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Year 13 Biology > 5.4 - Hormonal Communication > Flashcards

5.4 - Hormonal Communication Flashcards

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1
Q

Different hormone glands and what they produce

A
  • Adrenal Gland - Adrenaline
  • Testes - Testosterone
  • Ovaries - Oestrogen and Progesterone
  • Pancreas - Insulin and Glucagon
  • Pituitary gland - FSH and LH
  • Thyroid - Thyroxine
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2
Q

Endocrine system def

A

A communication system using hormones as signalling molecules

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3
Q

Hormones def

A
  • Molecules(proteins or steroids) that’s er released by endocrine glands directly into the blood
  • They act as messenger, carrying a signal from the endocrine gland to a specific target organ or tissue
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4
Q

Target cell def

A
  • For non-steroid hormones, cells that possess a specific receptor on their plasma(cell surface) membrane.
  • The shape of the receptor is complementary to the shape of the hormone molecule
  • Many cells together form a target tissue
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5
Q

Endocrine glands info

A
  • They produce and secret hormones directly into the blood
  • They are ductless glands
  • They consist of groups of cells that manufacture and release the hormone directly into the blood in capillaries running through the gland
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6
Q

Exocrine system info

A
  • They do not produce hormones

- They secrete molecules into a duct which carries them to where they are needed

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7
Q

Where is Adrenal medulla found and what does it do?

A
  • In the centre of the adrenal gland

- Produces and secretes adrenaline and noradrenaline

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8
Q

What effects does adrenaline have on the body?

A
  • relax smooth muscle in bronchioles -increase stroke volume of heart -increase heart rate
  • vasoconstriction
  • glycogen ‐‐> glucose
  • dilates pupils
  • increase mental awareness
  • inhibits action of gut
  • body hair erects
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9
Q

Adrenaline mechanism

A
  • Adrenaline is a non-steroid(protein/amino acid based hormones) ‐ these can’t dissolve in the cell surface membranes of target cells and get inside and must instead bind to a receptor
  • Non‐steroid hormones are known as first messengers because they transmit the signal around the body and cause an effect on the cell when they bind to a receptor.
  • The binding causes a G‐protein to activate adenyl cyclase which converts ATP into cyclic AMP (cAMP) which is the second messenger because it transmits the signal inside the cell to initiate a change inside the cell
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10
Q

What does adrenal cortex use to produce steroid hormones?

A

Adrenal cortex uses cholesterol to produce steroid hormones

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11
Q

3 layers of adrenal cortex

A
  • Zona Glomerulosa - (nearest outside)
  • Zona Fasciculata - (middle layer)
  • Zona Retcularis - (nearest medulla)
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12
Q

What do each of the three layers of the adrenal cortex do?

A
  • Zona Glomerulosa - secrete mineralocorticoids - help to control sodium and potassium levels in blood and blood pressure
  • Zona Fasciculata - secretes glucocorticoids e.g. cortisol - helps to control metabolism of carbs, fats and proteins in liver
  • Zona Reticularis - secretes precursors to the sex hormones
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13
Q

How steroid hormones cause a change in cells/(cell signalling)

A

Steroid hormones enter cells by dissolving in the cell surface membrane.

  • They then bind with a receptor in the cytoplasm, the receptor‐hormone complex enters the nucleus, binds to another receptor on the chromosome.
  • This causes mRNA to be made which then produces proteins.
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14
Q

Using the example of the adrenal glands, describe how different types of hormones are released and take affect on their target cells. (8)
- Model answer

A

-endocrine glands release hormones -hormones travel in blood to target cells

  • adrenal medulla releases non‐steroid hormones/adrenaline
  • (adrenaline) acts as first messenger
  • G‐protein activates adenyl cyclase that converts ATP into cyclic AMP (cAMP)
  • cAMP is the second messenger ‐ causes effect in cell
  • Adrenal cortex releases steroid hormones that dissolve in cell surface membrane (of target cells)
  • Bind with a receptor in the cytoplasm
  • Receptor‐hormone complex binds to receptor on the chromosome/DNA
  • Causes mRNA/proteins to be made
  • AVP: correct reference to Zona Glomerulosa, Zona Fasciculata, Zona Reticularis
  • AVP: ref to complementary shapes
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15
Q

How can hormones travel all around the body in the blood yet still have such specific effects?

