hormonal communication Flashcards

1
Q

examples of glands in exocrine system

A

salivary glands (secrete saliva, containing amylase w cofactor Cl-)
liver (secretes bile, which emulsifies fats & neutralises stomach acid)
stomach (secretes gastric juice)
pancreas (secretes pancreatic juice from acinar cells)

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2
Q

examples of glands in endocrine system

A

pituitary gland (secretes ADH, which increases permeability of CD to water so increase reabsorption)
thyroid (secretes thyroxine, which regulates metabolic rate: fight/flight)
adrenal gland (secretes adrenaline and noradrenaline)
pancreas (secretes insulin and glucagon to lower or increase BGL)
ovaries (secrete oestrogen and progesterone)
testes (secrete testosterone)

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3
Q

what do glands do

A

secrete a substance

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4
Q

exocrine vs endocrine

A

exocrine: secretes substances e.g. enzymes into ducts, which open out into the body cavity
endocrine: ductless, secretes hormones directly into the blood

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5
Q

hormone definition

A

chemical messenger
produced by endocrine gland
travels in blood plasma
bind to specific target cells in organ(s)/tissue(s)
can reach whole body and effective in minute quantities

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6
Q

2 types of hormones

A

non steroid
steorid

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7
Q

describe properties of non-steroid hormones

A

water-soluble/hydrophilic/polar
do NOT enter the cell bc not lipid soluble
bind to specific, complementary receptors on cell surface membrane

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8
Q

examples of non steroid hormones

A

GLOBULAR PROTEINS eg insulin, ADH, glucagon
AMINE e.g. adrenaline, noradrenaline

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9
Q

properties of steroid hormones

A

lipid-soluble, derived form cholesterol: carried by plasma proteins
diffuse through phospholipid bilayer and bind to intracellular complementary receptors in the cytoplasm
switch on/off genes to cause response

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10
Q

examples of steroid hormones

A

testosterone, aldosterone. oestrogen, progesterone

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11
Q

what are non-steroid hormones known as in their mode of action
why

A

first messengers
they are hydrophilic so cannot pass easily through cell membrane: therefore remain outside the cell, and bind to glycoprotein receptors in the cell membrane

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12
Q

mode of action of non-steroid hormones

A

first messenger (hormone) binds to glycoprotein receptor in plasma membrane bc cannot pass through membrane as hydrophilic
cause release of another signalling molecule inside the cell (called the second messenger)
leads to a response

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13
Q

what is a common second messenger for non-steroid hormones

A

G protein

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14
Q

mode of action of steroid hormones

A

steroid hormone passes through the phospholipid bilayer bc it is lipid soluble
binds to complementary intracellular receptor in cytoplasm
forms hormone receptor complex, which acts as transcription factor
transcription factor inhibits/switches on gene
protein is produced e.g. enzyme, channel protein, hormone etc

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15
Q

how can one hormone have different effects on different targets

A

different receptor may be present
second messenger may activate different enzymes/channels
different second messengers may be activated
second messenger level may increase or decrease within the cell

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16
Q

location of adrenal glands

A

2 above kidneys

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17
Q

size of adrenal glands

A

3x5cm
5g

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18
Q

3 layers of adrenal cortex from outside to inside

A

zona glomerulosa
zona fasciculata
zone reticularis
GFR

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19
Q

parts of adrenal gland

A

adrenal cortex
adrenal medulla

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20
Q

type of hormone secreted by zona glomerulosa

A

mineral corticoids
e.g. aldosterone

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21
Q

aldosterone function

A

controls concentrations of sodium and potassium in the blood
acts on cells in the distal tubules and collecting ducts in the kidney causing increased Na+ absorption leading to increased water retention

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22
Q

what type of hormone does the zona fasciculata secrete

A

glucocorticoids
e.g. cortisol

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23
Q

cortisol function

A

helps control metabolism of carbohydrates, fats and proteins in the liver:
e.g. inhibits protein synthesis causing blood increase in amino acids
also promotes fatty acid release form adipose tissue as an energy source
released in response to stress, or low blood sugar, bc stimulates production of glucose gluconeogenesis

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24
Q

what type of hormone does the zona reticularis secrete

A

cortisol or precursor molecules of sex hormones (ANDROGENS)
e.g. oestrogen in females and testosterone in males

