topic 6 Flashcards

1
Q
A
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2
Q

what is peristalsis ?

A

peristalsis is the contraction of circular and longitudinal muscle layers

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3
Q

what is the function of peristalsis in the small intestine?

A

to mix the food with enzymes and move it along the gut.

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4
Q

what is the function of the pancreas?

A

to secrete enzymes into the lumen of the small intestine.

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5
Q

what are the main enzymes present in pancreatic juice?

A

amylase, lipase, endopeptidase

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6
Q

amylase

A

starch->maltose

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7
Q

lipase

A

triglycerides-> fatty acids + glycerol
or
triglycerides-> fatty acids + monoglycerides

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8
Q

nucleases

A

DNA and RNA -> nucleotides

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9
Q

maltase

A

maltose -> glucose

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10
Q

lactase

A

lactose -> glucose + galactose

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11
Q

sucrase

A

sucrose -> glucose + fructose

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12
Q

proteases/peptidases

A

proteins/polypeptides -> shorter peptides

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13
Q

dipeptidases

A

dipeptides -> amino acids

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14
Q

what do enzymes do?

A

they digest most macromolecules in food into monomers in the small intestine.

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15
Q

describe the path of digestive enzymes from the pancreas to the small intestine

A
  1. synthesised in pancreatic gland cells on ribosomes on the rER
  2. processed in the Golgi apparatus
  3. secreted by exocytosis
  4. flow through pancreatic duct and into small intestine
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16
Q

what type of reactions are macromolecules->monomers

A

hydrolysis

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17
Q

what are the two functions of the villi in the small intestine?

A
  • to increase the surface area of epithelium over which absorption is carried out
  • to absorb monomers formed by digestion as well as minerals and vitamins
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18
Q

draw out a labelled diagram of a villus

A

check

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19
Q

list 6 substances absorbed by the villi in the small intestine

A
  • glucose, fructose, galactose and other monosaccharides
  • amino acids
  • fatty acids, monoglycerides, glycerol
  • bases (from nucleotides)
  • mineral ions (eg Ca, K, Na)
  • vitamins
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20
Q

to be absorbed into the body, nutrients must pass from the —– of the small intestine to the ——- or ——- in the villi

A

lumen; capillaries; lacteals

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21
Q

what happens before nutrients pass into the lacteal/capillaries of the villi?

A

they must first be absorbed into epithelium cells

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22
Q

describe how triglycerides are absorbed from the small intestine into the villi.

A
  1. triglycerides are digested into fatty acids and monoglycerides
  2. monoglycerides are absorbed into villus epithelium cells by simple diffusion
  3. fatty acids are absorbed by facilitated diffusion (via fatty acid transporters)
  4. inside the epithelium cells, fatty acids + monoglycerides form triglycerides, which cannot diffuse back out.
  5. triglycerides + cholesterol + phospholipids + protein -> lipoprotein particles
  6. these are released into the interstitial spaces of the villus by exocytosis
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23
Q

describe how glucose is absorbed from the small intestine into the villi

A
  1. Na-K pumps in the inwards-facing part of the plasma membrane pump Na ions by active transport from the cytoplasm to the interstitial spaces inside the villus and K ions in the opposite direction
  2. there is a low concentration of Na ions inside villus epithelium cells
  3. sodium-glucose co-transporter proteins in the microvilli transfer a Na ion and glucose molecule together from the intestinal lumen to the cytoplasm of the epithelial cell (facilitated diffusion).
  4. glucose channels allow the glucose to move from the cytoplasm to the interstitial spaces inside the villus and into the blood capillaries.
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24
Q

why can glucose not pass through the plasma membrane of the villus epithelium via simple diffusion?

A

because it is polar and therefore hydrophilic

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25
Q

mouth

A
  • mechanical digestion of food by chewing and mixing with saliva (contains lubricants and enzymes)
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26
Q

oesophagus

A
  • movement of food by peristalsis from the mouth to the stomach
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27
Q

stomach

A
  • churning and mixing with secreted water + acid which kills foreign pathogens in food
  • initial stages of protein digestion
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28
Q

small intestine

A
  • digestion of lipids, carbs, proteins, nucleic acids
  • neutralisation of stomach acid
  • absorption of nutrients
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29
Q

pancreas

A

secretion of lipase, amylase, and protease

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30
Q

liver

A

secretion of surfactants in bile to break up liquid droplets

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31
Q

gall bladder

A

storage and regulated release of bile

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32
Q

large intestine

A
  • re-absorption of water
  • further digestion by symbiotic bacteria (especially of carbs)
  • formation and storage of faces
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33
Q

describe the 4 layers of the wall of the small intestine

A
  • serosa (outer coat)
  • muscle layers (longitudinal muscle and inside it circular muscle)
  • sub-mucosa (tissue layer containing blood and lymph vessels)
  • mucosa (lining of SI, with epithelium that absorbs nutrients)
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34
Q

describe the processs of starch digestion

A

Starch can exist in one of two forms – amylose (linear, only 1,4) or amylopectin (branched, 1,4+1,6)

The digestion of starch is initiated by salivary amylase in the mouth and continued by pancreatic amylase in the intestines

Amylase digests amylose into maltose subunits (disaccharide) and digests amylopectin into branched chains called dextrins (it cannot break 1,6 bonds)

Both maltose and dextrin are digested by enzymes (maltase) which are fixed to the epithelial lining of the small intestine

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35
Q

how and why are the products of the digestion of starch transported to the liver?

A

via the hepatic portal vein; excess glucose is absorbed by liver cells and converted to glycogen for storage

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36
Q
A
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37
Q

what is the function of the arteries?

A

convey blood at high pressure from the ventricles to the tissues of the body

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38
Q

what are artery walls composed of?