A
  • Endocrine glands make and secrete hormones and release them directly into the blood.
  • Hormones bind to specific complementary receptors on the cell surface membranes of their target cells.
  • The hormones will not affect cells without these receptors. Target cells are grouped into target tissues.
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16
Q

Adrenaline def

A

Hormone released from the adrenal glands, which stimulates the body to prepare for fight or flight response

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17
Q

Beta cells def

A

Cells found in the Islets of Langerhans that secret the hormone insulin

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18
Q

Glucagon def

A

A hormone that cause an increase in blood glucose concentration

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19
Q

Insulin def

A

The hormone, released from the pancreas, that causes blood glucose levels to decrease

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20
Q

Two main secretions from the pancreas

A
  • Pancreatic juices - containing enzymes which are secreted into the small intestine
  • Hormones - secreted from the Islets of Langerhans into the blood
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21
Q

What is the ‘pancreatic juice’ and where is it produced?

A

-‘Pancreatic juice’ is made of digestive enzymes produced by the majority of cells in the pancreas

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22
Q

Substances in the pancreatic juice

A
  • Pancreatic Amlylase
  • Digests amylose/carbohydrates to maltose/monosaccharides
  • Trypsinogen
  • The precursor to trypsin- which breaks down proteins when it enters the duodenum(first part of the small intestine)
  • Lipase
  • Which digests lipid molecules
  • Sodium hydrogen carbonate(alkali)
  • Makes the blood alkaline and can neutralise acidic contents of blood of digestive system
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23
Q

Endocrine function of the pancreas mechanism

A
  • The islets of Langerhans contain alpha and beta cells
  • The cells detect changes in blood glucose levels (normal = 90mg per 100cm3)
  • Alpha cells ‐ produce and secrete glucagon (hormone)
  • Beta cells ‐ produce and secrete insulin (hormone)
  • They secrete the hormones directly into closely associated capillaries
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24
Q

How to distinguish between different pancreatic cells on a micrograph

A
  • Most cells: exocrine
  • Groups of cells surrounding smallest hollow tubes: acini
  • Slightly larger circular(ish) hollow tubes: tubules leading to pancreatic duct
  • Patches (circularish) with different staining: Islet of Langerhans
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25
Q

What is the acini in the pancreas?

A
  • Groups of cells that are grouped together that release digestive enzymes
  • They are grouped together into small lobules surrounded by connective tissue
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26
Q

Where do acini secrete their digestive enzymes?

A

Pancreatic duct

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27
Q

Why is insulin released into the bloodstream?

A
  • To control the blood-glucose levels in the blood when it is too high
  • It reduces the blood-glucose levels
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28
Q

How is insulin released from cells mechanism

A
  1. Cell membrane has potassium and calcium ion channels
  2. The potassium ion channels are normally open - so K+ ions flow out
  3. When blood-glucose concentration is too high, glucose moves into the cell
  4. Glucose is metabolised to produce ATP
    - (Glucose - Glucose Phosphate - ATP)
  5. ATP closes the K+ ion channels
  6. The accumulation of K+ ions alters the potential difference across the cell membrane
    - The inside of the cell becomes less negative
  7. The change in pot. difference opens the Ca2+ channels
  8. Ca2+ ions cause vesicles of insulin to fuse with plasma membrane
    - This releases insulin by exocytosis
29
Q

Regulation of blood glucose part to make

A

H

30
Q

Changes in body when blood-glucose levels get too high. Effect of insulin mechanism (6 Marks)

