Chapter 14: Homeostasis Flashcards

1
Q

Homeostasis

A

the maintenance of constant internal environment regardless of changes in external environment

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2
Q

Using examples, outline the importance of homeostasis in a mammal

A
  1. Homeostasis: the maintenance of constant internal environment regardless of changes in external environment.
  2. The internal environment of an organism refers to all the conditions inside the body.
  3. Homeostatic mechanisms work by controlling the composition of blood, which therefore controls the composition of the tissue fluid.
  4. The factor fluctuates around particular ideal value, or set point.
  5. Temperature - low temperatures slow down metabolic reactions. high temperatures proteins (enzymes) are denatured and cannot function.
  6. Water potential - if wp decreases, osmosis -> metabolic reactions in the cell slow/ stop, cell shrink. if wp increases, osmosis into the cell -> swell + burst
  7. Conc. of glucose - glucose is the fuel for respiration -> lack of it = slow down respiration/stop. too much glucose -> osmosis out of cell -> cells shrink.
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3
Q

Outline principles of homeostasis with reference to glucose conc

A
  1. Homeostasis: maintenance of constant internal environment regardless of changes in external environment
  2. Negative feedback: process in which a change in some parameter, such as blood glucose level, brings about processes which move its level back towards normal again.
  3. Receptors detect changes in glucose levels
  4. Alpha cells produces glucagon and beta cells produce insulin in the islets of Langerhans
  5. Action taken by the effector (liver, muscles)
  6. Restoration of norm
  7. Fluctuations around the set point
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4
Q

Explain how stimuli, receptors, central control, coordination systems and effectors are involved in maintaining the internal environment of a mammal.

A
  1. Receptor (or sensor) detects stimuli (any change in a factor, such as a change in blood temperature or the water content of the blood)
  2. Receptors send information about the changes they detect to a central control through nervous system (input)
  3. Central control instructs an effector to carry out an action (output)
  4. Corrective actions: correct changes; continuous adjustments to the output.
  5. The factor fluctuates around a particular ideal value, or set point.
  6. Mechanism to keep changes in the factor within narrow limits: negative feedback.
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5
Q

Nervous system

A

information in the form of electrical impulses is transmitted along nerve cells (neurones)

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6
Q

Endocrine system

A

uses chemical messengers called hormones travel in the blood, in a form of long-distance cell signalling

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7
Q

Negative feedback

A

a process in which a change in some parameter, such as blood glucose level, brings about processes which move its level back towards normal again.

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8
Q

Excretion

A

The removal of unwanted products of metabolism

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9
Q

Excretory products

A
  1. Carbon dioxide
    - respiring aerobically
    - transport by bloodstream to the lungs from respiring cells
  2. Urea
    - produced in the liver
    - produced from excess amino acids
    - transported from the liver to the kidneys, in solution in blood plasma.
    - Kidneys remove urea from blood and excrete it, dissolved in water as urine.
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10
Q

Deamination

A
  • In the liver cells, the amino group (-NH2) of an amino acid is removed, together with an extra hydrogen atom.
  • Combine to produce ammonia (NH3) and keto acid
  • Keto acid: converted to glucose/ glycogen or enter the Krebs cycle and be respired.
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11
Q

Ammonia

A
  • very soluble and highly toxic compound
  • Aquatic animals, ammonia diffuses from the blood and dissolves in the water around the animal.
  • Terrestrial animals, ammonia would rapidly build up in the blood and cause immense damage.
  • > Damage is prevented by converting ammonia immediately to urea, which is less soluble and less toxic.
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12
Q

Urea

A

2NH3 + CO2 -> CO(NH2)2 + H2O (urea)
- the main nitrogenous excretory product
- small quantities of other products: creatinine and uric acid
+ Creatinine: muscles, form of creatine phosphate, energy store.
+ Uric acid: breakdown of purines from nucleotides, not from amino acids

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13
Q

Explain why it is important that carbon dioxide and nitrogenous wastes are excreted and not allowed to accumulate in the body

A
  • Its conc in the blood would build up and become dangerous.
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14
Q