A

muscle and elastic fibres

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39
Q

name the 3 layers of arteries

A
  • tunica externa: tough outer layer of connective tissue
  • tunica media: thick layer containing smooth muscle and elastic fibres made of the protein elastin
  • tunica intima: a smooth endothelium forming the lining of the artery
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40
Q

what is the role of the arterial muscle and elastic fibres?

A

to assist in maintaining blood pressure between pump cycles

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41
Q

systolic pressure

A

the peak pressure reached in an artery

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42
Q

diastolic pressure

A

the minimum pressure inside an artery

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43
Q

role of elastic fibres in the maintenance of blood pressure

A
  1. systolic pressure pushes the wall of the artery outwards, widening the lumen and stretching elastic fibres in the wall, thus storing potential energy
  2. at the end of each heartbeat the pressure in the arteries falls sufficiently for the stretched elastic fibres to squeeze the blood in the lumen.

This mechanism saves energy and prevents the diastolic pressure from becoming too low.

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44
Q

role of muscle fibres in the maintenance of blood pressure

A

VASOCONSTRICTION
circular muscles in the wall form a ring so when they contract, the circumference is reduced and the lumen is narrowed, blood pressure increase

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45
Q

why do arterioles have a particularly high density of muscle cells?

A

so that they can respond to various hormone and neural signals to control blood flow to downstream tissues

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46
Q

artery:
- diameter
- relative thickness of wall and diameter of lumen
- number of layers in wall
- muscle and elastic fibres in wall
- valves

A
  • larger than 10µm
  • relatively thick wall and narrow lumen
  • 3
  • abundant
  • none
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47
Q

what is the role of capillaries?

A

to allow exchange of materials between cells in tissues and the blood in the capillary

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48
Q

general role of arterial muscle fibres in walls

A

help to form a rigid arterial wall that is capable of withstanding the high blood pressure without rupturing

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49
Q

general role of arterial elastic fibres in walls

A

allow the arterial wall to stretch and expand upon the flow of a pulse through the lumen

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50
Q

give 2 tissues that do not contain capillaries

A

tissues of the lens and cornea in the eye- these must be transparent

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51
Q

state and explain the adaptations of capillaries

A
  • very small diameter which allows passage of only a single red blood cell at a time (optimal exchange)
  • capillary wall is made of a single layer of cells to minimise the diffusion distance for permeable materials
  • surrounded by a basement membrane which is permeable to necessary materials
  • may contain pores to further aid in the transport of materials between tissue fluid and blood
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52
Q

describe plasma and tissue fluid

A

plasma is the fluid in which blood cells are suspended; tissue fluid contains oxygen, glucose, and all other substances in blood plasma apart from large protein molecules which cannot pass through capillary wall

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53
Q

describe the process of absorption from capillaries into tissues

A

fluid flows between the cells in a tissue, allowing the cells to absorb useful substances and excrete waste products as the tissue fluid then re-enters the capillary network

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54
Q

describe how capillary structure may vary depending on its location in the body and specific role

A
  • wall may be continuous (eg nervous tissue in blood-brain barrier) with endothelial cells held together by tight junctions to limit permeability of large molecules
  • In tissues specialised for absorption (e.g. intestines, kidneys), the capillary wall may be fenestrated (contains pores)
  • some capillaries are sinusoidal and have open spaces between cells and be permeable to large molecules and cells (e.g. in liver)
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55
Q

Arteries split into ? which in turn split into ?, decreasing arterial pressure as total vessel volume is ?

The branching of arteries into capillaries therefore ensures blood is moving ? and all cells are located near a blood supply

After material exchange has occurred, capillaries will pool into ? which will in turn collate into larger ?

A

arterioles; capillaries; increased;

slowly;

venules; veins

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56
Q

describe the flow of blood in capillaries

A
  1. blood flows through the capillaries very slowly and at a very low pressure in order to allow for maximal material exchange
  2. The higher hydrostatic pressure at the arteriole end of the capillary forces material from the bloodstream into the tissue fluid
  3. The lower hydrostatic pressure at the venule end of the capillary allows materials from the tissues to enter the bloodstream
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57
Q

what is the role of veins?

A

to collect blood at low pressure from the tissues of the body and return it to the atria of the heart

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58
Q

capillary:
- diameter
- relative thickness of wall and diameter of lumen
- number of layers in wall
- muscle and elastic fibres in wall
- valves

A
  • around 10µm
  • extremely thin wall
  • only one layer, tunica intimate which is an endothelium consisting of a single layer of very thin cells
  • none
  • none
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59
Q

why is the hepatic portal vein unusual

A

it carries blood from stomach and intestines to liver, not back to the heart

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60
Q

adaptations of veins

A
  • very wide lumen (relative to wall thickness) to maximise blood flow for more effective return
  • thin wall containing less muscle and elastic fibres as blood is flowing at a very low pressure
  • pressure is low so veins possess valves to prevent backflow and stop the blood from pooling at the lowest extremities
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61
Q

why do veins typically pass between skeletal muscle groups?

A

as they facilitate venous blood flow via periodic contractions; it would otherwise be difficult for the blood to move against the downward force of gravity

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62
Q

describe how valves in veins work

A
  • if blood starts to go backwards, it gets caught in the flaps of the pocket valve, which will with blood, blocking the lumen of the vein
  • when blood flows towards the heart, it pushes the flaps to the sides of the vein so the pocket valve opens
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63
Q

vein:
- diameter
- relative thickness of wall and diameter of lumen
- number of layers in wall
- muscle and elastic fibres in wall
- valves

A
  • variable but much larger than 10
  • relatively thin wall with variable but often wide lumen
  • three layers
  • small amounts
  • present in many veins
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64
Q

what is meant by the term ‘double circulation’?

A

in humans there is a separate circulation for the lungs:
- pulmonary circulation, to and from the lungs
- systemic circulation, to and from all other organs including the heart muscles

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65
Q

why do humans have double circulation?