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25
function of androgens
released and are converted to sex hormone which help secondary sexual characteristics develop and regulate production of gametes
26
what do the cells in the adrenal medulla produce
adrenaline
27
adrenaline structure/properties
polar molecule derived the amino acid tyrosine cannot pass directly across cell surface membrane so must be detected by specialised receptors in the target cell
28
why are the effects of adrenaline widespread
many cells and tissues have specialised adrenaline receptors
29
action of adrenaline on liver cells
adrenaline is hydrophilic so soluble in plasma binds to receptor on cell surface membrane (complementary binding) receptor changes shape, causing a G protein to be activated G protein binds to and activates adenyl cyclase enzyme this converts ATP into the 2nd messenger cyclic AMP this activates other enzymes (protein kinases) which activate other enzymes (cascade effect) this leads to a response (e.g. glycogenolysis and inhibition of glycogenesis)
30
why does adrenaline cause glucose to be released in a frightening situation?
muscles need glucose for respiration to release ATP to sustain muscle contraction to run away/ fight
31
how can the effect of adrenaline continue for hours when adrenaline only has a lifespan of 1-3 minutes in the body
adrenaline continues to be secreted form adrenal glands over a long period of time
32
what percentage of pancreatic tissue are the islets of langerhans
5%
33
parts of pancreas
islets of langerhans pancreatic duct acinar cells
34
pancreatic duct function
carries pancreatic juice to small intestine
34
acinar cells function
secrete pancreatic juice which drains into the duct
35
ducts in pancreas
intarglobular ducts feed into interlobular ducts, which feed into pancreatic duct
36
proportion of alpha and beta cells in islets of langerhans
more beta cells than alpha
37
beta cells make what
insulin, to prevent hyperglycaemia
38
alpha cells make what
glucagon, to prevent hypoglaecemia
39
how to distinguish between endocrine and exocrine tissue in pancreas
islets of langerhans (endocrine) are lightly staines, large spherical clusters which secrete and produce hormones pancreatic acini (exocrine) are darker stained, small berry-like clusters which produce and secrete digest enzymes
40
name of granules in acinar cells
zymogen
41
2 visible features that allow you to distinguish islets of langerhans form surrounding tissue
paler than surrounding more prominent nuclei cells more loosely packed bigger than surrounding acini
42
2 visible feature of islets of langerhans that relates to their function
contain capillaries for hormone distribution large prominent nucleoli for secretory function
43
normal range for blood sugar level
4-6 mol dm-3
44
value of 'too high' blood sugar level
consistently over 7mmol dm-3
45
consequence of high BSL
diabetes hyperglycaemia so glucose loss in urine so lower BP bc water lost so less blood to brain, causing a coma
46
value of 'too low' blood sugar level
consistently less than 4 mol dm-3
47
consequence of too low BSL
hypoglycaemia cells run short on glucose ketoacidosis coma
48
pathway of negative feedback when BGL too high
detected by beta cells, which secrete insulin, leading to an increased uptake and respiration of glucose, increased glycogenesis, increased lipogenesis, decreased glycogenolysis and gluconeogenesis this lowers BGL
49
pathway of negative feedback when BGL too low
detected by alpha cells, which secrete glucagon increased glycogenolysis, gluconeogenesis, release of glucose and lipolysis increased BGL
50
what is glycogenesis
the addition of glucose monomers to form glycogen
51
what is gluconeogenesis
the synthesis of glucose from non sugar precursors
52
what is glycogenolysis
the breakdown of glycogen into glucose
53
what do insulin and glucagon inhibit
the release of each other therefore control mechanism for blood glucose levels is an example of negative feedback as BGL fluctuates around a set point
54
step by step insulin secretion from beta cell
cell membrane has K+ and Ca2+ ion channels, the K+ ones are normally open so K+ flow out when BGL is too high, the glucose moves into the beta cell by FD glucose is metabolised to produce ATP, which is used to close the K+ channels the accumulation of K+ ions alter the potential difference across the cell membrane: the inside becomes less -ve the change in PD opens the Ca2+ channels Ca2+ ions caused the vesicles of insulin to fuse with the cell membrane, releasing insulin by exocytosis
55
how do some hormones inhibit insulin secretion
by opening K+ channels some diabetes drugs inhibits K+ channels, so trigger insulin release
56
describe insulin and glucagon action
insulin binds to complementary tyrosine kinase receptor tyrosine kinase enzyme is activated this activates other enzymes (2nd messengers) enzymes cause vesicles containing glut 4 transporters to move to and fuse with the membrane glucose transporter proteins inserted into the membrane extra glucose enters the cell by facilitated diffusion
57
differences between insulin and neurotransmitter secretion
cells carrying out secretion= beta cells in islets of langerhans and sensory/relay pre-synaptic neurone stimulus= high BGL and AP transmitted along axon membrane effect of stimulus on membrane= glucose enters cell->ATP closes K+ channels vs local current causes Na+ channels to open on synaptic knob vesicles contain insulin vs NT
58
what is diabetes
common metabolic disease in humans BGL cannot be controlled effectively
59
two types of diabetes proportions
10% have type 1 90% have type 2
60
describe type 1 diabetes
insulin dependent diabetes begins in early life pancreas doesn't secrete insulin so liver cannot store excess glucose as glycogen due to loss of B cells (caused by immune attack (autoimmune diseases)/ viral attack/ deficiency in human insulin gene)
61
describe type 2 diabetes