The structure of the kidney

A
  • Renal Vein
  • Renal Artery
  • Afferent arteriole: supply blood to glomerulus by a branch of the renal artery.
  • Efferent arteriole: leads off to form a network of capillaries running closely alongside the rest of the nephron. Blood flow into a branch of the renal vein.
  • Pelvis: where ureter joins
  • thousand of tiny cubes called NEPHRONS
  • Bowman’s capsule: a cup-shaped structure
  • Glomerulus: tight network of capillaries
  • Podocytes: tiny finger-like projections with gaps in between them
  • Glomeruli + capsules of all the Nephrons in cortex
  • Proximal Convoluted Tubule in Cortex
  • Loop of Henle in medulla (descending, ascending): hairpin loop runs deep into the medulla.
  • Distal convoluted tubule
  • Collecting duct: leads down through the medulla and into the pelvis of the kidney
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15
Q

Kidney makes urine in a two-stage process

A
  • Ultrafiltration

- Selective reabsorption

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16
Q

Ultrafiltration

A
  • Reducing blood vessels diameter
  • Increases hydrostatic pressure
  • 3 barriers:
    + Cappillaries wall-gaps
    + Basement membrane: collagen + glycoproteins
    + Podocytes , gaps between processes
  • Glomerular filtrate (< 68,000 RMM)
    + Urea
    + Glucose
    + Amino acid
    + Small protein
    + Inorganic ions (Chloride, Sodium, Potassium)
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17
Q

Endothelium

A
  • first cell layer is the lining of the capillary

- it has gaps, but more gaps in other capillary (each endothelial cell has thousands of tiny holes in it.

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18
Q

Epithelial cells

A
  • inner lining of the Bowman’s capsule

- these cells have many tiny finger-like projections with gaps in between them, and are called podocytes.

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19
Q

Factors affecting glomerular filtration rate

A
  • The rate at which the fluid filters from the blood in the glomerular capillaries into the Bowman’s capsule. (human: 125 cm3min-1)
  • Differences in WP between the plasma (glomerular capillaries) and filtrate (Bowman’s capsule)
  • WP is lowered by the presence of solutes, and raised by HIGH PRESSURES.
  • Inside the capillaries (glomerulus), high BLOOD PRESSURE (efferent < afferent) -> raise WP in blood plasma.
  • Concentration of solutes in blood plasma > than solutes in the Bowman’s capsule. (protein molecules are too big to get through - 68000 MM) -> WP lower than the filtrate in the Bowman’s capsule.
  • Effect of differences in PRESSURE outweighs the effect of differences in solute conc. The WP of the blood plasma > filtrate in the capsule. So water MOVES DOWN the WP gradient from the blood into the capsule.
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20
Q

Reabsorption in the proximal convoluted tubule

A
  • Selective reabsorption: many of the substances in glomerular filtrate need to be kept in the body
  • In proximal convoluted tubule (in cortex)
  • lining is made of a single layer of cuboidal epithelial cells
  • Adaptation of cuboidal epithelial cells for reabsorption:
    + MICROVILLI: increase the surface area of the inner surface facing the lumen.
    + TIGHT JUNCTIONS: hold adjacent cells together so that fluid cannot pass between the cells, but go through the cells.
    + MANY MITOCHONDRIA: provide energy for sodium - potasium (Na+ - K+) pump proteins in the outer membranes of the cells.
  • CO-TRANSPORTER PROTEINS in the membrane facing the lumen for sodium to move passively into the tubule down its conc gradient, b
  • Process:
    1. Basal membrane of PCT use ATP for sodium - potassium pump. DECREASE the conc of sodium ions in the cytoplasm. FOLDED BASAL MEMBRANE gives large surface area for carrier proteins.
    2. BLOOD PLASMA absobed Na*, Cl-, glucose and amino acids. This helps further uptake from the lumen of the tubule.
    3. Microvilli INCREASE surface area, helping uptake of solutes. Na+ moves passively into the cell down its conc gradient. It moves in using protein co-transporter molecules in the membrane, which bring in glucose and amino acids at the same time.
  • Urea is reabsorbed too since it is a small molecule which passes easily through cell membranes.Its conc in the filtrate is considerably higher than that in the capillaries, so it diffuses passively into the blood.
  • Other two nitrogenous excretory products: uric acid and creatinine: actively secreted by the cells of the proximal tubule into its lumen, not reabsorbed.
    -> reduces the V of liquid remaining. In adult, 125cm3min-1 enter PCT, only 64% passes on to the loop of Henle.
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21
Q

