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Biology A2 > Homeostasis > Flashcards

Homeostasis Flashcards

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1
Q

Homeostasis definition

A

physiological control systems maintaining an internal environment within restricted limits in organisms.

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2
Q

Importance of homeostasis - general

A

cells of the body are in an environment that suits their requirements and means they can function normally despite external change. There are constant fluctuations around the optimum point.

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3
Q

Why is maintaining a constant body temperature important?

A

Low temp - a decrease in enzyme activity and the rate of biochemical reactions as molecules have less KE. Eg low respiratory rate - ATP needed by cells cannot be produced fast enough.
High temp - enzymes and proteins may not function as efficiently of be denatured, so metabolic reactions cannot be catalysed.

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4
Q

Importance of maintaining a constant pH

A

Enzymes and proteins may function less efficiently or become denatured if pH fluctuates far away from the optimum.

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5
Q

Importance of maintaining a constant blood water potential

A

Changes to blood water potential can cause cells to shrink or expand/ burst by water entering or leaving by osmosis. This means the cell can’t function normally. Maintaining a constant blood glucose concentration is important in keeping WP constant, as well as for ensuring cells have a reliable glucose source for respiration.

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6
Q

Why is maintaining a constant BGC important?

A

For keeping WP constant, as well as for ensuring cells have a reliable glucose source for respiration.

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7
Q

Positive feedback

A

Deviation from the optimum point causes changes that lead to even greater deviation.

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8
Q

Examples of positive feedback

A

Stimulation of a generator potential and action potential in neurones, hyper/ hypothermia

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9
Q

Negative feedback

A

Deviation from the optimum triggers a mechanism to return it to the optimum. When this happens, corrective mechanisms are switched off.

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10
Q

The role of the pancreas in regulating BGC

A

The pancreas is a gland which produces the hormones insulin and glucagon. Groups of hormone producing cells = islets of Langerhans, including α cells which produce glucagon and β cells which produce insulin.

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11
Q

Where do the hormones produced by the pancreas have their effect?

A

The liver

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12
Q

3 important processes involved in BGC which occur in the liver

A

Glycogenesis, glycogenolysis, gluconeogenesis

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13
Q

What is glycogenesis?

A

conversion of glucose to glycogen, this occurs when BGC is high. Glucose is removed from the blood by the liver, then converted.

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14
Q

What is glycogenolysis?

A

the breakdown of glycogen to form glucose. This occurs when BGC is low - the liver converts glycogen back into glucose which diffuses into the blood to raise BGC.

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15
Q

What is gluconeogenesis?

A

The production of glucose from sources other than carbohydrates, eg glycerol and amino acids. This occurs when the liver’s glycogen supply runs out.

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16
Q

What is the advantage of having separate negative feedback mechanisms to control departure from the optimum in both directions?
BGC example

A

There are positive actions in both directions, giving a greater degree of homeostatic control.

eg if glucagon raises BGC above the optimum, it would take a while to fall if it could only be lowered through metabolic activity. However, insulin allows BGC to be lowered and returned to the optimum much more rapidly.

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17
Q

When is insulin secreted?

A

when BGC rises

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18
Q

The action of insulin

3

A
  • attaches to receptors on the surfaces of target cells
  • controls the uptake of glucose by regulating the inclusion of channel proteins in the surface membranes of target cells (by making vesicles containing the protein channels in their membrane fuse with the CSM)
  • activates enzymes involved in the conversion of glucose to glycogen
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19
Q

How is BGC returned to the opt when it increases?

A

increase is detected by receptor cells in the pancreas, which produce insulin. Insulin causes an increase in the rate of glucose uptake by cells and glycogenesis, eg in the liver, to BGC returns to opt.
Lowering BGC causes β cells to secrete less insulin - this is negative feedback.

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20
Q

How does BGC fall without the action of insulin (eg in diabetics)

A

Glucose is taken into cells to be used for respiration and is secreted in urine

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21
Q

When is glucagon released

A

when a fall in BGC is detected

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22
Q

What is the effect of insulin

A

To decrease BGC

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23
Q

The action of glucagon

A
  • Attaches to receptors on the CSM of target cells (eg liver cells).
  • Activates enzymes that convert glycogen to glucose. (glycogenolysis)
  • Activating enzymes involved in gluconeogenesis - conversion of amino acids and glycerol to glucose.
    (gluconeogenesis)
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24
Q

Negative feedback with hormones

A

the secretion of a hormone results in a reduction in its own secretion.

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25
Q

The role of adrenaline

A

Adrenaline is a hormone involved in the ‘fight-or-flight’ response. It is produced by the adrenal glands at times of stress, excitement or danger.