A

blood capillaries in the lungs cannot withstand high pressures so blood is pumped to them at relatively low pressure; after passing through the lung capillaries, pressure is still low so blood must return to the heart to be pumped again before it goes to other organs

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66
Q

draw and label a diagram of a heart

A
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67
Q

The contraction of the heart is called ? while the relaxation of the heart is called ?

A

systole; diastole

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68
Q

Atrial systole is the period when

Ventricular systole is when

A

the atria are contracting

the ventricles are contracting

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69
Q

Functions of atrial and ventricular systole

A

Atrial systole forces blood from the atria into the ventricles

During ventricular systole, blood is forced from the ventricles into the pulmonary artery and aorta

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70
Q

Initiation of the heartbeat by the sinoatrial node

A
  1. the heart beat is initiated by a group of cells in the wall of the right atrium called the sinoatrial node (SAN)
  2. the cells of the sinoatrial node depolarise, reversing the charge across their membranes
  3. Depolarisation of the cells in the sinoatrial node sends an electrical signal over the atria, causing them to contract in atrial systole
  4. The electrical signal then reaches a region of non-conducting tissue which prevents it from spreading straight to the ventricles; this causes the signal to pause for around 0.1 s
    This delay means that the atria can complete their contraction before the ventricles begin to contract
  5. The electrical signal is carried to the ventricles via the atrioventricular node (AVN), a region of conducting tissue between atria and ventricles
  6. The signal then travels to the base of the heart via conductive fibres in the septum known as the bundle of His
  7. it is then carried through conductive fibres called Purkyne fibres which spread around the sides of the ventricles, causing contraction of the ventricles from the apex, or base, of the heart upwards
  8. Blood is forced out of the heart into the pulmonary artery and aorta
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71
Q

why is the sinoatrial node is considered to be the pacemaker of the heart?

A

because it initiates the heart beat and so controls the speed at which the heart beats

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72
Q

why is the heart considered myogenic?

A

it will beat without any external stimulus from other organs or the nervous system

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73
Q

how can heart rate be increased or decreased?

A

with signals from branches of two nerves originating in the cardiovascular centre, a region in the medulla of the brain

  • signals from one of the nerves cause the pacemaker to increase the frequency of heartbeats
  • signals from the other decrease the rate
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74
Q

low blood pressure, oxygen concentration and pH suggests that

High blood pressure, oxygen concentration and pH suggests that

A

the heart rate needs to speed up to increase the flow rate of blood to the tissues, deliver more oxygen and remove more CO2

the heart rate may need to slow down

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75
Q

what is the function of epinephrine?

A

controlled by the brain, and increases the heart rate to prepare for vigorous physical activity because of a threat/opportunity

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76
Q

what responds to the secretion of epinephrine by the adrenal glands?

A

the sinoatrial node

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77
Q

describe Harvey’s discovery of the circulation of the blood with the heart acting as the pump

A
  • demonstrated blood flow through larger vessels is unidirectional, with valves to prevent back flow
  • showed the rate of flow through major vessels is too high for blood to be consumed in the body after being pumped out by the heart; it must therefore return to the heart and be recycled
  • showed the heart pumps blood out in arteries and returns it in veins
  • predicted presence of numerous fine vessels
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78
Q

describe the events leading up to occlusion of the coronary arteries

A
  1. Low density lipoproteins (LDL) containing fats and cholesterol accumulate in the artery wall of the coronary artery.
  2. phagocytes are then attracted by signals from endothelium cells and smooth muscle. The phagocytes engulf the fats and cholesterol by endocytosis and grow very large.
  3. Smooth muscle cells migrate to form a tough cap over the atheroma. The artery wall bulges into the lumen narrowing it and thus impeding blood flow.
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79
Q

describe the possible effects of coronary artery occlusion

A

Coronary occlusion is a narrowing of the arteries that supply blood containing oxygen and nutrients to the heart muscle.

Lack of oxygen (anoxia) causes pain, known as angina, and impairs the muscle’s ability to contract, so the heart beats faster as it tries to maintain blood circulation with some of its muscle out of action.

The fibrous cap covering atheromas sometimes ruptures, which stimulates the formation of blood clots that can block arteries supplying blood to the heart and cause acute heart problems.

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80
Q

give 6 factors that increase risk of atheroma

A
  • high blood concentrations of LDL (low density lipoprotein)
  • chronic high blood glucose concentrations, due to overeating, obesity or diabetes
  • chronic high blood pressure due to smoking, stress or any other cause
  • consumption of trans fats, which damage the endothelium of the artery.
  • infection of the artery wall with Chlamydia pneumoniae
  • production of trimethylamine N-oxide (TMAO) by microbes in the intestine.
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81
Q

define atherosclerosis

A

the development of an atheroma - plaque, or fatty tissue that blocks arteries

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82
Q

describe the pressure changes in the left atrium, left ventricle and aorta during the cardiac cycle using a diagram

A

0.0-0.1 seconds
The atria contract causing a rapid but relatively small pressure increase, which pumps blood from the atria to the ventricles, through the open atrioventricular valves.
The semilunar valves are closed and blood pressure in the arteries gradually drops to its minimum as blood continues to flow along them but no more is pumped in.

0.1-0.15 seconds
The ventricles contract, with a rapid pressure build up that causes the atrioventricular valves to close.
The semilunar valves remain closed.

0.15-0.4 seconds
The pressure in the ventricles rises above the pressure in the arteries so the semilunar valves open and blood is pumped from the ventricles into the arteries, transiently maximizing the arterial blood pressure.
Pressure slowly rises in the atria as blood drains into them from the veins and they fill.

0.4-0.45 seconds
The contraction of the ventricular muscles wanes and pressure inside the ventricles rapidly drops below the pressure in the arteries, causing the semilunar valves to close.
The atrioventricular valves remain closed.