Reabsorption in the loop of Henle and collecting duct

A
  • loop of Henle in medulla
  • Allows production of very concentrated urine, water is conserved in the body, helping to prevent DEHYDRATION.
  • Descending loop of Henle: permeable to Na+ and water
  • Ascending loop of Henle: permeable to Na+ and impermeable to water
  • The longer the loop, the more concentrated the fluid inside the loop.
    1. Na+ and Cl- are actively transported out of the ascending limb.
    2. This raises the conc of Na+ and cl- in the tissue fluid.
    3. This in turn causes the loss of water from the descending limb
    4. The loss of water concentrates Na+ and Cl- in the descending limb
    5. Na+ and Cl- ions diffuse out of this concentrated solution in the lower part of the ascending limb.
  • > Counter-current mechanism in the loop of Henle builds up high conc of Sodium ions and Chloride ions in the tissue fluid of the medulla.
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22
Q

Reabsorption in the loop of Henle and collecting duct

A
  • loop of Henle in medulla
  • Allows production of very concentrated urine, water is conserved in the body, helping to prevent DEHYDRATION.
  • Descending loop of Henle: permeable to Na+ and water
  • Ascending loop of Henle: permeable to Na+ and impermeable to water
  • The longer the loop, the more concentrated the fluid inside the loop.
    1. Na+ and Cl- are actively transported out of the ascending limb.
    2. Raises the conc of Na+ and cl- in the tissue fluid.
    3. Loss of water from the descending limb
    4. Concentrates Na+ and Cl- in the descending limb
    5. Na+ and Cl- ions diffuse out of this concentrated solution in the lower part of the ascending limb.
  • > Counter-current mechanism in the loop of Henle builds up high conc of Sodium ions and Chloride ions in the tissue fluid of the medulla.
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23
Q

Ability of some small mammals (rodents) produce very concentrated urine

A
  • Related to the relative thickness of the medulla in their kidneys.
  • Large medulla
  • Deep infolds with many Na+ - K+ pump in ascending loops of Henly
  • Many mitochondria with many cristae in cytoplasm, production of ATP -> energy for the pumping of sodium ions into the tissue fluid.
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24
Q

Reabsorption in the distal convoluted tubule and collecting duct

A
  • First part of distal convoluted tubule functions - same way as the ascending limb of the loop of Henle.
  • 2nd part fuction = same way as the collecting duct
  • In the distal convoluted tubule and collecting duct, Sodium ions (Na+) are actively pumped from the fluid in the tubule into the tissue fluid, from where they pass into the blood.
  • Potassium ions (K+)
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25
Q

Reabsorption in the distal convoluted tubule and collecting duct

A
  • First part of distal convoluted tubule functions - same way as the ascending limb of the loop of Henle.
  • The cells of the ascending limb of the loop of Henle and the cells lining of the collecting ducts are permeable to urea, which diffuses into the tissue fluid.
  • > Urea is also concentrated in the tissue fluid in the medulla.
  • Therefore, fluid passes once again through the regions where the solute concentration of the tissue fluid is very high and the WP is very low.
  • > Water can move out of the collecting duct, by osmosis, until the WP of urine is the same as the WP of tissue fluid in the medulla.
  • 2nd part fuction = same way as the collecting duct
  • In the distal convoluted tubule and collecting duct, Sodium ions (Na+) are actively pumped from the fluid in the tubule into the tissue fluid, from where they pass into the blood.
  • Potassium ions (K+) are actively transported INTO the tubule.
  • The rate at which these two ions are moved into and out of the fluid in the nephron can be varied.
  • > Helps to regulate the concentration of these ions in the blood.
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26
Q

Osmoregulation

A

the control of the water potential of body fluid. This regulation is an important part of homeostasis and involves the hypothalamus, posterior pituitary gland and the kidneys.