A

• Beta cells detect rise in blood glucose level
• Stimulates production of insulin by beta cells
• Glucagon production by alpha cells inhibited
• Insulin secreted into blood
• Insulin binds to receptors on target cells (hepatocytes and muscle cells)
‐ more glucose channels inserts into plasma membrane ‐ more glucose enters cells
‐ glucose converted to glycogen (glycogenesis)
‐ glucose converted to fats
‐ increased rate of glucose used in respiration
• This results in less glucose in the blood
• This is an example of negative feedback

31
Q

Changes in body mechanism when blood-glucose levels get too low

A

• Alpha cells detect fall in blood glucose level
• Stimulates production of glucagon by alpha cells
• Insulin production by beta cells inhibited
• Glucagon secreted into blood
• Glucagon binds to receptors on target cells (hepatocytes)
• Causes:
‐ hydrolysis of glycogen to glucose (glycogenolysis)
‐ conversion of fats and amino acids to glucose (gluconeogenesis)
‐ use of more fatty acids in respiration
• The glucose is released into the blood = more glucose in the blood

32
Q

Benefits of storing glucose as glycogen

A 
- insoluble
• unreactive
• can't diffuse out of cell
• compact
• easy to convert to glucose
• lots of branches for enzymes to work on in hydrolysis
33
Q

Gluconeogenesis - very simple mechanism

A
  • amino acids have amino group removed
  • creates pyruvate (used as carbon skeleton)
  • In the presence of enzyme triose phosphate
  • Controls condensation reaction into glucose
34
Q

What occurs in Glycogenolysis?

A

-Glyocgen is converted to glucose

35
Q

What is made in gluconeogenesis?

A

-Fatty acids/amino acids are converted into glucose

36
Q

What occurs in glycogenesis?

A

Glucose is converted into glycogen

37
Q

What are hepatocytes?

A

-Liver cells

38
Q

Diabetes mellitus def

A

A disease where you can’t control blood glucose levels effectively

39
Q

HYPERglycaemia def

A
  • Where blood glucose levels are too high

- This can lead to organ damage in the long term

40
Q

HYPOglycaemia def

- What effect can this have on cells?

A

-Disease where blood glucose levels are too low

  • Not enough glucose travels to cells
  • Less aerobic respiration
  • Can cause tiredness and irritability to brain damage, seizures and death
41
Q

Info about type 1 diabetes

A
  • Insulin dependent diabetes
  • Autoimmune response - attack own beta cells and destroys them
  • Or viral attack on beta cells
  • Can’t produce sufficient insulin
  • Cant store glucose as glycogen - excess glucose remains in blood - hyperglycaemia
  • When blood-glucose levels fall, no enough glycogen store to release glucose - this cause hypoglycaemia
42
Q

Info about type 2 diabetes

A
  • Non-insulin dependent diabetes
  • Receptors on target cells for insulin decline and cells become unresponsive to insulin
  • Can still produce insulin(less produced)
  • Risk factors:
  • Age
  • Obesity
  • Need for refined sugar rich diet
  • Certain ethnicities
  • Family History
43
Q

Treating type 1 diabetes

A
  • Monitor blood glucose levels
  • Insulin injections administered
  • Insulin pump - permanently pumps insulin at a steady rate into blood stream
  • Islet/beta cell transplant from a donor
  • Pancreas transplant
44
Q

Advantages of obtaining insulin form genetically engineered bacteria(rather than animals)

A

The old method of obtaining insulin was from pigs. Advantages over this method are:
• Engineered insulin is cheaper (as food stock is cheaper than that for pigs)
• Much larger amount of product is more readily available as the rate of
production is much faster
• There is less risk of infection than with pig insulin
• Human insulin is more effective for humans than pig insulin
• Avoids side effects/allergies/immune response that some people
experience with pig insulin
• Ethically it is advantageous to use bacteria as there are no animal rights issues associated with them as there are with pigs.
- This is also true for religious groups e.g. Jews who may not want pig insulin for religious reasons.