0.45-0.8 seconds
Pressure in the ventricles drops below the pressure in the atria so the atrioventricular valves open.
Blood from the veins drains into the atria and from there into the ventricles, causing a slow increase in pressure.

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83
Q
A
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84
Q

describe the body’s primary defence mechanism

A

the skin and mucous membranes form a primary defence mechanism against pathogens that cause infectious disease

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85
Q

skin

A
  • outermost layer is tough and provides a physical barrier against the entry of pathogens and physical/chemical damage
  • sebaceous glands are associated with hair follicles and secrete sebum, which maintains skin moisture and slightly lowering skin pH, which inhibits the growth of bacteria and fungi
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86
Q

mucous membranes

A

thinner and softer type of skin found in airways and reproductive organs

  • the mucus secreted is a sticky solution of glycoproteins and traps pathogens, which are either swallowed or expelled, acting as a physical barrier
  • also has antiseptic properties due to the presence of the anti-bacterial enzyme lysozyme
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87
Q

how are cuts in the skin sealed?

A
  1. platelets aggregate at the site forming a temporary plug
  2. they release clotting factors that trigger off the cascade of reactions involved in the clotting process
  3. this cascade results in the production of thrombin, an enzyme, which converts the soluble protein fibrinogen into the insoluble fibrin
  4. the resulting clot is initially a gel but if exposed to the air dries to form a hard scab
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88
Q

Use of phagocytes in defence

A
  • ingestion of pathogens by phagocytic white blood cells gives non-specific immunity to diseases
  • they engulf of pathogens by endocytosis and digest them with lysosomes (enzymes)
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89
Q

Use of antibody production in defence

A

Production of antibodies by lymphocytes in response to particular pathogens gives specific immunity

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90
Q

define an antigen

A

any chemical that stimulates an immune response

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91
Q

define a specific immune response

A
  • the production of one type of antibodies specific to a particular pathogen’s antigens by lymphocytes
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92
Q

describe the steps of antibody production

A
  1. antigens on the pathogen stimulate cell division of the small group of lymphocytes that produce the appropriate antibody
  2. plasma cells (large clones of lymphocytes) are produced within a few days and secrete large quantities of the antibody
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93
Q

describe the role of antibodies

A

antibodies are large proteins that have two functional regions: a hyper variable region that binds to a specific antigen and another that helps the body fight the pathogen by

  • making it more recognisable to phagocytes
  • preventing viruses from docking to and entering host cells
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94
Q

some of the lymphocytes produced during an infection are not active plasma cells but instead become

A

memory cells

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95
Q

immunity to a disease involves

A

either having antibodies against the pathogens or memory cells that allow rapid production of the antibody

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96
Q

describe the function of antibiotics

A

block processes that occur in prokaryotic cells but not eukaryotic cells. For example, bacterial DNA replication, transcription, translation, ribosome function and cell wall formation.

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97
Q

what is the issue with widespread antibiotic use?

A

some strains of bacteria have evolved with genes which confer resistance to antibiotics and some strains have multiple resistance

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98
Q

why can viral diseases not be treated using antibiotics?

A

Being non-living, they rely on the host cell’s enzymes for ATP synthesis and other metabolic pathways. These processes cannot be targeted by drugs as the host cell would also be damaged.

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99
Q

medical name for a blood clot

A

thrombus

100
Q

coronary thrombosis is

A

the formation of blood clots in the coronary arteries - this can be a fatal condition.

101
Q

give 4 things that increase the risk of coronary thrombosis

A

coronary occlusion, damage to the capillary epithelium, hardening of the arteries, rupture of an atheroma

102
Q

Effects of HIV on the immune system and modes of transmission

A

Production of antibodies by the immune system is a complex process and includes different types of lymphocyte, including helper T-cells. The human immunodeficiency virus (HIV) invades and destroys helper T-cells. The consequence is a progressive loss of the capacity to produce antibodies.

In the early stages of infection, the immune system makes antibodies against HIV. If these can be detected in a person’s body, they are said to be HIV-positive.

HIV is a retrovirus that has genes made of RNA and uses reverse transcriptase to make DNA copies of its genes once it has entered a host cell. The rate at which helper T-cells are destroyed by HIV varies considerably and can be slowed down by using anti-retroviral drugs. In most HIV-positive patients antibody production eventually becomes so ineffective that a group of opportunistic infections strike, which would be easily fought off by a healthy immune system.

A collection of several diseases or conditions existing together is called a syndrome. When the syndrome of conditions due to HIV is present, the person is said to have acquired immune deficiency syndrome (AIDS).

AIDS spreads by HIV infection. The virus only survives outside the body for a short time and infection normally only occurs if there is blood to blood contact between infected and uninfected people. There are various ways in which this can occur:
- sexual intercourse, during which abrasions to the mucous membranes of the penis and vagina can cause minor bleeding
- transfusion of infected blood, or blood products such as Factor VIII
- sharing of hypodermic needles by intravenous drug users.

103
Q

Florey and Chain experiments

A

Florey and Chain tested penicillin on infected mice
Eight mice were injected with hemolytic streptococci and four of these mice were subsequently injected with doses of penicillin
The untreated mice died of bacterial infection while those treated with penicillin all survived – demonstrating its antibiotic potential

104
Q

what is the function of ventilation?