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27
Q

Osmoregulation

A

the control of the water potential of body fluid. This regulation is an important part of homeostasis and involves the hypothalamus, posterior pituitary gland and the kidneys.

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28
Q

Osmoreceptors

A

The WP of the blood is constantly monitored by specialised sensory neurones in the hypothalamus

29
Q

Antidiuretic hormone (ADH)

A

a peptide hormone made of nine amino acids

30
Q

How ADH affects the kidneys

A
  • Low blood water potential detected by osmoreceptors in hypothalamus
  • Neurosecretory cells stimulated to produce ADH
  • ADH released by posterior pituitary gland
  • ADH transported in blood
  • Affects the collecting duct
  • Binds to receptors on cell surface membrane
  • Activate series of enzyme controlled reactions
  • Causes aquaporin to move to cell surface membrane, and fuse with it.
  • Cell become more permeable to water, so water moves out of lumen of collecting duct down a water potential gradient by osmosis into tissue fluid
  • Increases the water potential of the blood.
31
Q

Osmoreceptors

A
  • specialised sensory neurones in the hypothalamus constantly monitor the water potential of the blood.
  • send nerve impluses to posterior pituitary gland when there’s a decrease in water potential of the blood.
32
Q

How ADH affects the kidneys

A
  • Low blood water potential detected by osmoreceptors in hypothalamus
  • Neurosecretory cells stimulated to produce ADH
  • ADH released by posterior pituitary gland
  • ADH transported in blood
  • Affects the collecting duct
  • Binds to receptors on cell surface membrane
  • Activate series of enzyme controlled reactions, ending with the production of an active phosphorylase enzyme
  • Causes aquaporins to move to cell surface membrane, and fuse with it.
  • Cells become more permeable to water, so water moves out of lumen of collecting duct down a water potential gradient by osmosis into tissue fluid
  • Increases the water potential of the blood.
33
Q

Aquaporins

A

the number of the water-permeable channels

34
Q

Negative feedback in osmoregulation:

A
  • Homeostasis
  • Change in water potential in blood detected by osmoreceptors in hypothalamus
  • Response via effector, so that ADH is released and has its effect on the collecting duct
  • The water potential level return to normal/set point.
35
Q

Urea Cycle:

A
  • Deamination of excess amino acids to form ammonia, which, when combined with CO2, forms Urea.
  • Urea cycle/ ornithine cycle.
36
Q

How glomerular filtrate is formed:

A
  • Afferent arterioles lumen are wider than efferent arteriole lumen, so the higher pressure in glomerulus forces fluids into the capsule to the lower pressure in Bowman’s capsule
  • There are many large gaps between endothelium cells of endothelium of blood capillaries
  • Large gaps between podocytes
  • Basement membrane acts as a filter, so nothing more than 68000 RMM (relative molecular mass) passing through
  • No cells pass through
  • Glucose, water, urea,… does pass through
  • Filtrate passes to Bowman’s capsule
37
Q

Mechanisms used and adaptations in reabsorption in PCT

A
  • Active transport of Na+ out of PCT
    endothelium cells into blood, setting up a Na+ ion gradient
  • Facilitated diffusion using protein carrier or cotransport of glucose, amino acids, and ions
  • Osmosis down water potential gradient
  • Diffusion down a concentration gradient
  • Microvilli
  • Many mitochondria
  • Tight junctions
  • Folder basal membrane
  • Many transport proteins/ cotransporters/ pumps
  • Many aquaporins
38
Q

Reabsorption of Glucose from kidney nephron:

