Communication&homeostasis, nerves, hormones Flashcards

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1
Q

Why do multicellular organisms need communication systems?

A
  • to detect and respond to changes in the external and internal environment
  • ti regulate substances in the blood
  • to co- ordinate the activities of different organs
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2
Q

How do cells communicate with each other?

A

by cell signalling e.g. the hormonal (information is passed from cell to cell using hormones) and neuronal systems (information is passed by electrical impulses along neurones)

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3
Q

What is negative feedback?

A

occurs when a change in a system sets in motion a sequence of events that counteracts the change and restores the original state

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4
Q

What is positive feedback?

A

occurs when a change in a system sets in motion a series of events that result in further change, away from the original state, exaggerating the change.

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5
Q

What are the principles of homeostatic control?

A

Receptor - a specialised cell that detects a particular stimulus
Effector - part of the body that produces a response
If the receptor detects a change, it will signal the effector to bring about a response to reverse the change back to normal in NEGATIVE FEEDBACK.
Stimulus –> receptor –> control centre –> effector –> response: monitored by receptor until the factor that changed is back to normal.

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6
Q

describe the physiological and behavioural responses that maintain a constant core body temperature in endotherms when temp. FALLS below 37degrees C
with reference to peripheral temperature receptors, the hypothalamus and effectors in skin and muscles.

A

external temperature falls, detected by peripheral temp. receptors in the skin.
blood temperature falls, detected by thermoreceptors in the hypothalamus. These receptors send signals to effectors to produce a response in negative feedback to restore optimum conditions.
Physiological responses:
Effectors decrease heat loss by:
- vasoconstriction of skin arterioles
- contraction of hair erector muscles
- decreasing sweating
Effectors increase heat gain by:
- shivering
- increasing respiration in brown fat cells
Behavioural responses:
finding shelter, moving into sun, wearing more clothes, wrapping arms around you

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7
Q

describe the physiological and behavioural responses that maintain a constant core body temperature in endotherms when temp. RISES above 37degrees C

A

external temp. rises, detected by peripheral temperature receptors in the skin.
Blood temperature rises, detected by thermoreceptors in the hypothalamus. These receptors send signals to effectors to produce a response in negative feedback to restore optimum conditions.
Physiological:
Efectors increase heat loss by:
- vasodilation of skin arterioles
- increased sweating
- relaxation of hair erector muscles
Effectors decrease heat gain by:
- decreasing respiration in brown fat cells
Behavioural:
- moving into shade, taking off clothes, cool drinks

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8
Q

How do ectotherms regulate body temp?

Advantage? Disadvantages?

A

Ectotherms obtain heat from the outside rather than generating heat so rely on behavioural mechanisms to regulate their body temperature.
When cold: they move into the sun and flatten their body to absorb as much heat as possible from the surroundings
When hot: they move into the shade or enter water to cool down
Advantage: require less food
Disadvantage: body temp. fluctuates more, less active in cold conditions, limited to environments

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9
Q

outline the roles of sensory receptors in mammals

e.g.?

A

Convert different forms of energy into nerve impulses: transducers
A change in external/internal environment produces a nerve impulse
e.g.:
photoreceptors - electromagnetic energy from light intensity/wavelength stimulus –> electrical energy

electroreceptor - electromagnetic energy from electricity stimulus –> electrical energy

mechanoreceptor - mechanical energy from sound/pressure/touch/gravity stimulus –> electrical energy

thermoreceptor - thermal energy fro, temp. change –> electrical energy

chemoreceptor - chemical energy from humidity/smell/taste/water potential/ion concentration stimulus –> electrical energy

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10
Q

Describe the structure and function of sensory neurones

A

Act as transducers. Carry impulses form receptors to the CNS
Myelinated with Shwaan cells for electrical insulation.
Cell body at one side.
Short axon (carries impulses away from cell body) long dendron (carries impulses towards cell body)

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11
Q

Describe the structure and function of motor neurones

A

Carry nerve impulses from CNS to effector
Myelinated with Schwaan cells
Have their cell body at one end of the neurone
Many dendrites, several short dendrons, one long axon

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12
Q

describe and explain how the resting potential is established and maintained

A

Sodium-potassium pump uses ATP to pump Na+ out of the cell by active transport and K+ in.
Ratio 3Na+ pumped out to 2K+ pumped in, so there are more positive ions outside edge tissue fluid and fewer inside the axoplasm.
K+ ions therefore diffuse back out of the cell
Membrane is less permeable to Na+ so fewer Na+ diffuse back in, maintaining the potential difference.
Voltage-gated channels closed.
There is a potential difference of around -70mV across the membrane. Said to be polarised.