A

it maintains concentration gradients of oxygen and carbon dioxide between air in alveoli and blood flowing in adjacent capillaries

105
Q

draw a labelled diagram of an alveolus

A

pg311
- type 1 pneumocystis in alveolus walls
- phagocyte
- network of blood capillaries
- type 2 pneumocystis in alveolus walls

106
Q

give 4 ways of monitoring ventilation in humans at rest and after mild and vigorous exercise

A
  1. ventilation rate
    - observation of number of times air is exhaled and inhaled in a minute
    - data logging with inflatable chest belt that is placed around the thorax
  2. tidal volume
    - one normal breath is exhaled through a delivery tube into a vessel and the volume is measured. it is not safe to use this apparatus for repeatedly inhaling/exhaling air as the co2 concentration will rise too high
    - spirometers measure flow rate into and out of lungs and from these measurements lung volumes can be deduced
107
Q

structure and function of type 1 pneumocytes

A

extremely thin alveolar cells that are adapted to carry out gas exchange

  • located in epithelium, in wall of alveolus
  • flattened cells
  • distance over which co2 and o2 have to diffuse is very small, which increases the rate of gas exchange
108
Q

structure and function of type 2 pneumocytes

A

secrete a solution containing surfactant that creates a moist surface:
- allows oxygen to dissolve and diffuse to blood
- provides area from which co2 can evaporate into the air and be exhaled

hydrophobic heads face the water and the hydrophobic tails face the air:
- reduces surface tension and prevents water from causing the sides of the alveoli to adhere when air is exhaled from lungs, helping prevent the collapse of the lung

109
Q

give a flow diagram describing airways for ventilation

A

nose/mouth -> trachea -> two bronchi -> lung -> tree-like bronchioles -> groups of alveoli

110
Q

give the structure and function of trachea and bronchi

A

rings of cartilage in their walls to keep it open even when air pressure inside is low or pressure in surrounding tissues is high

111
Q

structure and function of bronchioles

A

smooth muscle fibres in their walls, allowing the width of these airways to vary

112
Q

draw a diagram for inspiration

A
  • ribs upwards and outwards
  • air in
  • diaphragm down
113
Q

draw a diagram for expiration

A
  • ribcage inwards and downwards
  • air out
  • diaphragm up
114
Q

describe the basic physics involved in ventilation

A
  • if particles of gas spread out to occupy a larger volume, the pressure of gas becomes lower
  • if gas is compressed to occupy a smaller volume, the pressure rises
  • if gas is free to move, it will flow from regions of higher pressure to regions of lower pressure
115
Q

describe the process of ventilation and how pressure is linked with it

A
  1. muscle contractions cause pressure inside the thorax to drop below atmospheric pressure
  2. air is drawn into the lungs from the atmosphere (inspiration) until lung pressure has risen to atmospheric pressure
  3. muscle contractions then cause pressure inside the thorax to rise above atmospheric, so air is forced out from the lungs to the atmosphere (expiration)
116
Q

muscles can be in two states

A

contracting and relaxing

117
Q

contracting

A
  • muscles do work
  • exert a pulling force (tension) that causes a particular movement
  • become shorter
118
Q

relaxing

A
  • muscles lengthen passively
  • pulled into an elongated state by the contraction of another muscle
  • do not exert a pushing force (compression) while relaxing so do no work
119
Q

describe an antagonistic pair of muscles

A

when one muscle contracts and causes a movement the second muscle relaxes and is elongated by the first . the opposite movement is caused by the second muscle contracting while the first relaxes

120
Q

why are antagonistic pairs of muscles needed?

A

muscles can only cause movement in one direction. if movement in opposite directions is needed at different timed, at least two muscles will be required

121
Q

draw a table for
diaphragm, ribcage
inspiration, expiration

A

p315

122
Q

draw a table for
volume and pressure changes, movement of diaphragm, movement of ribcage
inspiration, expiration

A

p.316

123
Q

causes of lung cancer

A
  • smoking: tobacco contains many mutagenic chemicals.
  • passive smoking
  • air pollution from diesel exhaust fumes, nitrogen oxides from all vehicle exhaust fumes, smoke from burning coal, wood, or other organic matter
  • radon gas: radioactive gas that leaks out of rocks like granite. accumulates in badly ventilated buildings so people inhale it
  • asbestos, silica, some other solids if dust or particles of them are inhaled, in construction sites, quarries, mines, or factories
124
Q

consequences of lung cancer

A
  • difficulties with breathing, persistent coughing, coughing up blood, chest pain, loss of appetite, weight loss, general fatigue
  • may lead to secondary tumours
  • chemotherapy or radiotherapy
125
Q

emphysema

A

Emphysema is a lung condition whereby the walls of the alveoli lose their elasticity due to damage to the alveolar walls
- The loss of elasticity results in the abnormal enlargement of the alveoli, leading to a lower total surface area for gas exchange
- The degradation of the alveolar walls can cause holes to develop and alveoli to merge into huge air spaces (pulmonary bullae)

126
Q

theories for formation of emphysema

A

in smokers, the number of phagocytes in the lungs increases and they produce more elastase.
- phagocytes inside alveoli normally prevent lung infections by engulfing bacteria and produce elastase, a protein-digesting enzyme, to kill them inside the vesicles formed by endocytosis.
- alpha 1-antitrypsin (A1AT) is an enzyme inhibitor and prevents elastase and other proteases from digesting lung tissue.
- genetic factors affect the quantity and effectiveness of A1AT produced in the lungs

127
Q

symptoms of emphysema

A
  • irreversible, chronic disease
  • low oxygen saturation in the blood and higher than normal co2 concentrations.
  • patient lacks energy
  • shortness of breath
  • ventilation laboured and more rapid than usual
128
Q

volume and pressure changes
- inspiration
- expiration

A

volume in thorax increases and pressure consequently decreases
volume in thorax decreases and pressure consequently increases

129
Q

movement of the diaphragm and abdomen wall muscles
- inspiration
- expiration

A

inspiration:
- diaphragm contracts and so it moves downwards and pushes the abdomen wall out
- muscles in the abdomen wall relax allowing pressure from the diaphragm to push it out

expiration:
- diaphragm relaxes so it can be pushed upwards into a more domed shape
- muscles in the abdomen wall contract pushing the abdominal organs and diaphragm upwards

130
Q

movement of the ribcage for the external intercostal muscles and internal intercostal muscles
- inspiration
- expiration

A

inspiration:
- the external intercostal muscles contract, pulling the ribcage upwards and outwards
- internal intercostal muscles relax and are pulled back into their elongated state

expiration:
- external intercostal muscles relax and are pulled back into their elongated state
- internal intercostal muscles contract, pulling the ribcage inwards and downwards

131
Q

Difference between nervous and endocrine system

A

endocrine system consists of glands that release hormones; nervous system consists of nerve cells called neurone

132
Q

What is the function of neurons?