A
  • All happens in PCT
  • Na+ actively transported out of cell into tissue fluid
  • Na+ conc decreases in the cell
  • Na+ enters cell from lumen by facilitated diffusion. This is called secondary active transport
  • Brings with it glucose by cotransport.
  • Glucose diffuse out into tissue fluid through GLUT proteins
  • Microvilli on lumen side increases surface area for reabsorption
  • Tight junctions separate proteins of front and basolateral membranes
39
Q

Adaptations of

A
- epithelial cells of PCT:
\+ Tight Junctions
\+ Folded basal membrane
\+ Many transport proteins
\+ Many aquaporins
\+ Microvilli
\+ Many mitochondria
- Glomerular Capillaries:
\+ Gaps in capillary endothelium
\+ Basement membrane acts as filter
\+ No substances larger than 68000 MM can get through
\+ So no cells can get through
- Podocytes:
\+ Have projections and gaps between projections.
40
Q

Glycogen

A

short-term energy store that is found in liver and muscle cells and is easily converted to glucose.

41
Q

Healthy human

A

Each 100cm3 of blood normally contains between 80 and 120 mg of glucose

42
Q

Conc of glucose below normal level

A
  • May not have enough glucose for respiration (brain cells)

- Unable to carry out normal activities

43
Q

Very high conc of glucose

A
  • Upsetting the normal behaviour of the cells.
44
Q

The homeostatic control of blood glucose concentration

A
  • Endocrine tissue in the pancreas has group of cells called islets of Langerhans
  • islets contain 2 types of cells:
    + a cells secrete GLUCAGON
    + b cells secrete INSULIN
  • The a and b cells act as the receptors and the central control for this homeostatic mechanism.
  • Hormones (glucagon and insulin) coordinate the actions of the effectors.
45
Q

Negative feedback control of high blood glucose concentration

A
  1. High blood glucose concentration (higher than set point)
  2. Receptors: a and b cells n the islets of Langerhans detect rise in blood glucose
    - > less glucagon and more insulin secreted
  3. Effectors:
    - Liver cells respond to less glucagon - no glycogen breakdown
    - Liver, muscle and fat cells respond to more insulin - increased uptake and use of glucose.
46
Q

Negative feedback control of low blood glucose concentration

A
  1. Low blood glucose concentration (lower than set point)
  2. Receptors: a and b cells in the islets detect fall in blood glucose
    - > more glucagon, less insulin
  3. Effectors:
    - Liver cells respond to move glucagon by breaking down glycogen into glucose
    - Liver, muscle and fat cells respond to less insulin - reduced uptake of glucose.
47
Q

Negative feedback control of low blood glucose concentration

A
  1. Low blood glucose concentration (lower than set point)
  2. Receptors: a and b cells in the islets detect fall in blood glucose
    - > more glucagon, less insulin
  3. Effectors:
    - Liver cells respond to move glucagon by breaking down glycogen into glucose
    - Liver, muscle and fat cells respond to less insulin - reduced uptake of glucose.
48
Q

Outline principles of homeostasis with reference to glucose conc

A
  • Homeostasis is the maintenance of constant internal environment regardless of changes in external environment
  • Negative feedback
    + Receptors detect changes in glucose levels
    + Alpha cells produces glucagon and beta cells produce insulin in the islets of langerhan
    + Action taken by the effector (liver, muscles)
    + Restoration of norm
    + Fluctuations around the norm
49
Q

After a meal containing carbohydrate

A
  • Glucose from the digested food is absorbed from the small intestine and passes into the blood.
  • As this blood flows through the pancreas, the a and b cells detect the increase in glucose concentration.
  • > a cells respond by stopping the secretion of glucagon
  • > b cells respond by secreting insulin into the blood plasma.
  • The insulin is carried to all parts of the body, in the blood.
50
Q

Insulin

A
  • signalling molecule
  • Protein: cannot pass through cell membranes to stimulate the mechanisms within the cell directly.
  • BINDS to a receptor in the cell surface membrane in muscle cells
  • CONVERT Glucose -> Glycogen
  • STIMULATES the activation of the enzyme glucokinase, which phosphorylates glucose.
  • > TRAPS glucose inside cells. Phosphorylated glucose cannot pass through the transporters in the cell surface membrane .
  • STIMULATES the activation of 2 enzymes: phosphofructokinase and glycogen synthase: together add glucose molecules to glycogen. THIS INCREASES the size of the glycogen granules inside the cell.
51
Q

