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Biology Module 5 > 5.4 Hormonal Communication > Flashcards

5.4 Hormonal Communication Flashcards

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1
Q
A

D

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2
Q

Heart rate can be increased by the hormone adrenaline, which binds to cardiac cells.
Describe how adrenaline binds to cardiac cells.

A

Binds to receptor in cell surface membrane + glycoprotein

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3
Q
A

No production of hCG until 4 weeks

Rapid increase until 8 weeks
Levels peak at 8 weeks
Levels fluctuate after 19 weeks

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4
Q
A

hCG is a peptide hormone
Binds to cell surface receptor
Uses cAMP to bring about response in cell

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5
Q

Which molecule does oestrogen interact w when it changes cell activity

A

DNA

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6
Q
A

Cells produce more hCG than normal due to depression of genes synthesising more hCG

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7
Q

Regulation of metabolism

A

Glucocorticoids

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8
Q

What secretes adrenaline

A

Medulla

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9
Q

Aldosterone

A

Controls blood pressure by controlling na+ concentration in blood and water reabsorption

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10
Q
A

A
B

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11
Q

Why’s it necessary to increase concentration of glucose surrounding cells before measuring insulin secretion

A

Glucose causes release of insulin
Change in insulin secretion high enough to be measured

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12
Q

Why’s standard deviation better

A

Less affected by anomaly
Takes into account every value in the data

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13
Q

Aspects of experimental design needed to be considered when comparing blood glucose concentration in patients

A

Blood glucose measured same number of times a day

Take into account patients age

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14
Q

Contractions cause more oxytocin to be released which causes more contractions. What’s this an example of

A

Positive feedback

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15
Q

Neuronal communication

A

Fast and short term

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16
Q

Hormonal communication

A

Slow and long term

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17
Q

Exocrine function

A

Synthesis of products to be released into ducts

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18
Q

Hormones

A

chemical messengers, signalling molecules
Glands that produce hormones = endocrine glands

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19
Q

Endocrine glands

A

Pituitary gland
Thyroid gland
Thymus
Adrenal glands
Pancreas
Ovaries
Testes

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20
Q

Which gland produces ADH

A

Posterior pituitary

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21
Q

Types of hormones

A

Peptide and steroid

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22
Q

Peptide hormones

A

made from amino acids e.g. adrenaline, insulin and glucagon = not lipid soluble so binds to receptors at the cell membrane

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23
Q

Steroid hormones

A

usually made from cholesterol e.g. oestrogen and testosterone and progesterone = lipid soluble = receptor found inside a cell

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24
Q

Endocrine glands

A

ductless glands = bundle of cells next to eachother that make the hormones + release them directly into the blood = travels directly to the target tissue

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25
Q

Target cell/tissue

A

has complementary receptors for a specific hormone

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26
Q

Peptide hormones

A
  • Hormone = first messenger
  • When the hormone binds to its receptor on a target cell it activates a G protein
  • G protein activates enzyme adenylyl cyclase
  • Adenyl cyclase converts ATP to cAMP (cAMP = secondary messenger)
  • cAMP causes an enzyme cascade
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27
Q

Steroid hormones

A
  • steroid hormone crosses the cell membrane and binds to a complementary receptor in the cytoplasm = receptor-hormone complex
  • Receptor-hormone complex goes into the nucleus and can bind to specific receptors on the chromosome + can act as a transcription factor = stops, starts, amplifies or dampens
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28
Q

Adrenal gland diagram

A
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29
Q

3 sections of adrenal cortex from outer to inner

A

GFR
zona glomerulosa
Zona fasciticulata
Zona reticularis

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30
Q

What type of hormones are in the adrenal cortex

A

Steroid hormones

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31
Q

Zona glomerulosa

A

produces mineralocorticoids e.g. aldosterone

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32
Q

Function of aldosterone

A

controls body’s salt concentration = affects blood pressure

33
Q

Zona fasciculata

A

produces glucocorticoids e.g. cortisol.