A

to transmit electrical impulses

133
Q

draw a diagram of a standard neuron

A
134
Q

dendrite

A

short branched nerve fibres, for example those used to transmit impulses between neurone in one part of the brain or spinal cord

135
Q

axons

A

very elongated nerve fibres, for example those that transmit impulses from the fingers to the spinal cord

136
Q

how are nerve fibres adapted?

A

they are myelinated, which allows for saltatory conduction

137
Q

saltatory conduction

A

in myelinated nerve fibres the nerve impulse can jump from one node of ranvier to the next

138
Q

describe myelin

A
  • consists of many layers of phospholipid bilayer
  • deposited by Schwann cells, which grow round and round the nerve fibre
139
Q

node of ranvier

A

gap between the myelin deposited by adjacent Schwann cells.

140
Q

why is saltatory conduction faster than continuous transmission?

A

action potential to be conducted much faster and prevents the loss of the electrical signal through the cell membrane.

141
Q

define resting potential

A

the potential difference or voltage across the membrane of a neuron that is not transmitting a signal

142
Q

why is there a resting potential?

A

due to the imbalance of positive and negative charges across the membrane

143
Q

describe resting potential and how it is maintained

A
  • sodium-potassium pumps transfer sodium and potassium ions across the membrane. Na+ ions pumped out and K+ ions pumped in. The number of ions pumped is unequal - when 3 Na+ ions are pumped out, only two K+ ions are pumped in, creating concentration gradients for both ions
  • the membrane is about 50x more permeable to K+ ions than Na+ ions, so K+ ions leak back across the membrane faster than Na+ ions. As a result, the Na+ concentration gradient across the membrane is steeper than the K+ gradient, creating a charge imbalance
  • there are proteins inside the nerve fibre that are negatively charged (organic anions) which increase the charge imbalance
144
Q

define an action potential

A

a rapid change in membrane potential, consisting of:
- depolarisation - a change from negative to positive
- repolarisation - a change back from positive to negative

145
Q

value of resting potential

A

-70mV

146
Q

describe depolarisation

A

due to the opening of sodium channels in the membrane, allowing Na+ ions to diffuse into the neuron down the concentration gradient. The entry of Na+ ions reverses the charge imbalance across the membrane, so the inside is positive relative to the outside. This raises the membrane potential to a positive value of about +30mV

147
Q

describe repolarisation

A

happens rapidly after depolarisation and is due to the closing of the sodium channel and the opening of potassium channels in the membrane. This allows K+ ions to diffuse out of the neuron, down their concentration gradient, which makes the inside of the cell negative again relative to the outside. The potassium channels remain open until the membrane has fallen to a potential close to -70mV

148
Q

why does it take a few milliseconds for the neuron to be able to transmit another nerve impulse?

A

the diffusion of potassium depolarises the neuron, but does not restore the resting potential as the concentration gradients of sodium and potassium ions have not yet been re-established.

149
Q

define a nerve impulse

A

action potentials propagated along the axons of neutrons

150
Q

why does the propagation of the action potential happen?

A

because the sodium ion movements that depolarise one part of the neutron trigger depolarisation in the neighbouring part of the neuron

151
Q

what is the function of the refractive period after a depolarisation?

A

prevents propagation of an action potential backwards along an axon

152
Q

describe how local currents, or propagation of the action potential, come about

A
  1. depolarisation of part of the axon reduces the concentration of sodium ions outside the axon and increases it inside
  2. depolarised part of the axon therefore has different sodium ion concentrations to the neighbouring part of the axon that has not yet depolarised
  3. inside the axon sodium ions diffuse along inside the axon to the neighbouring part that is still polarised
  4. outside the axon the sodium ions diffuse from the polarised part back to the part that has just depolarised
153
Q

state the effect of local currents

A

reduce the concentration gradient in the part of the neuron that has not yet depolarised. this makes the membrane potential rise from the resting potential of -70mV to about -50mV. sodium channels in the axon membrane are voltage-gated and open when a membrane potential of -50mV is reached (known as threshold potential). this causes depolarisation

154
Q

draw a diagram for local current

A

pg 323

155
Q

draw and describe an action potential peak

A

pg 324

156
Q

define a synapse

A

a junction between neurons and between neurone and receptor or effector cells

157
Q

when pre-synaptic neurons are depolarised, they release

A

a neurotransmitter into the synapse

158
Q

describe synaptic transmission

A
  1. a nerve impulse is propagated along the pre-synaptic neuron until it reaches the end of the neuron and the pre-synaptic membrane
  2. depolarization of the pre-synaptic membrane causes calcium ions (Ca2+) to diffuse through channels in the membrane into the neuron
  3. influx of calcium causes vesicles containing neurotransmitter to move to the pre-synaptic membrane and fuse with it
  4. neurotransmitter is released into the synaptic cleft by exocytosis
  5. the neurotransmitter diffuses across the synaptic cleft and binds to receptors on the post-synaptic membrane
  6. the binding of the neurotransmitter to the receptors causes adjacent sodium ion channels to open
  7. sodium ions diffuse down their concentration gradient into the post-synaptic neuron, causing the post-synaptic membrane to reach the threshold potential
  8. an action potential is triggered in the post-synaptic membrane and is propagated on along the neuron
  9. the neurotransmitter is rapidly broken down and removed from the synaptic cleft
159
Q

function of acetylcholine

A

used as the neurotransmitter in many synapses

160
Q

how is acetylcholine produced

A

in the presynaptic neuron by combining choline, absorbed from the diet, with an acetyl group produced during aerobic respiration