Insulin

A
  • signalling molecule
  • Protein: cannot pass through cell membranes to stimulate the mechanisms within the cell directly.
  • BINDS to a receptor in the cell surface membrane in muscle cells
  • CONVERT Glucose -> Glycogen
  • STIMULATES the activation of the enzyme glucokinase, which phosphorylates glucose.
  • > TRAPS glucose inside cells. Phosphorylated glucose cannot pass through the transporters in the cell surface membrane .
  • STIMULATES the activation of 2 enzymes: phosphofructokinase AND glycogen synthase: together add glucose molecules to glycogen. THIS INCREASES the size of the glycogen granules inside the cell.
52
Q

The insulin receptors

A
  • on many cells: liver, muscle and adipose (fat storage) tissue.
53
Q

Glucose transporter protein (GLUT)

A
  • Glucose can only enter cells through transporter proteins.
  • Muscles: GLUT4
  • Brain: GLUT1 (ON SURFACE)
  • Liver: GLUT2 (ON SURFACE)
  • Normally are kept in cytoplasm (as aquaporins)
  • When insulin binds to receptors, the vesicles with GLUT4 proteins moved to the cell surface membrane, and fuse with it.
  • Facilitated diffusion for glucose.
54
Q

Low conc of glucose - glucagon?

A
  1. Glucagon binds to membrane receptor
  2. Activation of G protein and then enzyme.
  3. Active enzyme produces cyclic AMP from ATP.
  4. Cyclic AMP activates protein kinase to activate an enzyme cascade
  5. Enzyme cascade leads to activation of many molecules of glycogen phosphorylase that break down glycogen.
55
Q

Low conc of glucose - glucagon?

A
  • MUSCLE CELLS don’t have glucagon.
    1. Glucagon binds to membrane receptor
    2. Activation of G protein and then enzyme.
    3. Active enzyme produces cyclic AMP from ATP.
    4. Cyclic AMP activates protein kinase to activate an enzyme cascade
    5. Enzyme cascade leads to activation of many molecules of glycogen phosphorylase that break down glycogen.
56
Q

Gluconeogenesis

A

Glucose is made from amino acids and lipids in a process.

57
Q

Glucagon

A
  • BINDS to a different receptor molecules in the cell surface membrane of LIVER cells
  • ACTIVATES a G protein -> ACTIVATES an enzyme within the membrane that catalyses the conversion of ATP to cyclic AMP, which is a SECOND MESSENGER.
  • Cyclic AMP binds to kinase enzymes within cytoplasm that activate other enzymes by ADDING phosphate groups to them (Phosphorylation)
  • > This enzyme cascade AMPLIFIES the original signal from glucagon.
  • Glycogen phosphorylase at the end of the enzyme cascade: when activated, it catalyses the breakdown.
58
Q

The hormone adrenaline

A
  • INCREASES the concentration of blood glucose.
  • BINDING to different receptors on the surface of liver cells that activate the SAME enzyme cascade and lead to the breakdown of glycogen by glycogen phosphorylase.
  • STIMULATES the breakdown of glycogen stores in muscle during exercise.
59
Q

Diabetes/ Diabetes mellitus

A
  • Type 1 diabetes: insulin-dependent diabetes:
    + Pancreas seems to be incapable of secreting sufficient insulin
    + Might be due to a deficiency in the gene that codes for the production of insulin.
    + because of an attack on the b cells by the persom’s own immune system.
    + begins very early in life.
  • Type 2 diabetes: non-insulin-dependent diabetes
    + the pancreas does secrete insulin, but the liver and muscle cells do not respond preperly to it.
    + begins relatively late in life, associated with diet and obesity
60
Q