45
Q

Treating type 2 diabetes

A
  • Control of carbohydrate intake
  • Regular exercise
  • Insulin injections or drugs used to slow absorption of glucose
46
Q

Future treatment for type 1 diabetes

A
  • Stem cells:
  • Could be used to grow new Islets of Langerhans and beta cells
  • This can produce insulin
  • So type 1 diabetes would cure type 1 diabetes
47
Q

Effect of insulin on the cell

A

-More glucose enters the cell
-Glucose in the cells is converted to glycogen for storage - glycogenesis
-More glucose is converted to fats
-More glucose is used in respiration
-More transporter proteins specific to glucose are placed into the cell surface membrane
This is achieved by causing vesicles containing these transporter proteins to fuse with the membrane

48
Q

Effect of glucagon on body cells

A

-More fatty acids are used in respiration
-Amino acids and fats are converted into additional glucose
This is gluconeogenesis
-Glycogen is converted into glucose(glycogenolysis) by phosphorylase A
This is one of the enzyme’s activated in the cascade

49
Q

Outline negative feedback loop of blood-glucose regulation when B-G levels are too high

A
  • Detected by beta cells in the Islets of Langerhans
  • Beta cells secrete insulin into the blood
  • Insulin detected by receptors on liver and muscle cells
  • Liver and muscle cells remover glucose from the blood and convert glucose to glycogen
  • Glucose conc falls and returns to normal levels
50
Q

Outline negative feedback loop of blood-glucose regulation when B-G levels are too low

A
  • Fall in B-G level conc detected by alpha cells in the Islets of Langerhans
  • Alpha cells secrete glucagon into the blood
  • Glucagon detected by receptors on liver cells
  • Liver cells converts glycogen to glucose and release glucose into the blood
  • Glucose concentration rises to normal levels
  • Glucagon inhibits the production and secretion of insulin form beta cells
51
Q

Blood glucose too high mechanism

A
  • Beta cells detect high glucose levels
  • They release insulin(peptide) hormone into the blood
  • The effector is the liver, muscle and fat cells
  • Liver and muscle cells take up glucose through GLUT 4 channel proteins
  • They convert glucose to glycogen for storage
  • Fat cells take up glucose as well but converts it into fats for storage
52
Q

Glucose levels too low mechanism

A

-Sensor is the Alpha cells in Islet of Langerhans
-Glucagon is secreted into the blood
Effector cells/Target Organs:
-Fat Cells - release fatty acids
-Liver cells - can convert glycogen into glucose by Glycogenolysis
-Muscle cells can release glucose from glycogen

  • Glycogenolysis will occur
  • Gluconeogenesis can also occur - glucose can be synthesised from fatty acids and amino acids
53
Q

Type 1 diabetes mechanism

A
  • There is no production of insulin
  • Due to a genetic defect
  • Or Beta cells have been destroyed by illness
  • Treatment is lifetime insulin injections
54
Q

Type 2 diabetes mechanism

A

-AKA - late onset diabetes

  • Symptoms usually appear in middle-aged people
  • Associated with ethnicity/genes and a high sugar diet
  • Insulin receptors decrease in sensitivity and insulin secretion declines
  • Can be treated by diet improvements(remove sugars and carbs from diet)
  • Can also be treated with drugs
  • Insulin injections may also be needed
55
Q

Where is adrenaline produced?

Maybe not part of this topic

A

Adrenal glands

Adrenal medulla

56
Q

Describe how adrenaline causes a change in target cells

A
  1. Adrenaline binds to receptor
  2. Complementary / specific, fit / shape
    3 G protein activated
    4 adenyl cyclase activated
    5 ATP converted to cAMP
    6 cAMP activates, proteins / enzymes
  3. By altering 3D structure by phosphorylation
57
Q

Suggest how having a number of steps in the signalling pathway enables a small number of adrenaline molecules to rapidly cause large effects.