161
Q

describe the use of acetylcholine as a neurotransmitter

A
  • loaded into vesicles and then released into the synaptic cleft during synaptic transmission
  • receptors for acetylcholine in the post-synaptic membrane have a binding site to which acetylcholine will bind
  • acetylcholine only remains bound to receptor for a short time, during which only one action potential is initiated in the post-synaptic neuron
  • enzyme acetylcholinesterase is present in the cleft and rapidly breaks down acetylcholine down into choline and acetate
  • choline reabsorbed into pre-synaptic neuron, where it is converted back into active neurotransmitter by recombining it with an acetyl group
162
Q

what do neonicotinoids do?

A

insecticides:
- they bind to the acetylcholine receptor in cholinergic synapses in the CNS of insects
- acetylcholinesterase does not break them down, so binding is irreversible
- receptors blocked so acetylcholine is unable to bind and synaptic transmission is prevented
- results in insect paralysis and death

163
Q

give an advantage and disadvantage of neonicotinoid use

A

+ not highly toxic to humans and other mammals: greater proportion of synapses in CNS are cholinergic in insects than in mammals and neonicotinoids bind less strongly to acetylcholine receptors in mammals than insects
- effects on honeybees and other beneficial insects

164
Q

a nerve impulse is only initiated if…

A

the threshold potential is reached

165
Q

nerve impulses follow an —- why?

A

all or nothing principle; only at the threshold potential do voltage-gated sodium channels start to open, causing depolarisation

166
Q

what determines whether a nerve impulse travels to the neighbouring neuron? explain

A

the amount of neurotransmitter secreted following depolarisation of the pre-synaptic membrane may not be enough to cause the threshold potential to be reached in the post-synaptic membrane, which then does not depolarise.

167
Q

what happens when the post-synaptic membrane does not depolarise?

A

sodium ions that have entered the post-synaptic neuron are pumped out by sodium-potassium pumps and the post-synaptic membrane returns to the resting potential

168
Q

what mechanism can be used to process information from different sources in the body to help in decision-making?

A
  • a typical post-synaptic neuron in the brain or spinal cord has synapses with many pre-synaptic neurone
  • it may be necessary for several of these to release neurotransmitter at the same time for the threshold potential to be reached and nerve impulse to be initiated
169
Q

function of cells in the pancreas

A

to respond to changes in blood glucose levels

170
Q

set point of blood glucose concentration

A

5 mmol/L

171
Q

what region of the pancreas secretes hormones directly into the bloodstream?

A

small regions of endocrine tissue islets of Langerhans

172
Q

alpha cells

A

synthesise and secrete glucagon if blood glucose levels fall below set point.

173
Q

function of glucagon

A

stimulates breakdown of glycogen into glucose in liver cells and its release into the blood, increasing the concentration

174
Q

beta cells

A

synthesise insulin and secrete it when the blood glucose concentration rises above the set point

175
Q

function of insulin

A

stimulates uptake of glucose by various tissues, particularly skeletal muscle and liver, in which it also stimulates conversion of glucose to glycogen, reducing blood glucose concentration

176
Q

why must secretion of insulin be ongoing?

A

it is broken down by the cells it acts upon

177
Q

define diabetes

A

a condition where a person has consistently elevated blood glucose levels

178
Q

effects of continuously elevated glucose

A
  • damages tissues, particularly their proteins
  • impairs water reabsorption from urine while it is forming in the kidney, resulting in an increase in the volume of urine and body dehydration
179
Q

symptoms of diabetes

A
  • urinate more frequently
  • constantly thirsty
  • feels tired
  • cares sugary drinks
180
Q

type 1 diabetes (early onset diabetes)

A
  • characterised by an inability to produce sufficient quantities of insulin
  • autoimmune disease arising from the destruction of beta cells in the islets of Langerhans by the body’s own immune system
181
Q

type 2 diabetes (late onset diabetes)

A
  • characterised by an inability to process or respond to insulin because of a deficiency of insulin receptors or glucose transporters on target cells
182
Q

main risk factors of type 2 diabetes

A
  • sugary, fatty diets
  • prolonged obesity due to habitual obesity and lack of exercise
  • genetic factors that affect energy metabolism
183
Q

treatment of type 1 diabetes

A
  • testing blood glucose concentration regularly and injecting insulin when it is too high or likely to become too high
  • injections often done before a meal to prevent peak of blood glucose as the food is digested/absorbed
184
Q

treatment of type 2 diabetes

A
  • adjusting diet to reduce peaks and troughs of blood glucose.
  • small amounts of food eaten frequently rather than infrequent large meals
  • foods with high sugar content avoided; starchy foods only allowed if low glycemic index (digested slowly); high-fibre foods included to slow digestion of other foods
  • strenuous exercise and weight loss
185
Q

what is thyroxin secreted by

A

thyroid gland (in neck) §

186
Q

why is thyroxin unusual?

A
  • chemical structure - contains four atoms of iodine
  • almost all cells in body are targets
187
Q

what prevents synthesis of thyroxin?

A

prolonged deficiency of iodine in the diet

188
Q

function of thyroxin

A
  • regulates body’s metabolic rate, so all cells need to respond
  • main targets are most metabolically active such as liver, muscle and brain
  • control of body temperature
189
Q

higher metabolic rate ->

A

more protein synthesis and growth and increases the generation of body heat

190
Q

in a person with normal physiology, cooling triggers…

A

increased thyroxin secretion by the thyroid gland, which stimulates heat production so body temperature rises

191
Q

effects of hypothyroidism

A

thyroxin deficiency:
- lack of energy/persistent tiredness
- forgetfulness and depression
- weight gain
- persistent feeling cold
- constipation
- impaired brain development

192
Q

explain weight gain despite of loss of appetite in hypothyroidism

A

less glucose and fat are being broken down to release energy by cell respiration

193
Q

explain constipation in hypothyroidism

A

contractions of muscle in the wall of the gut slow down

194
Q

define leptin

A

a protein hormone secreted by adipose cells (fat storage cells)

195
Q

what controls the concentration of leptin in the blood?

