Biology A Level- Homeostasis

1. Chapter 14: Homeostasis

2. Homeostasis
• Maintenance of constant internal environment
• Keep set point within narrow limits in body
• Irrespective of changes in external environment
• Factors such as temperature, water potential,
glucose concentration must be maintained in the
tissue fluid because its affects cell function
• So that internal environment can:
• be stable
• function optimally

4. Negative feedback mechanism
• The body works in negative feedback mechanism

5. Stimulus
• Refers to Internal or external
changein factor awayfrom
norm/set-point
Receptor • Cells/Tissue/organwhich detect
the stimulus
Coordinating
Centre
• Receives and processesmessages, in the from
of hormonesor nerve impulses, from the
receptore, and determinestheappropriate
response
• Only if the stimulusreachesthethreshold, it
will send messagesto the effector
Effector
• Receive messagesfrom
coordinatingcentreand carry
out the correctivereaction
Response
• The reaction
carried out by the
effectors
• Returnto the
norm/set-point

6. Negative Feedback
• Continuous monitoringof the factor affecting the internal
environment
• Results in many ‘corrective actions’
• Factors thus fluctuates around the norm/set-point

7. Positive feedback vs. Negative feedback
Response reinforce the original
stimulus
Response counteracts the
original stimulus
Very uncommon Common in the body
Response worsen / intensifies the
initial changes
To maintain homeostatis / stable
internal environment
e.g: labor pains, ripening of the fruit,
inhalation of CO2
e.g: maintaining blood glucose levels,
temperature, oxygen level, water
content

8. Osmoregulation
Chapter outline
• Deamination and the urea cycle
• Structure of the kidney
• Structure of the nephron
• Mechanism of excretion in the kidney
▫ Ultrafiltration
▫ Selective reabsorption
• Osmoregulation

9. Excretion
• Removal of unwanted products of metabolism
•  Toxic, poisonous, will cause damage to the tissue
• Main excretory products
a) Carbon dioxide
• -> aerobic respiration
• -> excreted via bloodstream and lungs
b) Urea (nitrogenous waste)
• Produced in liver
• From excess amino acids
• Excreted via kidneys

10. • C) Creatinine
• Small amounts produced in liver
• From certain amino acids
• Most used as energy storage in muscles
• Excreted via kidney
• D) Uric acid
• Produced in liver
• From excess purine of nucleotides
• Excreted via kidney

11. Urea
• Main nitrogenous excretory product
• Formed in excess amino acids
• In liver cells
• 1. Deamination
• Remove the amine group and a H atom from amino acid
• Produce ammonia,NH3
• 2. Urea cycle (ornithine cycle)
• Ammonia + carbon dioxide+ urea  excreted (kidney)
• Keto acid remains  respired or converted to glucose/glycogen/fat

13. Structure of Kidney
• Capsule
•  Tough, protective layer
• 3 main region
• A. Cortex
• B. Medulla
• C. Pelvis
• Nephrons- tiny tubes in the kidney in the cortex
and medulla

14. Structure of the Kidney

16. Structure of the Nephron
1. 1. Bowman’s capsule
2. a.k.a renal capsule
3. Proximal convoluted tubule @ cortex
4. Loop of Henle @ medulla
1. Descending limb
2. Ascending limb
5. Distal convoluted tubule @ cortex
6. Collecting duct
•  ureter @pelvis

17. Nephron stucture

18. Structure of a Nephron
• Branch of renal artery
 afferent arteriole
 glomerulus (tangle of capillaries in the ‘cup’ of
the capsule
Efferent arteriole
 Network of blood capillaries surrounding the
the rest of the nephron
Branch of renal vein

24. Mechanism of Excretion in Kidney
• 2 stages:
• 1. Ultrafltration
• Filtering of small molecules (including urea)
@ Bowman’s capsule
• 2. Selective Reabsorption
• Absorbing any useful molecules from fluid in
nephron
@ proximal convoluted tubules, loop of Henle,
distal convoluted tubules and collecting duct

