12. Homeostasis Flashcards

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1
Q

When insulin binds to receptors on liver cells, it causes the formation of glycogen from glucose, lowering the concentration of glucose in liver cells.

Explain how the formation of glycogen in liver cells leads to a lowering of blood glucose concentration.

A
  • Glucose concentration in liver falls
  • Below that in blood/ plasma
  • Creates/ maintains glucose concentration/ diffusion gradient
  • Glucose enters cells/ leaves blood by facilitated diffusion/ via carrier/ channel protein
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2
Q

Destruction of developing follicles during chemotherapy can lead to a much higher
concentration of FSH in the young female patients’ bodies than normal.
Use your knowledge of hormonal interactions to explain why.

A
  • No/ less oestrogen produced by follicles/ ovaries
  • No/ less negative feedback (by oestrogen)
  • On pituitary gland
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3
Q

Picture of two hormones, one artificial and one normal.
During cancer treatment follicles are destroyed by the radiation which leads to a much higher concentration of FSH than normal. Suggest how the artificial hormone reduces the release of FSH

A

-Artificial hormone has a similar shape/ binding site to normal hormone (REJECT references to active site, enzyme inhibitors and substrates)
-So binds to same receptor and stops normal hormone binding
Accept references to binding sites and competitive inhibition of hormone binding sites.

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4
Q

Give 3 reasons why homeostasis is important.

A
  • Enzymes and other proteins are sensitive to temperature and pH so can be denatured so they are no longer functional if conditions fluctuate too far.
  • Changes in water potential may cause cells to shrink or expand so the cell cannot operate normally- constant blood glucose is important to ensure a constant water potential
  • Organisms that can maintain a constant internal environment have a wider geographical range and therefore a greater chance of finding food and surviving
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5
Q

Describe the 5 stages of a self regulating system.

A

1) Set point, a desired level at which the system operates. Monitored by a…
2) Receptor which detects deviations from the set point and informs the…
3) Controller which coordinates information from various receptors and sends instructions to an appropriate…
4) Effector which brings about the changes to return to the set point
5) Feedback loop- informs the receptor of changes brought about by the effector

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6
Q

Give two methods (each) for an organism to

  • Gain heat
  • Lose heat
A

Gain heat
>Production of heat by increasing the metabolic rate
>Gain of heat from the environment by conduction, convection or radiation

Lose heat
>Evaporation of water (eg sweating)
>Loss of heat to environment by conduction, convection and radiation

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7
Q

How is body temperature regulated in ectotherms?

A
  • Exposing themselves to the sun
  • Taking shelter from sun when too hot/ go into a burrow to conserve heat when it is too cold
  • Gaining warmth from the ground by pressing themselves up against it to transfer heat into their bodies
  • Generating metabolic heat (not the main source of heat)
  • Colour variations (eg darker colours absorb more heat whereas lighter colours reflect more heat)
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8
Q

How is body temperature regulated in endotherms?

A
  • Metabolic activities
  • Behavior- shelter from cold wind or hot sunshine
  • Curl up when its cold and stretch out when its hot
  • (Genetics) large surface area to volume ratio in hot climates and small surface area to volume ratio in cold climates
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9
Q

How do endotherms respond to a cold environment?

A
  • Vasoconstriction- diameter of arterioles near skin’s surface are made smaller so most of the blood entering the skin passes beneath the insulating layer of fat, reducing heat loss to the environment
  • Shivering- involuntary muscle contractions produces more metabolic heat
  • Increased metabolic rate so more heat is generated
  • Hair erector muscles contract so a warm layer of air is trapped close to the skin so there is more insulation
  • Decrease in sweating
  • Behavioral mechanisms- sheltering from the wind, basking in the sun, huddling together
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10
Q

How do endotherms respond to a hot environment?

A
  • Vasodilation- diameter of arterioles near skin’s surface becomes larger so warm blood passes close to the surface where heat can be radiated to the environment
  • Increased sweating- evaporating water from the skin requires energy in the form of heat
  • Lowering of body hair-hairs flatten against the body so there is no insulating layer of air close to the skin
  • Behaviour- avoiding the heat and sheltering in burrows
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11
Q

What is the coordinator in the case of temperature homeostasis?

A

Hypothalamus

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12
Q

Describe the thermoregulatory centre in the hypothalamus.

A
  • HEAT GAIN CENTRE which is activated by a fall in blood temperature and is responsible for controlling the mechanisms that increase the body temperature.
  • HEAT LOSS CENTRE-which is activated by an increase in blood temperature and is responsible for controlling the mechanisms that decrease the body temperature
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13
Q

Where are thermoreceptors located and how do they work?

A
  • Located in the skin and hypothalamus
  • Thermoreceptors in the hypothalamus monitor the temeperature of the blood passing through. Thermoreceptors in the skin monitor environmental conditions and send impulses along the autonomic nervous system to the hypothalamus which can therefore coordinate a response considering both the blood and skin temperatures.
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14
Q

Hormones are..

  • Produced in…
  • Carried by…
  • Effective?
A
  • Produced by glands (endocrine glands) and secreted directly in the blood stream
  • Carried by blood plasma to the cells on which they act (target cells which have hormone receptors on their cell surface membranes which are complementary to the hormone)
  • Effective in small quantities but often have widespread and long lasting effects
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15
Q

Describe the second messenger model of how hormones work.

A
  • Hormone is the first messenger- binds to specific receptors on the cell surface membrane to form a hormone-receptor complex
  • Hormone-receptor complex activates an enzyme inside the cell that results in the production of a chemical that acts as the second messenger
  • Second messenger causes a series of chemical changes that produce the required response
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16
Q

Describe how the second messenger model works in terms of adrenaline.