34
Q

Function of cortisol

A

stress hormone + helps when your blood sugar is low = allows you to release stored glucose from your liver

35
Q

Zona reticularis

A

helps produce sex hormones = produces the precursors which are then released + go to the site e.g. testes + ovaries and become the complete sex hormone

36
Q

Adrenal medulla

A
  • produces adrenaline = fight or flight hormone = peptide hormone = increases heart rate, increases blood glucose concentration, increases blood flow to muscles, causes pupils to dilate, decrease blood flow to gut, dilation of bronchioles

Noradrenaline has the same typa functions

37
Q

Where is the pancreas

A

Organ Behind the stomach

38
Q

Pancreas endocrine role

A

to produce hormones e.g insulin and glucagon

39
Q

Exocrine role of pancreas

A

to produce pancreatic juice = helps you digest food, contains pancreatic enzymes which includes amylase, trypsinogen (inactive protease until needed then converted to trypsin), lipase and sodium hydrogen carbonate

40
Q

Exocrine cells in pancreas

A
  • have a duct in a bundle known as acinis = make all digestive enzymes + release them into the duct in the middle which travels to the small intestines (duodenum)
41
Q

Compare endocrine and exocrine in pancreas

A
  • endocrine are ductless, exocrine has ducts
  • Exocrine function of pancreas is to release digestive enzymes + pancreatic juice, endocrine function is to produce hormones
  • Exocrine cells used = acinis, endocrine cells are alpha and beta cells found I. The islets of langerhans
42
Q

Endocrine cells in pancreas

A

Alpha and beta cells

43
Q

Alpha cells in pancreas

A

produce glucagon (increase blood glucose concentration)

44
Q

Beta cells in pancreas

A
  • beta cells produce insulin (decreases blood glucose concentration)
  • Beta cells usually smaller than alpha cells
45
Q

Pancreas cells diagram

A
46
Q

Role of insulin

A
  • once blood glucose concentration is really high = steep concentration gradient, glucose diffuses into the cell
  • Glucose metabolised into ATP using glucokinase
  • ATP closes the potassium ion channels = potassium builds up in the cell so charge becomes less negative
  • Change in voltage opens voltage gated calcium ion channels
  • Calcium ions enter which causes vesicles containing insulin to move towards the plasma membrane to fuse + release the content via exocytosis
47
Q

Blood glucose concentration

A

normal blood glucose concentration is between 4-6 mmol dm^-3 = if below this then hypoglycaemia, if above this then hyperglycaemia

48
Q

Hypoglycaemia

A

tiredness, if brain doesn’t get enough glucose it can lead to coma or death = brain cells die

49
Q

Hyperglycaemia

A

if only happens once it’s fine, if permanently above 7 it can cause vascular damage + damage to organs. If above 7 for a long time = diabetes

50
Q

If blood glucose rises too high

A
  • insulin produced = peptide hormone
  • When it binds to the receptor it activates an enzyme called tyrosine kinase = phosphorylates an inactive enzyme into an active enzyme
  • Active enzyme promotes conversion of any glucose to glycogen (glycogenesis), any excess glucose into fat, promotes use of glucose into respiration and promotes addition of glucose transporters into the cell membrane = more glucose can enter your liver cells = less in blood so blood glucose concentration should decrease
51
Q

Glycogenesis

A

Glucose to glycogen

52
Q

Glycogenolysis

A

Glycogen to glucose

53
Q

Gluconeogenesis

A

Glucose from amino acids + fats

54
Q

If blood glucose drops too low

A
  • glucagon released = works in G protein system
  • converts glycogen to glucose (glycogenolysis), make glucose from amino acids + fats (gluconeogenesis)
55
Q

Negative feedback loop for blood glucose concentration

A
56
Q

How is someone classified as diabetic

A
  • when your blood glucose concentration is above 7mmol dm^-3 for a prolonged period of time
57
Q

Blood glucose and insulin graph

A
  • Normal people when they eat something their blood glucose concentration will rise and then go back down
58
Q

Type 1 diabetes

A

Results from shortage of beta cells = not enough insulin produced

autoimmune disease, when your own immune cells attack your beta cells which means you don’t produce insulin. Usually genetic or triggered by a virus. Because they don’t have insulin they don’t know how to store glucose into glycogen so even if they have a low glucose concentration they have nothing to release glucose from. This means they’re prone to getting hypoglycaemia as well as hyperglycaemia.