25. Ultrafiltration
• Filtering of small
molecules
• Out of blood in
glomerulus
•  into filtrate in
Bowman’s capsule
space / lumen
• Glomerular filtrate is
produced
• Flows along the entire
nephron

26. Ultrafiltration
Structure of Glomerular wall and Bowman’s capsule
• Refer to Figure 14.9 pg. 355
• 1. Endothelium of blood capillaries of the glomerulus
• Wtih many gaps / fenestrations
• 2. basement membrane
• Mesh of collagen and glycoprotein fibres
• Acts as main selective barrier / filter
• 3. Epithelial cells of Bowman’s capsule (podocytes)
• Inner lining of Bowman’s capsule
• Wrap around capillaries of the glomerulus
• Podocytes have many finger-like projections that forms
gaps/filtration slits

29. How the structure adapted for
ultrafiltration?
1. Many large gaps in capillary endothelium &
filtration slits between foot processes of podocytes
• Allow movements of substances from blood plasma
easily into Bowman’s capsule
2. Diameter of the lumen of afferent arteriole is wider
than the efferent arterioles
• Leads to high blood pressure / hydrostatic pressure
in the glomerulus than the Bowman’s capsule
• Fluid forced out of glomerulus into Bowman’s
capsule

30. 3. Basement membraneacts as the filter
• prevents RBCs, WBCs, & large plasma protein
from passing through (68k Da)
• Resulting glomerular filtrate contains:
• No cells and large proteins
• Soluble molecules: water, amino acids, glucose,
urea, inorganic ions (Na, K, Cl), uric acid, creatinine,
vitamins
• Glomerular filtrate passes through gaps between
podocytes and into renal capsule

31. 2) Selective Reabsorption
• Necessary
• To reabsorp essential substances from filtrate
back into blood
• Selective reabsorption so only certain substances
are reabsorbed; glucose, amino acids, vitamins,
Cl, Na, H2O
• @ proximal convoluted tubules, loop of Henle,
distal convoluted tubule and collecting duct

34. • Selective Reabsorption at Proximal convoluted
tubule:
- main site for glucose/ amino acid/ vitamins/ Cl
reabsorption
- Walls made up of single layer of cuboidal
epithelial cells

35. 1. active transport for Na ions
from PCT cells into blood
• Via Na/K ions pumps
• Concentration of Na ions in PCT cells decrease

36. 2. Na ions in PCT lumen diffuse down its
concentration gradient into cells lining in the PCT
• By facilitated diffusion
• Via co-transporter carrier proteins
• Na ions co-transported with glucose/amino
acids/ vitamins/ Cl ions into cells
3. Glucose/amino acids/ vitamins/ Cl ions
transported via transport protein
• By facilitated diffusion

37. • Glucose is all reabsobed into blood
• Hence, no glucose in blood
• Amino acid, vitamins, Cl ions
 actively reabsorbed
• Water, urea
 some passively reabsorbed
• Uric acid & creatinine
 not reabsorbed
• Creatinine actively secreted/transported into lumen
of PCT

38. Adaptations of PCT cells
1. numerous microvilli (facing lumen)
-large surface area for absorption
2. High density of mitochondria
-provide energy in the form of ATP
3. High infolding of basal membrane (facing blood capillaries
4. Presence of different transport proteins in membranes (facing
lumen)
-i.e co-transporters, pumps, aquaporins
5. Tight junctions holding adjacent cells together
• - separate proteins of front and basal meembrane so fluid
cannot pass between cells, substance must pass through cells

39. Selective Reabsorption @ Loop of
Henle
• LOH located at medulla
• Mainly for water reabsorption
• 2 parts:
1. Descending limb
-permeable to both water and Na & Cl ions
2. Ascending limb
-Impermeable to water
-Permeable to Na & Cl ions

40. • @ascending limb
1. Na & Cl ions move out of
the tube
 by active transport
 into tissue fluid of medulla
space
2. High concentration of Na
& Cl ions in the medulla
space
 Renal fluid become more
dilute and enters distal
convoluted tubule
 Longer loop results in
higher concentrations of
solute built up in the medulla
space, more water
reabsorption, more
concentrated urine formed!