Adrenaline raises BGC:

  • Attaching to protein receptors on the CSM of target cells
  • Activating enzymes involved in converting glycogen to glucose.
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26
Q

Why is it important that adrenaline increases BGC

A

muscles need more glucose for stronger contractions under the influence of adrenaline.
- fight or flight response.

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27
Q

The second messenger model of glucagon/ adrenaline action

A
  1. Adrenaline/ glucagon binds to a transmembrane protein receptor on a liver cell CSM.
  2. This binding causes the protein to change shape on the inside of the membrane.
  3. The shape change leads to activation of an enzyme called adenylate cyclase.
  4. Adenylate cyclase converts ATP to cyclic AMP (cAMP).
  5. cAMP acts as a second messenger, binding to protein kinase enzyme, changing its shape and activating it.
  6. Active protein kinase enzyme catalyses the conversion of glycogen to glucose, which leaves liver cells by facilitated diffusion into the blood.
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28
Q

The effect of glucagon

A

an increase in BGC, which returns to its optimum. This causes α cells to secrete less glucagon. (negative feedback)

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29
Q

How is type 1 diabetes caused?

A

the body cannot produce insulin. This could be due to an autoimmune response where the body attacks its own β cells. Type I diabetes normally begins in childhood, develops quickly and has obvious symptoms.

30
Q

Which type of diabetes is ‘insulin dependent’ and which is not?

A

Type 1 is insulin dependent.

31
Q

How is type 1 diabetes managed?

A

by injecting insulin. The dose of insulin must be matched to the glucose intake, so BGC is monitored using biosensors. Carbohydrate intake and exercise must also be managed.

32
Q

How is type 2 diabetes caused?

A

glycoprotein receptors on body cells become lost or unresponsive to insulin, or the supply of insulin from the pancreas is inadequate. Type II generally develops slowly in middle-aged people and has less severe symptoms. People who are overweight or have a poor diet are more likely to develop type II diabetes.

33
Q

How is type 2 diabetes controlled?

A

by carefully managing carbohydrate intake and the amount of exercise taken. Drugs which stimulate insulin production may also be taken.

34
Q

Where are receptors which detect changes in BGC levels located?

A

The pancreas

35
Q

Where are receptors which detect changes in blood temperature located?

A

The hypothalamus

36
Q

Name 1 organ in the human body containing cells with glucagon receptors.

A

The liver

37
Q

Name the processes stimulated to occur when glucagon is secreted

A

Gluconeogenesis, glycogenolysis

38
Q

How is high BGC returned to normal?

A

High BGC detected by the pancreas, stimulates B cells to release insulin. Insulin causes increased glucose uptake, eg glucose to glycogen by the liver, uptake by muscles.

39
Q

Which cells have large glycogen stores?

A

liver and muscle

40
Q

Which cell types produce insulin?

A

Beta cells in the pancreas/ islets of Langerhans

41
Q

Which cell types produce glucagon?

A

Alpha cells in the pancreas/ islets of Langerhans

42
Q

Why is osmoregulation important?

A

An optimum concentration of water and salts needs to be maintained in tissue fluid and blood plasma, as changes to water potential of these fluids can cause osmotic problems - cells expand or shrink and cannot function properly.

43
Q

Nephron structure

A

Nephron structure
Renal (Bowman’s) capsule: cup-shaped, surrounds the glomerulus. The inner layer is formed of specialised cells called podocytes.
Proximal convoluted tubule: loops surrounded by blood capillaries, epithelial cell walls with microvilli.
Loop of Henle: long, hairpin look extending from the cortex into the medulla and back. Surrounded by blood capillaries.
Distal convoluted tubule: series of loops surrounded by (fewer) blood capillaries with epithelial cell walls.
Collecting duct: tube into which several distal convoluted tubules connect. It becomes wider as it empties into the renal pelvis.

44
Q

Why does ultrafiltration occur in the glomerulus?

A

The diameter of the afferent arteriole is larger than that of the efferent arteriole, so hydrostatic pressure increases in the glomerulus. This means small molecules such as water and mineral ions are forced out of the capillary and into the renal capsule to form glomerular filtrate. Blood cells and proteins are too large to be forced out.

45
Q

Where in the nephron does ultrafiltration occur?

A

the glomerulus

46
Q

Where does reabsorption of water and glucose occur?

A

the proximal convoluted tubule

47
Q

Adaptations of PCT cells for reabsorption of water and glucose

A

microvilli provide LSA
mitochondria provide ATP for active transport
Carrier proteins for active transport
Channel proteins for facilitated diffusion

48
Q

Substances present in glomerular filtrate

A 
water
glucose
urea
amino acids/ fatty acids
ions, eg sodium
49
Q

substances not present in glomerular filtrate

A

blood cells, large proteins, platelets

50
Q

How is glucose reabsorbed in the PCT?

