is this insulin currently obtained from?
In the past, insulin was derived from animals. However, the extraction process was expensive and could cause allergic reactions. As a result, we now obtain insulin from genetically modified bacteria.
124
what is the cause of type 1 diabetes
unknown but could be autoimmune response, attacking beta cells, receptors seen as foreign
125
what is type 2 diabetes
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
126
risk factors of type 2 diabetes
excess body mass, lack of exercise, overeating of refined carbohydrates
127
what are the 2 ways insulin have been produced
isolation of pig/cow insulin
genetically engineered human insulin
128
what is wrong with isolated pig/cow insulin
it is a difficult, expensive process, caused allergic reactions in some diabetics
129
what was genetically engineered human insulin first come from
E.coli and then it was biosynthetic
130
transplant and injections for diabetes
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
131
what is the potential use of stem cells in diabetes treatment
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
132
advantages of using stem cells in diabetes treatment
overcomes donor organ problem
reduced cell transplant rejection
insulin injections become redundant
133
disadvantages of using stem cells in diabetes treatment
destruction of human embryos (problematic)
injected stem cells could become cancerous tumors
134
which type of diabetes is insulin depended diabetes and why
type 1 as they need insulin injections
135
the risk for which type of diabetes increases with age
type 2
136
the control of heart rate is under which nervous system
the autonomic nervous system
137
what part of the ans/brain is responsible for controlling hr and what exactly is it
medulla oblongata, a cone shaped neuronal mass responsible for autonomic (involuntary) functions eg vomiting and sneezing
138
where is the medulla oblongata located and what does it connect
in the brainstem connecting the higher levels of the brain to the spinal cord
139
what control centres does the medulla oblongata contain and so which autonomic functions does it control
cardiac, respiratory, vomiting, vasomotor centres and so deal with the autonomic functions of breathing, hr and bp
140
what is normal bp and what does this mean
120/80 mmHg
120 is systolic pressure from the ventricles so is larger
80 is diastolic pressure and so is lower
141
what is the name of the control centre which increases heart rate and how does it work
cardio acceleratory centre
increases hr through sympathetic NS using the accelerator nerve connected to the SAN
142
which control centre decreases hr and how does it work
inhibitory centre
decreases hr through the parasympathetic NS using the vagus nerve connected to the SAN
143
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
heart rate is controlled by the autonomic nervous system
parasympathetic/vagus nerve reduces heart rate
heart rate reduces by 30bpm approx
144
what are the 2 sets of receptors in blood vessels
baroreceptors and chemoreceptors
145
what do baroreceptors detect and where are they located
detect changes in blood pressure, located in aorta, vena cava, carotid arteries
146
what do chemoreceptors detect and where are they located
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
147
what happens when blood pressure is too high
and too low
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
148
what happens when blood co2 is too high and what is it caused by
and too low
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
149
what hormones influence/control hr by affecting the SAN directly and what affect is it
adrenaline- increases hr
noradrenaline- increases hr
150
which glands have one of the largest blood supplies and what is it
one of the biggest blood supply rates per gram of tissue of any organ, up to 60 small arteries may enter each gland
151
in the f+f r what is a "threat" detected by and what does this cause communication between
detected by ANS
hypothalamus communicated with SNS and adrenal-cortical system
152
what is the difference in sns and a-c s and what do they work together for
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
153
what does the sns do in the f/f r
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
154
suggest long term adverse effects of continued exposure to stress on body function
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
155
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)
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
156
157
what leads to type 2 diabetes
Cell-surface membrane receptors lose their sensitivity to insulin.
The pancreas stops producing enough insulin.
158