41. • @decending limb
permeable to both water and
Na & Cl ions
Due to high concentration of
solute in the medulla
• 3. Water is moves out into
medulla tissue fluid
 by osmosis
 Water is reabsorbed
4. Urea, Na & Cl ions in
medulla space diffuse into
descending limb
 Fluid in descending limb
become very concentrated as
it moves down the loop

43. Selective Reabsorption @ Distal
Convoluted Tubule
• Located at the cortex
1st part of DCT = similar to LoH (ascending
limb)
• Na & Cl ions again actively transported into
blood
• Plus secretion of K, H ions and urea into lumen
from blood

44. Selective Reabsorption @ Distal
Collecting Duct
• Located at the medulla
• Tissue fluid af medulla has high concentrations
of solutes
• So water moves out of collecting duct
• High reabsorption of water back into blood
•  formation of urine
• Rate of water reabsorption is controlled by Adh
(antidiuretic hormone)

45. Osmoregulation
• Hypothalamus
-Conrol of water potential of body fluids
-Uses negative feedback mechanism
• Stimuli: water potential of blood is low
• Receptor: Osmoreceptors at the hypothalamus
detect water potential of blood
• Effector: Neurosecretory cells of th hypothalamus
send nerve impulse to poterior pituitary gland
-Anditdiuretic hormone (ADH) released from
posterior pituitary
entering bloodstream
 Target organ: distal convluted tubule / collecting
duct of kidneys

46. ADH
• Response:
1. ADH in blood bind to receptors on plasma
membrane of distal convoluted tubulue /
collecting duct
2. activates a series of enzyme-controlled
reactions/ enzyme cascade in cells  production
of active phosphorylase enzyme
3. Vesicles containing aquaporins fuse with
plasm membrane of lumen side

48. • Result:
1. Increase membrane permeability of collecting
duct
2 Increase water reabsorption
3. More water flows out of distal convoluted
tubule into blood down water potential gradient
4. so, smaller volume of more concentrated
urine produced
water potential of blood increases
return to norm/set point

49. What if there is an increase of water potential of
blood?
• Osmoregulation no longer stimulated
• Neurons stop secreting ADH
• Aquaporins move out of cell surface membrane of
collecting duct, back into vesicles in the cytoplasm
• Collecting duct is less permeable to water
• Dilute urine and larger volume of urine
produced
• Water potential of blood decreases
• Return to set point

52. Blood Glucose Concentration Control

53. Endocrine Vs Exocrine Glands
• 1. Endocrine Gland
-Secretory cells
-Release secretions into blood capillaries
- secretions = hormones
-e.g: pituitary gland, thyroid, adrenal, ovary,
testes, pancreas
2. Exocrine Gland
-Secretory cells
- Releases secretion into duct/tubes
-secretion- not hormones
e.g: stomach, salivary glands, pancreas

54. Hormones
• Secreted by endocrine gland
• Can be globular OR steroids
eg: Insulin – protein hormone
testosterone- steroid hormone
• Characteristics:
1. Small molecules, chemical messengers
2. Needed in small quantities
3. Secreted quickly upon receeiving stimulus
4. Short lifespan; quiskly broken down by enzymes
5. Transported in blood stream to target cells
6. Specific binding on receptorsof target cells
7. Receptors can be on surface cell membrane or inside
cells
*enzyme-signaling cascade?