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13
Q

describe and explain how an action potential is generated

A

If the stimulus energy reaches above threshold potential the membrane becomes depolarised and the p.d across membrane reaches -40mV causing voltage Na+ channels to open and Na+ ions rush in by diffusion down the electrochemical gradient, making it positive inside and p.d = +40mV.
Na+ ion channels now close and voltage-gated potassium ion channels open and K+ diffuse out of the cell so that p.d. becomes negative once again, falling to -75/-90mV and is said to be hyper polarised.
Most of the K+ channels close and the sodium-potassium pump restores resting potential.

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14
Q

how is an action potential transmitted in a myelinated neurone?

A

Impulses jump from one gap (node of Ranvier) to the next in saltatory conduction. Local circuits set up by the presence of an action potential at one node depolarise the membrane at the next node as Na+ ions rush in then K+ ions rush out and a new action potential is generated. The previous node is returned to its resting potential thanks to the sodium-potassium pumps.

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15
Q

What does the frequency of impulse transmission signify?

A

A strong stimulus causes many action potentials to be generated per second - increased frequency - which is interpreted by the brain, despite all action potentials having the same electrical strength provided they exceed threshold value - the all or nothing law.

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16
Q

compare and contrast the structure and function of myelinated and non-myelinated neurones

A

myelinated:
- are sensory/motor neurones
- have a myelin sheath of schwaan cells
- longer axons and dendrons
- neurones electrically insulated
- faster transmission of impulses as saltatory conduction occurs
non-myelinated:
- are relay neurones/neurones in invertebrates
- no Schwaan cells
- shorter axons and dendrons
- neurones not insulated
- slower transmission, no saltatory conduction
BOTH have voltage-gated channels and sodium-potassium exchange pumps in their membranes

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17
Q

describe, with the aid of diagrams, the structure of a cholinergic synapse

A

synaptic knob/presynaptic membrane + synaptic cleft + postsynaptic membrane
Synaptic knob contains mitochondria to provide ATP for vesicle formation/movement of vesicles to presynaptic membrane/exocytosis of vesicles containing neurotransmitter/absorption of choline
Synaptic cleft 15nm across, too wide to be crossed by action potential so neurotransmitter used instead
Postsynaptic membrane has receptors which are complementary to ACh

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18
Q

outline the role of neurotransmitters in the transmission of action potentials;

A

At the axon terminal action potentials cannot diffuse across the synaptic cleft so neurotransmitters such as ACh are used instead.

19
Q

outline the roles of synapses in the nervous system.

A
  • unidirectional transmission of impulse from presynaptic to postsynaptic membrane
  • may be excitatory/inhibitory = flexibility of response
  • allow spatial (two action potentials arrive at the same time causing greater depolarisation of postsynaptic membrane) and temporal (greater depolarisaing effect when action potentials arrive closely after one another) summation
  • allow facilitation, in which the arrival of each action potential leaves the membrane more responsive to the next
20
Q

Describe the sequence of events that take place in the transmission of a nerve impulse across a cholinergic synapse

A
  1. Action potential arrives at axon terminal
  2. Calcium ion channels open and Ca2+ ions diffuse into synaptic knob
  3. this causes the synaptic vesicles containing ACh to move to the presynaptic membrane (active process- requires ATP)
  4. the vesicles fuse with the presynaptic membrane, releasing ACh into synaptic cleft by exocytosis
  5. ACh diffuses across cleft and attaches to receptors on postsynaptic membrane
  6. This causes sodium ion channels to open and Na+ ions enter the cell depolarising the membrane and starting a new action potential
  7. ACh broken down by acetylcholinesterase and choline is absorbed and recycled (requires ATP)
21
Q

What are hormones?

