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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
Q

function of androgens

A

released and are converted to sex hormone which help secondary sexual characteristics develop and regulate production of gametes

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26
Q

what do the cells in the adrenal medulla produce

A

adrenaline

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27
Q

adrenaline structure/properties

A

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

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28
Q

why are the effects of adrenaline widespread

A

many cells and tissues have specialised adrenaline receptors

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29
Q

action of adrenaline on liver cells

A

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)

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30
Q

why does adrenaline cause glucose to be released in a frightening situation?

A

muscles need glucose for respiration to release ATP to sustain muscle contraction to run away/ fight

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31
Q

how can the effect of adrenaline continue for hours when adrenaline only has a lifespan of 1-3 minutes in the body

A

adrenaline continues to be secreted form adrenal glands over a long period of time

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32
Q

what percentage of pancreatic tissue are the islets of langerhans

A

5%

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33
Q

parts of pancreas

A

islets of langerhans
pancreatic duct
acinar cells

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34
Q

pancreatic duct function

A

carries pancreatic juice to small intestine

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34
Q

acinar cells function

A

secrete pancreatic juice which drains into the duct

35
Q

ducts in pancreas

A

intarglobular ducts feed into interlobular ducts, which feed into pancreatic duct

36
Q

proportion of alpha and beta cells in islets of langerhans

A

more beta cells than alpha

37
Q

beta cells make what

A

insulin, to prevent hyperglycaemia

38
Q

alpha cells make what

A

glucagon, to prevent hypoglaecemia

39
Q

how to distinguish between endocrine and exocrine tissue in pancreas

A

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
Q

name of granules in acinar cells

A

zymogen

41
Q

2 visible features that allow you to distinguish islets of langerhans form surrounding tissue

A

paler than surrounding
more prominent nuclei
cells more loosely packed
bigger than surrounding acini

42
Q

2 visible feature of islets of langerhans that relates to their function

A

contain capillaries for hormone distribution
large prominent nucleoli for secretory function

43
Q

normal range for blood sugar level

A

4-6 mol dm-3

44
Q

value of ‘too high’ blood sugar level

A

consistently over 7mmol dm-3

45
Q

consequence of high BSL

A

diabetes
hyperglycaemia so glucose loss in urine so lower BP bc water lost so less blood to brain, causing a coma

46
Q

value of ‘too low’ blood sugar level

A

consistently less than 4 mol dm-3

47
Q

consequence of too low BSL

A

hypoglycaemia
cells run short on glucose
ketoacidosis
coma

48
Q

pathway of negative feedback when BGL too high

A

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
Q

pathway of negative feedback when BGL too low

A

detected by alpha cells, which secrete glucagon
increased glycogenolysis, gluconeogenesis, release of glucose and lipolysis
increased BGL

50
Q

what is glycogenesis

A

the addition of glucose monomers to form glycogen

51
Q

what is gluconeogenesis

A

the synthesis of glucose from non sugar precursors

52
Q

what is glycogenolysis

A

the breakdown of glycogen into glucose

53
Q

what do insulin and glucagon inhibit

A

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
Q

step by step insulin secretion from beta cell

A

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
Q

how do some hormones inhibit insulin secretion

A

by opening K+ channels
some diabetes drugs inhibits K+ channels, so trigger insulin release

56
Q

describe insulin and glucagon action

A

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
Q

differences between insulin and neurotransmitter secretion

A

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
Q

what is diabetes

A

common metabolic disease in humans
BGL cannot be controlled effectively

59
Q

two types of diabetes proportions

A

10% have type 1
90% have type 2

60
Q

describe type 1 diabetes

A

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
Q

describe type 2 diabetes

A

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
Q

risk factors associated with type 2 diabetes

A

obesity
high sugar/fat diet
genetics
lack of exercise
Asian and Afrocaribbean people have higher incidence

63
Q

symptoms of diabetes

A

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
Q

LT effects of diabetes

A

damage to blood vessels
eye and gum problems
higher risk of heart attack/ stroke. kidney failure

65
Q

examples of treatment of type 1 diabetes

A

insulin treatments e.g. animal insulin (pig), GM bacteria
Transplants e.g. pancreas, islets of langerhans, stem-cell derived islets

66
Q

advantages and disadvantages of using insulin extracted from animal pancreas e.g. pigs

A

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
Q

advantages of using GM bacteria to produce human insulin

A

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
Q

disadvantages of using GM bacteria to produce human insulin

A

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
Q

advantages of pancreas transplant to cure t1 diabetes

A

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
Q

disadvantages of pancreas transplant to cure t1 diabetes

A

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
Q

how does transplant of islets of langerhans work

A

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
Q

advantages of islet transplant to treat t1 diabetes

A

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
Q

disadvantages of islet transplant to treat t1 diabetes

A

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
Q

how are iPSCs made

A

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
Q

how are stem cells used to treat diabetic patients?

A

transplant of pancreatic stem cell-derived pancreatic islet cells
immunotherapy
gene therapy
developmental biology

76
Q

how are stem cells used to treat diabetic patients?: transplant of pancreatic stem cell-derived pancreatic islet cells

A

pluripotent stem cells could differentiate into B cells and increase the mass of the islets and increase the secretion of insulin

77
Q

how are stem cells used to treat diabetic patients?: immunotherapy

A

pluripotent stem cells can protect B cells from autoimmune attack by inhibiting T cell proliferation and reduce the inflammatory response

78
Q

how are stem cells used to treat diabetic patients?: gene therapy

A

opportunities to use genetic modification to provide enhanced endocrine function and survival and modulate the immune response

79
Q

how are stem cells used to treat diabetic patients?: developmental biology

A

opportunities to study function and longevity of human islet cells with varied genotypes and develop nw drugs for treatment

80
Q

advantages of using stem cells to treat t1 diabetes

A

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
Q

disadvantages of using stem cells to treat t1 diabetes

A

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
Q

examples of treatment of t2 diabetes

A

lifestyle changes
medication
insulin therapy

83
Q

treatment of t2 diabetes: lifestyle changes

A

losing weight
regular exercise
low sugar diet

84
Q

treatment of t2 diabetes:medication

A

metformin acts on liver cells to decrease glucose released and increase glucose uptake
sulfonylureas stimulate pancreas ti produce more insulin

85
Q

treatment of t2 diabetes: gestational diabetes

A

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
Q
A

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