59
Q

Type 2 diabetes

A

Insulin resistance = insulin still produced but livers cells no longer respond to insulin bc of damaged receptors Causes: obesity, lack of exercise, diet

60
Q

What cells do glucagon and insulin primarily bind to

A

Liver cells

61
Q

Type 1 diabetes treatment

A
  • insulin injections
  • Islet cell transplantation
  • Complete pancreas transplant
  • In the future = use stem cells to grow islet of langerhans cells and put those into patients
62
Q

Type 2 diabetes treatment

A
  • low sugar diet
  • exercise
  • manage weight
  • If still can control diabetes then take medication = reduces release of glucose from the liver + promotes release of insulin from the pancreas (control glucose levels e.g. metformin)
63
Q

How to get insulin for diabetes - past and advantages and disadvantages of it

A

From animal pancreas e.g. pig
Advantages: tried and tested method, early treatment kept people alive
Disadvantages: risk of allergic reaction, high production cost, ethical issues of animal products

64
Q

Advantages of genetically modifying insulin

A

exact copy of human insulin so faster acting + more effective, less risk of infection, less chance of rejection due to immune response, cheaper, less likely to have moral objections

65
Q

Why does diabetes cause excessive hunger

A
  1. The food eaten isn’t being processed into energy so the body assumed they aren’t getting energy and thus hungry
66
Q

Why does diabetes cause weight loss

A
  1. Can’t use the glucose so your body breaks down fat stores for energy
67
Q

Why does diabetes cause tiredness

A
  1. The cells aren’t taking in the glucose so it isn’t able to be converted into energy.
68
Q

Why does diabetes cause dehydration

A

Low water potential so water moves out of the cells which mean they don’t have enough water = dehydrated so can’t carry out action so send message to brain that they’re dehydrated

69
Q

State 3 differences between type 1 and type 2 diabetes

A

T1 = childhood. T2 = adulthood
T1 = doesn’t produce enough insulin, T2= inability to effectively use the insulin bc doesn’t bind to glycoprotein receptors
T1= insulin injections. T2= might not need insulin injections instead work on diet and environment

70
Q
A

D

71
Q
A
  • IV: conc of GH injected
  • DV: rate of growth
  • control: animal species
  • trial populations over several months
  • control group to ensure validity
  • method for assessing growth = growth rate to allow comparability
  • ensure food consistent across all trial groups
  • large sample size to reduce effect of anomalies
  • ethical concerns = chickens should be reared in humane conditions
72
Q
A

K = islet of langerhans
L = blood vessel

73
Q

Suggest and explain which statistical test the researchers would have used to analyse their data.

A

Unpaired t-test because they’re comparing means

74
Q
A

Probability less than 0.1% so results due to chance

75
Q

Stem cell therapy is a potential future treatment for diabetes mellitus.
In the future, it might be possible to differentiate stem cells in a laboratory (in vitro) before they are implanted into the pancreas of a patient with diabetes.

Which type of diabetes mellitus is most likely to be improved by stem cell therapy?

A
  • type 1 bc it results from shortage of beta cells so stem cell therapy might increase insulin production and type 2 diabetes usually results from insulin resistance rather than lack of insulin so unlikely to help type 2
76
Q
A

Type of diabetes
Age
Gender

77
Q

How to get insulin for diabetes - current

A
  • from genetic modification
  • transplant of pancreas
  • transplant of stem cells
78
Q

Advantages and disadvantages of human insulin

A

Advantages: less risk of allergic reaction, lower production cost, overcomes ethical issues of animal products
Disadvantages: side effects of pumps e.g. hard lumps forming under skin, people persuaded to change from previous insulin regime

79
Q

Advantages and disadvantages of transplant as diabetes treatment

A

Advantages: no need for insulin injections, improved quality of life, stem cells turned into functioning b-cells

Disadvantages: need to take immunosuppressants, ethical issues associated with stem cells, risk of cancer with stem cells

Biology Module 5 (8 decks)

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