A

-

17
Q

What role does the pancreas play in maintaining a constant blood glucose level? Hormones produced etc…

A

Islets of langerhans in the pancreas come in two types

  • Alpha cells- produce glucagon to increase the blood glucose
  • Beta cells- produce insulin to decrease the blood glucose
18
Q

What are the three sources of blood glucose?

A
  • Directly from the diet- from the break down of carbohydrates (starch, maltose, lactose and sucrose)
  • Glycogenolysis- from the breakdown of glycogen stored in the liver and muscle cells
  • Gluconeogenesis- production of new glucose from sources other than carbohydrates (eg. the liver can produce glucose from glycerol and amino acids)
19
Q

How does the secretion of insulin from the beta cells in the pancreas control blood glucose?

  • What does insulin binding with glycoprotein receptors on cell surface membranes cause?
  • Therefore in which ways is the blood glucose level lowered?
A

-Insulin binds with glycoprotein receptors on the cell surface membrane which
>changes the specific tertiary structure of the glucose transport protein channels, allowing them to open to let more glucose into the cells
>Increase in the number of carrier molecules in the cell surface membrane
>Activation of enzymes that convert glucose into fat and glycogen

Blood glucose is lowered by:
>Increasing the rate of absorption of glucose into cells
>Increasing respiratory rate of cells (therefore causing them to absorb more glucose)
>Increasing rate of conversion of glucose into glycogen in the muscles and liver cells (glycogenesis)
>Increasing rate of conversion of glucose into fat

20
Q

How does glucagon respond to a fall in blood glucose?

A
  • Activates enzyme that converts glycogen to glucose

- Increasing conversion of amino acids and glycerol into glucose (gluconeogenesis)

21
Q

How does adrenaline increase blood glucose levels?

A
  • Activates an enzyme which causes the breakdown of glycogen into glucose in the liver
  • Inactivating an enzyme that synthesises glycogen from glucose.
22
Q

How do insulin and glucagon interact?

A

They interact antagonistically

23
Q

What is diabetes?

A

A chronic illness where the person is unable to metabolise

24
Q

Describe the differences between type one and type 2 diabetes

A

Type 1:

  • (insulin dependent)
  • Body is unable to produce insulin
  • May have arisen in childhood when the body’s immune system attacked its own cells (beta cells in the islets of langerhans)

Type 2:

  • When glycoprotein receptors on the body cells lose their responsiveness to insulin
  • Or an inadequate supply of insulin from the pancreas
25
Q

How is type 1 diabetes controlled?

A
  • Insulin injections

- Injected a few times a day

26
Q

How is type 2 diabetes controlled?

A
  • Regulating the intake of carbohydrate
  • Matching this to the amount of exercise taken
  • Either stimulating insulin production or supplementary insulin injections
  • Other drugs slow down the rate at which the body absorbs glucose from the intestine
27
Q

(2 marks)

Describe how hormones and local chemical mediators reach the cells they affect.

A
  1. Hormones in blood;
  2. Local chemical mediators spread by diffusion / spread
    directly;
28
Q

(2 marks)
Adrenaline binds to receptors in the plasma membranes of liver cells. Explain how this
causes the blood glucose concentration to increase.

A
1. Adenylate cyclase activated /
cAMP produced / second
messenger produced;
2. Activates enzyme(s) (in cell);
3. (So) glycogenolysis/
gluconeogenesis occurs /
glycogenesis inhibited;
29
Q

(1 mark)
Scientists made an artificial gene which codes for insulin. They put the gene into a
virus which was then injected into rats with type I diabetes. The virus was harmless to
the rats but carried the gene into the cells of the rats.
The treated rats produced insulin for up to 8 months and showed no side-effects. The
scientists measured the blood glucose concentrations of the rats at regular intervals.
While the rats were producing the insulin, their blood glucose concentrations were
normal.

The rats were not fed for at least 6 hours before their blood glucose concentration was
measured. Explain why

A
1. Glucose/sugar in food would
 affect the results;
2. Food/eating would affect
 blood glucose (level);
3. (Allows time for) blood
 glucose (level) to return
 to normal;
30
Q

(1 mark)
Scientists made an artificial gene which codes for insulin. They put the gene into a
virus which was then injected into rats with type I diabetes. The virus was harmless to
the rats but carried the gene into the cells of the rats.
The treated rats produced insulin for up to 8 months and showed no side-effects.

The rats used in the investigation had type I diabetes. This form of gene therapy may
be less effective in treating rats that have type II diabetes. Explain why.

A

Type 2 diabetes is a failure to
respond to insulin / still produces
insulin / is not insulin-dependent;

31
Q

(4 marks)
Scientists made an artificial gene which codes for insulin. They put the gene into a
virus which was then injected into rats with type I diabetes. The virus was harmless to
the rats but carried the gene into the cells of the rats.
The treated rats produced insulin for up to 8 months and showed no side-effects.

Research workers have suggested that treating diabetes in humans by this method of
gene therapy would be better than injecting insulin. Evaluate this suggestion.

A
1. Avoids injections / pain of
injections;
2. Long(er) lasting / permanent
/ (new) cells will contain/
express gene;
3. Less need to measure blood
sugar / avoids the highs and
lows in blood sugar;
4. Less restriction on diet;
(Against) – 3 max
5. Rats are different to humans;
6. May have side effects on
humans;
7. Long(er) term effects (of
treatment) not known / may
have caused effects after 8
months;
8. (Substitute) insulin may