A

co-transport

51
Q

Describe the reabsorption of glucose in the PCT by co-transport

A
  1. Sodium ions are actively transported out of PCT cells into blood capillaries which carry them away, hence lowering sodium ion conc. in these cells.
  2. Sodium ions diffuse down a concentration gradient from the PCT lumen into epithelial lining cells via special facilitated diffusion carrier proteins.
  3. These carrier proteins also carry another molecule (glucose, amino acids, chloride ions … ) with the sodium ions - this is cotransport.
  4. The cotransported molecules then diffuse into the blood.
52
Q

How is the renal capsule adapted for ultrafiltration?

A

Podocytes, the specialised cells lining the renal capsule, have spaces between them to allow filtrate to pass through.
(capillaries in glomerulus also have spaces between endothelial cells)

53
Q

What is the role of the loop of Henle?

A

To maintain a gradient of sodium ions in the medulla

54
Q

Describe the gradient of sodium ions/ water potential in the medulla maintained by the loop of Henle

A

Sodium ion concentration increases and water potential decreases the further into the medulla you go,

55
Q

Describe the permeabilities of the ascending and descending limbs of the loop of Henle.

A

Descending - thin walls which are permeable to water

Ascending - wider with thicker walls which are impermeable to water

56
Q

Explain the role of the loop of Henle in the absorption of water from the filtrate

A
  • sodium ions are actively removed from the ascending limb
  • the ascending limb is impermeable to water
  • water moves out of the descending limb
  • the water potential in the medulla becomes more negative
  • the longer the loop, the greater the osmotic gradient, so more water is reabsorbed
  • water leaves the collecting duct by osmosis
57
Q

Explain the role of ADH in the production of concentrated urine

A
  • If the water potential of the blood is too low, this is detected by osmoreceptors in the hypothalamus.
  • The hypothalamus stimulates the pituitary gland to release more ADH
  • ADH increases the permeability of the collecting duct to water by increasing the number of aquaporins
  • more water is reabsorbed by osmosis, from the nephron into the blood
58
Q

Where is ADH produced and released into the blood?

A

produced in the hypothalamus and released at the pituitary gland

59
Q

What does ADH stand for?

A

antidiuretic hormone

60
Q

How does the binding of ADH to receptors in the kidney lead to an increase in blood WP?

A

ADH binds to specific protein receptors on the CSM of collecting duct and DCT cells, leading to the activation of the enzyme phosphorylase, which causes vesicles in the cell which contain aquaporins in their membrane to fuse with the CSM. The increase in numbers of aquaporins makes the membrane more permeable to water. water passes out of CD/DCT by osmosis and is reabsorbed by the blood.

61
Q

What happened once ADH has caused a rise in blood WP?

A

The rise in WP is detected by osmoreceptor cells, which send fewer impulses to the pituitary. Less ADH is released and the permeability of collecting ducts returns to normal. This is negative feedback.

62
Q

Compare and contrast the features of hormonal and nervous transmission

A

Hormones - have slow, long-lasting and widespread effects

Nerve impulses - rapid, short-lived and localised

63
Q

Why do hormones only have an effect on certain cells?

A

as only the target cells have the specific protein receptors which are complementary to the shape of the specific hormone

64
Q

How do hormones reach their target cells?

A

they travel in blood plasma

65
Q

What happens if blood WP rises above the optimum?

A

hypothalamus detects this, stimulating pituitary to release less ADH, so collecting duct becomes less permeable to water etc.

66
Q

Importance of the counter-current multiplier

A

needed to make urine which is more concentrated than blood plasma.
Counter-current flow between fluid in the descending and ascending limbs increases/ multiplies the osmotic gradient between fluid in the tubules and the medulla.
Counter-current flow between fluid in the collecting duct and ascending limb means that filtrate in the CD meets fluid in the medulla with an even lower WP - a WP gradient exists for the whole length of the collecting duct.

67
Q

Name the blood vessels associated with the nephron

A

Afferent arteriole, glomerulus, efferent arteriole, blood capillaries

68
Q

Role of the afferent and efferent arterioles in the nephron

A

Afferent arteriole - brings blood to the glomerulus

Efferent arteriole - recombined glomerulus - takes blood away from the renal capsule and glomerulus, has a smaller diameter than the afferent arteriole - this means blood in the glomerulus is under high pressure and small molecules are forced out. It then branches to form blood capillaries.

69
Q

Role of the glomerulus in the nephron

A

Glomerulus - branched knot of capillaries in the renal capsule from which fluid is forced out of the blood. (ultrafiltration). Glomerular filtrate is formed.

70
Q

Role of the blood capillaries in the nephron

A

a network of capillaries surrounding PCT, loop of Henle and DCT. This is where reabsorption of mineral salts, glucose and water occurs. Blood capillaries re-merge to form venules, which merge to form the renal vein.

Biology A2 (12 decks)

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