Symptoms of diabetes mellitus

A
  • After a carbohydrate meal, glucose is absorbed into the blood, the conc increases and stays high.
  • Kidney CANNOT REABSORB all the glucose, so that some passes out in the urine.
  • Extra water and salts accompany with glucose, and the person consequently feels extremely HUNGRY and THRISTY.
  • UPTAKE of glucose into cells is slow, cells lack of glucose, metabolise fats and proteins as alt. enery sources.
  • > Build-ip of keto-acids in blood, decrease the blood pH. The combination of DEHYDRATION, SSALT LOSS and LOW BLOOD pH -> coma in extreme situations
  • Blood glucose conc of a person with untreated diabetes may decrease steeply, because there’s no glycogen to mobilise, not stored. -> coma, laco of glucose for respiration.
61
Q

Treatment for Diabetes

A

Type 1:
+ receive regular injections of insulin (do themselves) - by mini pumps
+ Take blood samples to check that the insulin is effective
+ Carefully controlled diet
Type 2:
+ Use diet and regular and frequent exercise to keep blood glucose within normal limits.
- Receive insulin made by genetically enginerred cells.

62
Q

Unrine analysis

A
  • Early indications of health problems.
  • Presence of glucose and ketones in urine:
    + Diabetes
    + Blood glucose conc increases above a certain value (renal threshold) -> not all glucose is reabsorbed from the filtrate in the PCT.
  • Presence of protein
    + sth wrong with kidneys because proteins are too large to be filtered.
    + in short time: high fever, after vigorous exercise, during pregnancy.
    + long-term: disease affecting the glomeruli or there is a kidney infection.
    + associated with high blood pressure, risk factor in heart disease.
63
Q

Dip sticks

A
  • Test strips
  • Test urine for a range of different factors (pH, glucose, ketones, protein)
  • Contain enzymes glucose oxidase and peroxidase IMMOLBILISED on a small pad at one end of the stick
  • Pad is immersed in urine
  • Glucose present: glucose oxidase catalyses a chemical reaction in which glucose is oxidised into gluconolactone.
  • Hydrogen peroxide produced: peroxidase catalyses a reaction between and a colourless chemical in the pad to form a BROWN compoud.
  • The more glucose present, the darker the colour (green, reddish, brown)
64
Q

Biosensor

A
  • Allows people with diabetes to check their blood to see glucose conc.
  • A pad impregnated with glucose oxidase
  • Small sample of blood is placed on the pad -> inserted into the machine.
  • Glucose oxidase CATALYSES the reaction to produce gluconolactone + tiny electric current is GENERATED.
  • Current is detected by an electrode, amplified and read by the meter which produces a reading for blood glucose conc within seconds.
  • The more glucose, the greater the reading.
65
Q

Stomata open in respond to changes in environmental conditions. Open in response to:

A
  • increasing light intensity
  • low carbon dioxide conc in the air spaces within the leaf
  • > gain CO2 for photosynthesis, but tend to lose much water in transpiration.
66
Q

Stomsta close in response to:

A
  • Darkness
  • High carbon dioxide conc in the air spaces in the leaf
  • Low humidity
  • High temperature
  • Water stress, when the supply of water from the roots is limited and there are high rates of transpiration.
  • > Daylight, supply of CO2 decreases -> Photosynthesis decreases.
  • > Water retained inside the leaf (important in times of water stress)
67
Q

Opening and closing of stomata

A
  1. ATP -powered proton pumps in the cell surface membrane actively transport H+ out of the guard cell
  2. The low H+ conc and the negative charge inside the cell causes K+ channels to open. K+ diffuses into the cell down an electrochemical gradient.
  3. The high conc of K+ inside the guard cell lowers the water potential
  4. Water moves in by osmosis, down a WP gradient
  5. The entry of water increases the volume of the guard cells, so they expand, The thin outer wall expands most, so the cells curve apart.
68
Q

Mechanism of guard cells

A
  • Open when they gain water to become TURGID and close when they lose water and become FLACCID
  • gain and lose water by OSMOSIS.
  • A decrease in WP
69
Q

Electrochemical gradient

A

a gradient across a cell surface membrane that involves both a difference in conc of ions and a potential difference.