HOMEOSTASIS Flashcards
Homeostasis
Ability of an organism to maintain a constant internal environment
Negative Feedback
When a change to the normal initiates a response which reduces the effect of the change
Positive Feedback
change stimulates further change; can be dangerous if it is not natural; often associated with breakdown of control systems
Endotherms (warm blooded)
control their body temperature by physiological and behavioural means, thus keeping it constant
Ectotherms (cold blooded)
control their body temperature by behavioural means only, NO physiological cooling/heating mechanism, therefore usually Air Temperature = Body Temperature
Too Cold
When we are too cold, ‘heat gain’ centre in hypothalamus detects this via a receptor in the skin and inhibits the ‘heat loss’ centre, then the ‘heat gain’ centre sends nerve impulses to appropriate part of the body to do the following
Shivering: creates heat
Vasoconstriction: constriction of arteriole walls allows less heat in blood to be lost from skin
Making your hair stand on end: traps layer of insulating air
Increasing metabolic and respiration rate: achieved via hormones; respiration and metabolism releases heat
(REMEMBER: metabolic rate is measured by measuring the uptake of Oxygen or production of CO2)
Less blood flow to surface capillaries
Role of blood vessels in conserving heat
Vasoconstriction of arterioles
Therefore less radiation
Therefore less blood to the surface
Too Hot
When we are too hot, ‘heat loss’ centre in hypothalamus detects this due to a receptor in the skin via nervous impulses, and inhibits the ‘heat gain’ centre, then the ‘heat loss’ centre sends nerve impulses to appropriate part of the body to do the following
Sweating
Vasodilatation: dilation of arterioles, allowing heat in blood to be transferred to sweat
More blood flow to surface capillaries
Lowering of hairs causes less insulation
Decreasing metabolic rate and respiration rate
Why we produce heat during exercise
Respiration is carried out for muscular activity
However respiration is INEFFICIENT and therefore releases extra energy as heat
Why we get tired from exercise in hot conditions quicker than we do when it is cold
The heated conditions cause vasodilatation and cause more blood flow to the surface capillaries
This results in less blood flow to muscles requiring oxygen
Large mammals with small surface area to volume ratio will heat up a lot quicker than smaller animals as they have reduced heat loss through skin, therefore large animals will activate their ‘heat loss’ centre in hypothalamus a lot quicker than small mammals
As temperature increases, respiration rate increases in ECTOTHERMS, (in us it decreases), this is because
Increased temperature increases kinetic energy
Increased kinetic energy increases rate of reactions
More ATP is produced
Therefore more ATP used, therefore higher respiration rate required to remake lost ATP
Importance of maintaining a constant body temperature (i.e. importance of homeostasis)
If body temperature is too high, the excess heat denatures active sites of enzymes
Therefore substrate can no longer form a complex with it therefore reactions are ceased
If body temperature is too low, there is too little kinetic energy, therefore molecules move too slowly
Therefore few collisions and thus fewer enzyme-substrate complexes formed, therefore too slow reactions
Why the activity of Ectotherms that live in deserts varies so much
1) Their body temperature varies with that of environment
2) Temperature of desert fluctuates greatly
3) Metabolic reactions inside the Ectotherm are controlled by enzymes
4) Enzyme activity changes according to body temperature
5) Speed of bodily actions dependent on metabolic rate
6) Reptiles seek shade when hot and seek Sun when cool
Hyperglycaemia
too much glucose in blood, lowers water potential of blood and produces symptoms of thirst
Hypoglycaemia
too little glucose in blood, produce symptoms of dizziness, tiredness, etc. As the brain does not have glucose
Pancreas
Contains Islets of Langerhans that make two types of cells:
α-cells produce the hormone glucagon
β-cells produce the hormone insulin
Glycogenesis
the production of glycogen by the polymerisation of glucose
Glycogenolysis
the breakdown of glycogen to release glucose
Gluconeogenesis
the production of glucose from non-carbohydrate sources
If blood glucose levels too high
β-cells detect the rise and secret insulin (notice how the β-cells are the RECEPTORS and EFFECTORS.)( α-cells are inhibited)
Insulin fits into specific receptor proteins on membranes of cells
This causes extra glucose channels to open allowing glucose to enter cell via facilitated diffusion (this is done through the second messenger IRS) and allow it to become metabolised, in Liver cells, insulin causes IRS to activate glycogen synthase enzyme which causes glucose to be converted to glycogen (Glycogenesis)
Once glucose levels stabilise, β-cells reduce secretion of insulin
Type 1 Diabetes
body cannot make insulin; therefore glucose cannot pass from blood into cells, therefore starving the cells
Type 2 Diabetes
body does not make enough insulin or the receptors are not responding well to insulin, therefore glucose cannot be fully passed from blood into cells which is the job of the insulin
How diet and exercise may help maintain low glucose concentration in the blood of a type II diabetic person
Eat polysaccharides therefore slower digestion, therefore no surge in blood sugar level
Exercise increases respiration
If blood glucose levels too low
α-cells detect the low levels and secret glucagon
Glucagon fits into specific receptor proteins on membrane of cells that CONTAIN glycogen which are called liver cells
Glucagon activates an enzyme that converts glycogen to glucose (Glycogenolysis) and proteins/lipid to glucose (Gluconeogenesis), glucose can pass through cell membrane, therefore increasing glucose concentration of blood
Once glucose levels stabilise, α-cells reduce the secretion of glucagon
Even though people with diabetes have high glucose levels, their glucose levels can still go down without insulin, this is through
The loss of glucose in urine
Glucose gets used up in cell respiration
When a diabetic person takes an insulin injection, and then does not eat a meal, his glucose levels do not fall dangerously low because:
Glucagon is still active which produces glucose using Glycogenolysis
Person is not active so little glucose used up in respiration
Adrenaline
1) Activates an enzyme called Adenyl Cyclase that causes the breakdown of glycogen to glucose
2) Glucose produced is then used for respiration (this is why you can run much faster with adrenaline)
3) Inhibits enzyme that synthesises glycogen from glucose
In any experiment on blood glucose concentrations, we ensure the candidates are not fed at least 6 hours before the test because:
Glucose in food would affect results
Allows time for blood glucose level to return to normal
Menstrual Cycle:
There are 4 key hormones (REMEMBER: hormones are globular proteins!)