non-insulin dependent diabetes pancreas secretes insulin but receptors on liver and muscle cells don't respond (insulin resistance) OR less insulin secreted due to fatty pancreas (stops B cells functioning properly)
62
risk factors associated with type 2 diabetes
obesity high sugar/fat diet genetics lack of exercise Asian and Afrocaribbean people have higher incidence
63
symptoms of diabetes
BGL remains high after high-carb meal glucose lost in urine, so excessive urination, so dehydration, hunger and thirst fat & proteins used as respiratory substrates, leading to ketoacidosis and low blood pH no glycogen stores so low BGL between meals, causing hypoglycaemia bc blood sugar plummets
64
LT effects of diabetes
damage to blood vessels eye and gum problems higher risk of heart attack/ stroke. kidney failure
65
examples of treatment of type 1 diabetes
insulin treatments e.g. animal insulin (pig), GM bacteria Transplants e.g. pancreas, islets of langerhans, stem-cell derived islets
66
advantages and disadvantages of using insulin extracted from animal pancreas e.g. pigs
A: tried and tested method early treatment kept people alive D: needs to be purified risk of allergic reaction high production lost religious/ethical issues of animal products
67
advantages of using GM bacteria to produce human insulin
high purity less risk of allergic reaction lower production cost, can make large quantities to meet demand overcomes religious/ethical issues of animal products allows use of smart pumps/pens pumps can be monitored by app
68
disadvantages of using GM bacteria to produce human insulin
people had to be persuaded to change form previous regime e.g. animal insulin some may not understand the technology eg. injection routine (risk of hypoglycaemia if inject too much) side effects of pumps e.g. hard lumps under skin
69
advantages of pancreas transplant to cure t1 diabetes
patient can now produce insulin so more physiological control of BGL less risk of hypos and decreases longtime risk of mortality form severe hypos (hypos common if too much insulin injected) increased QoL 80% success rate (most of the time, no need to inject)
70
disadvantages of pancreas transplant to cure t1 diabetes
not enough pancreases available due to donor shortage patients require immunosuppressants for life (can lead to side effects) use of immunosuppressant drugs leaves patients vulnerable to infections
71
how does transplant of islets of langerhans work
doctors use enzymes to remove islets from pancreas of organ donor purified and counted (around 400,000 islets transplanted in each procedure) doctors insert the cells into hepatic portal vein towards the Liver
72
advantages of islet transplant to treat t1 diabetes
proven curative measure patient can now produce insulin so more physiological control of BGL less risk of hypos and decreases longtime risk of mortality form severe hypos (hypos common if too much insulin injected) increased QoL slows development of diabetes complications e.g. heart diseases, kidney disease and nerve eye damage
73
disadvantages of islet transplant to treat t1 diabetes
limited donor supply risk of rejection need lifelong immunosuppressants still classed as an experimental treatment- only performed in certain clinical trials not all people are good candidates for transplantation. doctors must weigh up risk of taking immunosuppressants risks to treatment e.g. bleeding and blood clots low success rate so chance that transplanted cells may not work well/ stop working
74
how are iPSCs made
reprogrammed from somatic cells e.g. skin fibroblasts from diabetic patient, have similar ability to differentiate and proliferate like ESCs ESC-derived B cells can be successfully generated by stepwise application of specific factors
75
how are stem cells used to treat diabetic patients?
transplant of pancreatic stem cell-derived pancreatic islet cells immunotherapy gene therapy developmental biology
76
how are stem cells used to treat diabetic patients?: transplant of pancreatic stem cell-derived pancreatic islet cells
pluripotent stem cells could differentiate into B cells and increase the mass of the islets and increase the secretion of insulin
77
how are stem cells used to treat diabetic patients?: immunotherapy
pluripotent stem cells can protect B cells from autoimmune attack by inhibiting T cell proliferation and reduce the inflammatory response
78
how are stem cells used to treat diabetic patients?: gene therapy
opportunities to use genetic modification to provide enhanced endocrine function and survival and modulate the immune response
79
how are stem cells used to treat diabetic patients?: developmental biology
opportunities to study function and longevity of human islet cells with varied genotypes and develop nw drugs for treatment
80
advantages of using stem cells to treat t1 diabetes
no longer need to inject insulin so money saved functioning B cells in pancreas improved QoL no hypoglycaemia or need for immunosuppressants could reprogram immune system to prevent B cell damage
81
disadvantages of using stem cells to treat t1 diabetes
still in early stages so need more clinical trials ethical issues with use of stem cells risk of cancer might still need low dose insulin initially high cost not suitable for all people
82
examples of treatment of t2 diabetes
lifestyle changes medication insulin therapy
83
treatment of t2 diabetes: lifestyle changes
losing weight regular exercise low sugar diet
84
treatment of t2 diabetes:medication
metformin acts on liver cells to decrease glucose released and increase glucose uptake sulfonylureas stimulate pancreas ti produce more insulin
85
treatment of t2 diabetes: gestational diabetes
gestational diabetes affects pregnant women: high levels of glucose in blood even though normal levels of insulin produced. caused by hormones released by placenta, which prevent body using insulin effectively TREATMENT: diet, exercise, medicines e.g. metformin, or insulin if not working
86