A
  • One adrenaline molecule can cause the production of multiple cAMP molecules
  • This multiplying effect is repeated at every step - idea of a cascade of cAMP production
58
Q

Summarise the action of steroid hormones

A
  1. Steroid hormone passes through the cell membrane of the target cell
  2. The steroid hormone binds with a specific receptor, with a complementary shape to the hormone, in the cytoplasm
  3. The receptor-steroid hormone complex enters the nucleus of the target cell and binds to another specific receptor on the chromosomal material
  4. Binding stimulate the production of mRNA molecules - these code for the production of proteins
59
Q

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 Marks)

A
  • Continues to be secreted as long as blood-glucose concentration remains higher than normal
  • Sufficient ATP will still be present and so K+ channels remain closed
  • Exocytosis still being triggered by Ca2+ ions
60
Q

Where are corticosteroids secreted from?

A

Cells in the cortex region in the brain

61
Q

A patient was sent for a further blood test, known as the haemoglobin A1C (HbA1C) test, to test for diabetes mellitus
• Glucose combines with haemoglobin in the bloodstream to form a ‘glycosylated
haemoglobin’ molecule, HbA1C.
• The concentration of HbA1C is directly proportional to the mean concentration of glucose in the blood over an eight to twelve week period.
Suggest why a single HbA1C test cannot indicate accurately the mean blood glucose concentration for a period longer than twelve weeks.
(2 Marks)

A
  • HbA1C contained within erythrocytes
  • Erythrocytes have a limited life span - of around 12 weeks
  • After 12 weeks they are broken down in hepatocytes by Kupffer cells
62
Q

Explain how emphysema could result in fatigue.

2 Marks

A
  • Less ventilation/less oxygen entering blood and capillaries
  • Less oxygen for aerobic respiration in cells
  • Less oxygen for oxidative phosphorylation
  • Less ATP produced
  • (Increased acidity from increased lactate production - denatures enzymes present in aerobic respiration/ox phosph)
63
Q

Suggest why fatigue may occur in a person with Type 2 diabetes who is NOT taking medication.
(2 Marks)

A
  • Receptors on target cells are less responsive to insulin
  • not enough glucose uptake into cells
  • not enough glucose used in aerobic respiration/ATP production in oxidative phosphorylation
  • Glucose isn’t stored as glycogen in cells - less energy stores when needed - hypoglycaemia
  • Less gluocse for aerobic respiration
64
Q

Certain heart conditions result in a weak and irregular heart beat.
Suggest how a weak and irregular heart beat could result in fatigue.
(2 Marks)

A
  • Lower blood pressure
  • Less oxygen reaches cells for aerobic respiration/oxidative phosphorylation
  • less glucose reaches cells for aerobic respiration
  • Less ATP produced
  • increased lactate - increased acidity - denature enzymes present in aerobic respiration
65
Q

What ion channels are present beta cell plasma membranes

A

Calcium and potassium ion channels

66
Q

Describe the body’s response to an increase in blood-glucose concentration

A
  • Increase in blood-glucose conc. detected by Islets of Langerhans in the pancreas
  • This causes beta cells to increase secretion of insulin into the blood
  • Insulin binds to receptors on target cell plasma membrane of liver cells/hepatocytes
  • Liver causes excess glucose monomers to be joined to form glycogen - glycogenesis
  • Glycogen can be stored in the liver
  • In addition,
  • The use of glucose in respiration is increased
  • Once blood glucose levels have been restored with the normal range
  • Negative feedback loop reduces the secretion of insulin
67
Q

Gluconeogenesis def

A

Metabolic pathway that results in the generation of glucose from pyruvate or lactate

68
Q

Describe the body’s response to a decrease in blood-glucose concentration - model answer

A

-

  • Causes alpha cells to increase the secretion of glucagon into the blood
  • Glucagon binds to receptors on cell membrane of liver cells
  • Liver breaks down stored glycogen into glucose into Glycogenolysis
  • In addition, pyruvate and lactate can be converted back into glucose in gluconeogenesis
  • Once blood glucose levels have been restored with the normal range
  • Negative feedback loop reduces the secretion of glucagon

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