A

chemical signals produced from endocrine glands which are carried in the blood/lymph to specific target tissues, where they have their effect

22
Q

What are endocrine glands?

A

ductless glands - hormones are secreted directly into the blood stream

23
Q

What are exocrine glands?

A

Substances are secreted into ducts

24
Q

What is meant by a first messenger? e.g.?

A

A hormone that binds to a specific receptor in the cell membrane of its target tissues - e.g. adrenaline binds to the complementary membrane receptor on liver cells and changes its shape causing it to interact with a g-protein in its membrane

25
Q

What is meant by a second messenger? e.g.?

A

Hormone that works inside the target cells, e.g. cAMP, involved in converting stored glycogen into glucose

26
Q

describe how adrenaline acts on target cells/tissue

A

First messenger adrenaline binds to the membrane receptor on the surface of target cells and changes its shape, causing it to interact with a glycoprotein in the membrane which splits and part of it activates an enzyme that converts ATP into cyclic AMP, the second messenger , which activates a ‘cascade’ of enzymes to produce a response/s

27
Q

describe the functions of the adrenal glands

A

release adrenaline hormone in times of stress, danger or excitement.
The cortex and the medulla of the adrenal glands secrete different hormones with different roles:
Adrenal cortex - secretes glucocortids and mineralocortids
Adrenal medulla - secretes adrenaline

28
Q

describe, with the aid of diagrams and photographs, the histology of the pancreas, and outline its role as an endocrine and exocrine gland

A

In part endocrine, made up of alpha cells, which secrete the hormone glucagon, and beta cells which secrete the hormone insulin
grouped together to form islets of Langerhans.
Other cells are exocrine which produce pancreatic juice and secreting this into the pancreatic duct which carries the juice into the duodenum.
This release is triggered by nervous / hormonal stimulation.
Pancreatic secretions into duodenum ;
alkaline secretions containing enzymes including lipase, amylase, trypsin

29
Q

why is it important that the blood glucose concentration is kept stable at 80-120mg/100cm3 blood?

A
  • glucose is the main respiratory substrate, and the only respiratory substrate for brain cells
  • excess glucose would lower the water potential of the blood, causing body cells to lose water by osmosis and toxins would build up in them, resulting in coma
  • lack of glucose would result in insufficient ATP for cell processes including nerve impulses which could also result in coma
  • changes in blood glucose levels affect blood pressure and in turn kidney functioning
30
Q

describe the sequence of events that occur when the blood glucose concentration increases, e.g. right after eating carbohydrates to restore the normal concentration

A
  1. blood glucose level is detected by glucose receptors in the islets of langerhans (both alpha and beta cells)
  2. alpha cells stop secreting glucagon but beta cells secrete insulin into the blood
  3. insulin travels in the blood to target tissues where is binds to receptors on the cell surface membranes of the target cells: liver cells (first messenger)
  4. liver cells take up more glucose from the blood and respire more of it
  5. excess glucose is converted to glycogen for storage in glycogenesis (further excess converted to triglycerides and stored in liver cells and adipose tissue)
    this is NEGATIVE FEEDBACK
31
Q

describe the sequence of events that occur when the blood glucose concentration decreases, e.g. after fasting/exercise to restore the normal concentration

A
  1. alpha and beta cells in islets of Langerhans detect the falling glucose conc.
  2. beta cells stop secreting insulin, alpha cells secrete glucagon into the blood
  3. glucagon binds to specific membrane receptors on target tissues - liver cells
  4. liver cells are stimulated by glucagon to hydrolyse glycogen into glucose in glycogenolysis. Fatty acids and amino acids in the liver cells can be converted into glucose too, in gluconeogenesis. Meanwhile respiration of glover decreases and fats/amino acids respired instead
  5. glucose is released into the blood
    NEGATIvE FEEDBACK
32
Q

outline how insulin secretion is controlled, with reference to potassium channels and calcium channels in beta cells

A

beta cells in the islets of Langerhans have potassium and calcium channels in their cell membranes. The ATP sensitive K+ channels ensure that the resting potential across its membrane is kept negative. When plasma glucose conc. rises glucose enters the beta cell and is respired, allowing ATP production which causes the K+ channels to close and the membrane to depolarise. Calcium ions rush into the cell, causing secretory vesicles to move toward the plasma cell membrane. Insulin is released by exocytosis

33
Q

What are the causes of Type 1 (insulin-dependent) diabetes compared with those of Type 2 (non-insulin-dependent)?