FSH: stimulates development of follicles in ovary, the follicle contain eggs, and stimulates follicles to produce oestrogen
Oestrogen: causes rebuilding of uterus lining and inhibits LH and FSH production (NEGATIVE FEEDBACK), on day 10, oestrogen reaches a critical point and it stimulate pituitary gland to release FSH and LH (POSITIVE FEEDBACK)
LH: causes one of the follicles in the ovary to release its egg (ovulation-day 14) and stimulates empty follicle to develop into a structure called Corpus Luteum which produces progesterone, therefore evidence of ovulation will be a peak in LH and a drop in the diameter of the follicle which is now empty
N.B. The diameter of a follicle will be largest just before ovulation
Progesterone: maintains lining of uterus in readiness for sperm and inhibits production of FSH and LH from pituary gland (NEGATIVE FEEDBACK)
How you describe Menstrual Cycle in the exam
FSH increase causes follicles to develop
Developing follicles produce Oestrogen
Oestrogen inhibits FSH
High Oestrogen stimulates FSH and LH release from pituary gland
LH causes ovulation which results in the production of Progesterone
If egg is not fertilised
Corpus Luteum degenerates and stops producing progesterone
No more progesterone causes uterus lining to break and also allows FSH to be released which causes follicle development, thus restarting the cycle
Evidence that fertilisation has not occurred
Progesterone levels drop
Another follicle develops
If egg is fertilised
A hormone called Human Chorionic Gonadotrophin (HCG) acts as a signal to Corpus Luteum to keep producing progesterone
Progesterone maintains uterus lining
How FSH release is controlled by negative feedback
FSH stimulates development of follicles which release Oestrogen
Oestrogen inhibits FSH
How LH concentration is controlled by negative feedback
LH rise causes a rise in Progesterone
Progesterone inhibits LH
Role of LH and FSH in the Menstrual Cycle
FSH stimulates growth of a follicle which produces Oestrogen
LH causes ovulation
LH stimulates formation of Corpus Luteum which produces Progesterone
Fall in FSH would result in no Oestrogen
Role of Progesterone in the Menstrual Cycle
Maintains uterus lining
Stimulates growth of blood vessels in uterus lining
REMEMBER: ovulation will coincide with a rise in progesterone and a fall in LH because
Progesterone is produced by the corpus luteum
Corpus Luteum is formed after ovulation
LH is now inhibited by the Progesterone produced
How excess Oestrogen causes infertility
Oestrogen inhibits production of FSH through negative feedback
Therefore prevents follicles developing
Oestrogen inhibits LH, this prevents ovulation
Some oral contraceptives add Progesterone as well as Oestrogen as progesterone also inhibits FSH and LH, FSH causes follicle development and LH causes ovulation.
Why women who have passed menopause will have low levels of oestrogen
Their follicles are no longer active
Therefore oestrogen is secreted by follicles, due to the follicles being inactive, the oestrogen concentration is low
Therefore oestrogen is not enough to inhibit pituary gland
Therefore there will remain a high concentration of FSH (which won’t do anything because follicles are inactive)
Plant Growth Factors
They are a type of hormone, but unlike animal hormones, they are made by cells throughout the plant rather than by particular organs
Unlike animal hormones, some plant growth factors actually affect the tissues that release them
They move around the plant using diffusion
Difference between Hormones and Chemical Mediators
Hormones have widespread effect
Hormones only affect cells with right receptor
Hormones travel in blood whereas Chemical Mediators travel by diffusion
How IAA causes root tips to grow towards gravity
IAA moves to lower side of root and inhibits growth of lower side
Upper side grows more therefore causing the root to bend downwards
Auxin is produced by the root TIP; therefore if I cut of the tip, the root will continue to grow horizontally
When light is directed towards the plant, IAA builds up on the shaded side causing the shaded side to elongate, resulting in the plant bending towards the light. This is called POSITIVE PHOTOTROPISM
Why growth of IAA on the shaded side helps to maintain the leaves in a favourable environment
Causes plant to bend towards light
Light is required for photosynthesis
IAA can be sprayed onto plant’s leaves, allowing it to diffuse through the leaves; however, the surface of the leaves has to be thin to allow a short diffusion pathway.
Why plants that reproduce sexually are very variable in their yield
Meiosis is involved which includes independent assortment and crossing over
Fertilisation is random
However plants grown from tissue culture will be clones as they are produced via mitosis
Paracrine Signalling
communication between close cells using chemicals called Local Chemical Mediators
Chemical mediators are released into tissue fluid but not into the blood; therefore they only affect cells that are in their immediate vicinity
Examples of chemical mediators are Histamine and Prostaglandins