55. Hormone Receptors
• 1. Protein hormone: on plasma membrane
 water soluble, cannot pass through plasma
membrane
• 2. Steroid hormones- in cytoplasm
 lipid soluble, can easily pass through plasma
membrane

56. The Pancreas
• Acts as BOTH endocrine and exocrine gland
Exocrine: secretes pancreatic juice (to
duodenum)
Endocrine: secretes insulin and glucagon
hormones into blood
 Islets of Langerhans: composed of
1. Alpha cells: Glucagon
2. Beta cells: Insulin

59. Insulin Vs. Glucagon
• Acts antagonistically for each other
-Glucagon (alpha cells): increase blood sugar
-Insulin (beta cells): decrease blood sugar

61. Insulin
• Stimuli: Blood glucose level increase
• Receptors: detected by α cells and β cells in
islets of Langerhans
• Effectors:
- β cells secrete more insulin into blood
- α cells stop secreting glucagon
• Insulin acts on liver cells, muscle cells and
adipose cells,

62. Insulin
1. Insulin bind to receptors on cell surface
membraneof cells
2. Increase permeability of membrane to glucose in
liver and muscle cells
-trigger vesicles with glucose transporter protein
(GLUT protein) to move & fuse with plasma
membrane
-more facilitated diffusion of glucose into cells
3. Increase glucose uptake / absorption from blood
-stimulate activation of enzyme glucokinase
phosphorylates glucose
-glucose trapped in cells
4. Increase rate of respiration of glucose

63. 5. Increaseconversion of glucoseto glycogen(glycogenesis)
-activatin g2 enzymes (phosphofructokinase,glycogen synthase)
 store in liver and muscle cells
6. Increaseprotein and lipd synthesis
7. Inhibit secretion of glucagonfrom α cells
 inhibit glycogen breakdowninto glucose(glycogenolysis)
8. Inhibit productionof glucosefrom protein and fats (gluconeogenesis)
Results:Decrease in glucoseconcentrationand return to set point

64. Glucagon
Stimuli: Blood glucose level decrease
Receptors: α cells and β cells in islets of
Langerhans
Effectors:
- α cells secretes glucagon into blood
- β cells stop production of insulin
Glucagon acts on liver cells ONLY

65. Glucagon
1. Glucagon binds to receptors on cell surface of liver
cells
-receptors changes shape
2. Activates G proteins
-activates adenyl cyclase
3. Acdenyl cyclase produces cyclic AMP (cAMP)
-from ATP
-cAMP acts as second messenger
-activates protein kinase
-triggers enzyme cascade (series of controlled
reactions)

67. • Response:
4. cAMP activates enzyme glycogen phosphorylase
-increasebreakdown of glycogen to glucose
(glycogenolysis)
5. Use fatty acids and proteins as respiratory
substrate instead of glucose
6. Increase production of glucose from proteins
and fats (gluconeogenesis)
-glucose diffuse through GLUT proteins from liver
-increase in blood glucose concentraion; return to
set point

68. Adrenaline
• Fight or flight hormone
• Produced during exercise and stress
• Secreted by adrenal gland into blood
• To increase glucose levels in blood
 muscles can undergo aerobic / anaerobic
respiration and produce more ATPs
• Same pathway as glucagon

70. Diabetes Mellitus
• High glucose concentration in blood
Type I
Insuline-Dependent DM
Type II
Non Insulin Dependent DM
Usually occur during childhood
(early onset)
Usually occur during adulthood
(late onset)
Body does not produce sufficient
insulin
Body does not respond to insulin
production
Caused by destruction of β cells
(autoimmune)
Caused by down-regulation of
insuline receptors
Requires insulin injections to
regulate blood glucose
Conrolled by managing diet and
lifestyle

71. • Symptoms same in both types; high glucose conc. In blood
and urine
due to glucose not taken up by cells
less glucose converted into glycogen/fat
not all glucose can be reabsorbed in kidneys
• Decrese in water potential of blood
 water and salts moves out of cells down the conc. Gradient
 dehydration production of dilute urine, loss of salts and
cramps
detected by osmoreceptors in hypothalamus; feeling thirsty
• Fats and proteins used in respiration instead of glucose
weight loss
• Build up of keto acids/ketones in blood  blood pH lowered,
can cause coma