What is the difference in how the disease operates?

A

Type 1:
- genetic defect
- auto-immune disease - immune system attacks beta cells
Insufficient insulin is secreted so the blood glucose level increases dramatically after carbohydrates are eaten.
Begins in early childhood.

Type 2:
- obesity
- genetic defect
Insulin is secreted, but the target tissues do not respond to it as the insulin receptors are defective
Begins in adults.
34
Q

How is Type 1 treated compared with Type 2 diabetes?

A

Type 2 can usually be controlled by diet e.g. avoiding high carb foods whereas Type 1 requires regular injections of insulin - previously obtained fro dead pigs/cows, now produced from bacteria genetically modified to produce human insulin.

35
Q

Potential treatments for Type 1 diabetes?

A

Stem cell treatment for Type 1 diabetes is currently being researched whereby stem cells could be transplanted into a pancreas and stimulated to develop into beta cells and produce insulin
However, only embryo stem cells are can be made to develop into beta cells and not adult stem cells.

36
Q

Discuss the use of human insulin from bacteria to treat individuals with Type 1 diabetes compared to the use of insulin from pigs

A
  • has the correct shape to bind to insulin receptors so more efficient control of blood glucose
  • no risk of transferring animal disease
  • no risk of rejection by the immune system
  • no ethical or religious objections about the use of pigs
  • cheaper as it ca be produced on a large scale
37
Q

what systems are involved in changing the heart rate?

A

both hormonal and neuronal systems can be used to control the heart rate.
Nervous control acts quicker than hormonal

38
Q

How doe the nervous system control heart rate?

A

To slow down heart rate:
Impulses passing to the SAN via the vagus nerve (parasympathetic) cause the release of ACh which slows down the SAN so that the heart rate decreases
To speed up heart rate:
Impulses to the SAN via the accelerator nerve (sympathetic) cause noradrenaline to be releases which speeds up the SAN and the heart rate increases

39
Q

How does the hormonal system change heart rate?

A

Adrenaline is secreted from the adrenal glands in times of stress and reaches the SAN via the blood stream, speeding it up and increasing heart rate.

40
Q

Describe the roles of the adrenal cortex

A

Adrenal cortex - secretes glucocortids (target the liver and stimulate synthesis of glucose) and mineralocortids (target the kidney and gut causing an increase in uptake of Na+ and raises blood pressure)

41
Q

Describe the role of the adrenal medulla

A

Adrenal medulla - secretes adrenaline which targets the heart, liver, and smooth muscle of gut, increasing heart rate by binding to SAN, stimulating breakdown of glycogen to glucose and inhibits peristalsis, dilates pupils etc……

42
Q

Describe how heart rate is controlled

hormonal + nervous

A

Adrenaline released by adrenal medulla binds to SAN increasing heart rate.
Also a nervous connection to SAN - cardiovascular centre in medulla oblongata sends impulses via parasympathetic nerve (neurotransmitter: ACH, for decreasing heart rate) or sympathetic nerve (neurotransmitter noradrenaline, for increasing heart rate.)
Whether the heart rate needs to be sped up/slowed down is detected receptors -
high blood pressure is detected by stretch receptors
low blood pH (build up of CO2) detected by chemoreceptors
receptors in aorta/carotid sinus

43
Q

Describe the function of Schwaan cells

A

produces myelin for electrical insulation: prevents movements of ions out of axon/prevents depolarisation.
The presence of a myelin ss oheath speeds up conductions as local circuits occur only at nodes of ranvier and impulses jump from node to node in saltatory conduction.