72. Urine Analysis
• Presence of glucose and keto acids in urine:
-not all glucose is reabsorbed at PCT
-may have DM
• Long term presence of proteins in urine:
-most proteins molecules does not pass through the
Bowman’scapsule basementmembrane
-other proteins should be reabsorbed at the PCT
-may have kidney infections or disease affecting
glomeruli
-also may associated with high blood pressure
• *short term common during high fever, vigorous
exercise, pregnancy

73. Dip stick test
• Used to measure glucose concentration in urine (not
blood)
• Specific test for glucose detection
• 1. glucose oxidase and peroxidase immobilised onto
pad on dipstick
• 2. dip stick lowered into urine
• 3.
• 4. Compare with colour chart

75. Biosensors
• Biosensors can directly measure glucose conc. in
blood
• Reusable, more precise
1. Glucose oxidase immobilised on pad
2. Place small sample of blood on pad and insert into
machine
3. Small electric current is generated at the same time
glucose gluconolactone + hydrogen peroxide
4. Current detected by electrode
-current amplified and reading is produced
-numerical value of glucose concentration  more
precise

76. Homeostasis in Plants

77. Homeostasis in Plants
• Important for plants to keep constant internal
environment
• E.g: carbon dioxide needed for photosynthesis
(limiting rate factor)
• stomata control the diffusion of gases in and
out of leaves and thus, control the entry of
carbon dioxide into the leaves.

78. Stoma
• The aperture (hole) between guard cells
• Guard cells are highly specialised in respond to a
wide range of environmental stimuli to control
the internal atmosphere of the leaf.

80. • Stomata are distributed on leaves, green
stemsand flowers.
• Lower epidermis of the leaf has the highest
density of stoma
• Surrounded by elliptical shape of guard cell
(kidney shape)

81. Features of Guard Cells
1. Thick cell walls facing outward the air outside f
leafe and stomatal pore.
- Outer wall has thick waxy cuticle, often
extended to into ledges.
2. Cellulose microfibrils arranged into bands
around the cells
3. No plasmodesmata on the cell wall.

82. 4. Cell surface membrane often folded and
contains many channels and carrier proteins
5. Cytoplasm has high density of choloplasts and
mitochondria
6. Have thylakoids, but few grana
starch grains increases in size as starch
stored at night and decrease during the day
7. Many cristae inside mitochondria
8. Nucleus is same size as mesophyll cells
*but occupy larger space inside cells (the size
of guard cell is smaller than mesophyll cells.
9. Several small vacuole rather than one large
vacuole.

83. Stomata Opening and Closing
• Stomata opens due to:
-High light density
-Low concentration of CO2
• Stomata closes due to:
-darkness
-high concentration of CO2
-low humidity
-High temperature
-water stress (water supply is limited or high rate of
transpiration)

84. Stomata Opening & Closing Mechanism
1. ATP powers proton pumps to actively transport H+ out of
cell
2. There is a low concentration of H+ and negative charge
inside the cell  K+ channels open  K+ diffuse in
3. High concentration of K+ inside the cell decreases water
potential
4. Water moves in via osmosis
5. Water entry increases the volume of the guard cell, causing
it to expand  open

86. • Guard cells:
-open when turgid (gain water)
-close when flaccid (lose water)

88. Absicic Acid and Stomatal Closure
• Abscisic acid (ABA) is a stress hormone that is
secreted in response to difficult environmental
conditions such as very high temperatures or much
reduced water supplies.
• ABA triggers the closure of stomata to reduce
transpiration and prevent water loss.
• ABA binds to cell surface receptors
-inhibits proton pumps: stop H+ pumped out
-stimulates movement of Ca2+ through the cell
surface membraneand tonoplast

89. • Ca2+ acts as a 2nd messenger to activate channel
proteins to open that allow negatively charged ions
to leave the guard cell. This will:
-opens channel proteins that allow K+ to leave the
cell
-closes channel proteins that allow K+ to enter the
cell
 net movement: K+ leaves cell
• Hence, loss of ions = higher water potential inside
cell = water passes out by osmosis = guard cells
become flaccid  stomata close

90. Effects of Absicic Acid on Stomata