A

food intake and amount of adipose tissue in the body

196
Q

target of leptin

A

group of cells in the hypothalamus of the brain that contribute to the control of appetite - leptin binds to receptors in the membrane of these cells.

197
Q

if adipose tissue increases,

A

blood leptin concentrations rise, causing long-term appetite inhibition and reduced food intake

198
Q

describe experiments done on obese mice

A
  • they had two copies of recessive allele, ob, causing their adipose cells to be unable to produce leptin
  • feed ravenously, become inactive and gain body weight, mainly through increased adipose tissue
  • when these mice were injected with leptin their appetite declined, energy expenditure increased, and body mass dropped
199
Q

why did leptin injections not work as a weight loss method?

A
  • in contrast to ob/ob mice, most obese humans have exceptionally high blood leptin concentrations
  • target cells in hypothalamus have become resistant to leptin so fail to respond to it, even at high concentrations
  • appetite not inhibited and food intake is excessive
  • more adipose tissue develops, causing a rise in blood leptin concentration but leptin resistance prevents inhibition of appetite
200
Q

a very small proportion of cases of obesity in humans are due to

A

mutations in the genes for leptin synthesis or its various receptors on target cells

201
Q

trials in people with such obesity have shown

A

significant weight loss while the leptin injections are continuing; however, leptin is a short lived protein and has to be injected several times a day. also affects the development and functioning of the reproductive system, so is not suitable to children and YAs

202
Q

circadian rhythms

A

humans are adapted to live in a 24-hour cycle and have rhythms in behaviour that fit this cycle

203
Q

what do circadian rhythms depend on?

A

two groups of cells in the hypothalamus - suprachiasmatic nuclei (SCN).

204
Q

function of SCN

A

control secretion of melatonin (hormone) by pineal gland.

205
Q

describe melatonin secretion

A

increases in the evening and drops to a low level at dawn

206
Q

why do blood concentrations of melatonin rise and fall rapidly in response to changes in secretion?

A

the hormone is rapidly removed from the blood by the liver

207
Q

state three effects of melatonin

A
  • the sleep-wake cycle: high levels of melatonin cause drowsiness and promote sleep through the night. falling levels encourage waking at the end of the night
  • night-time drop in core body temperature
  • decreased urine production at night: melatonin receptors have been discovered in the kidney
208
Q

describe how melatonin secretion is regulated

A

a special type of ganglion cell in the retina of the eye detects light of wavelength 460-480nm and passes impulses to cells in the SCN. This indicates to the SCN the timing of dusk and dawn and allows it to adjust melatonin secretion so that it corresponds to the day-night cycle.

209
Q

how does jet lag come about?

A

the SCN and pineal gland are continuing to set a circadian rhythm to suit the timing of day and night at the point of departure rather than destination.

210
Q

initially, the development of the embryo is

A

the same in all embryos and embryonic gonads develop that could either become ovaries or testes

211
Q

what does the developmental pathway of the embryonic gonads and thereby the whole baby depend on?

A

the presence or absence of one gene

212
Q

if the gene SRY is present

A

the embryonic gonads develop into testes.

213
Q

what does SRY do?

A

it codes for a DNA binding protein called TDF (testis determining factor(, which stimulates the expression of other genes that cause testis development

214
Q

where is SRY located?

A

on the Y chromosome

215
Q

when would embryonic gonads develop as ovaries?

A

when embryos have 2 X chromosomes and so do not have a copy of the SRY gene. TDF is not produced and the embryonic gonads develop as ovaries

216
Q

when do the testes develop from the embryonic gonads?

A

in about the eighth week of pregnancy

217
Q

the testes develop 1, 2, 3, at an early stage and these produce 4 which causes male genitalia to develop

A

testosterone-secreting cells
testosterone

218
Q

what happens at puberty in males?

A

the secretion of testosterone increases

219
Q

effects of increased testosterone secretion

A
  • sperm production in the testes (primary sexual characteristic of males)
  • secondary sexual characteristics: enlargement of the penis, growth of pubic hair, deepening of voice due to growth of the larynx
220
Q

describe female hormone secretion

A
  • estrogen and progesterone are always present in pregnancy
  • at first they are secreted by the mother’s ovaries and later by the placenta
  • in the absence of fetal testosterone and the presence of maternal oestrogen and progesterone, female reproductive organs develop
221
Q

effects of increased oestrogen and progesterone secretion during puberty

A
  • female secondary secondary sexual characteristics: enlargement of the breasts, growth of pubic and underarm hair
222
Q

draw a labelled diagram of the female and male reproductive systems

A
223
Q

testis

A

produce sperm and testosterone

224
Q

scrotum

A

hold testes at lower than core body temperature

225
Q

epididymis

A

store sperm until ejaculation

226
Q

seminal vesicle and prostate gland

A

secrete fluid containing alkali, proteins and fructose that is added to sperm to make semen

227
Q

urethra

A

transfer seen during ejaculation and urine during urination

228
Q

penis

A

penetrates the vagina for ejaculation of semen near the cervix

229
Q

ovary

A

produce eggs, oestrogen, and progesterone

230
Q

oviduct

A

collect eggs at ovulation, provide a site for fertilisation then move the embryo to the uterus

231
Q

uterus

A

provide the needs of the embryo and then foetus during pregnancy

232
Q

cervix

A

protect the foetus during pregnancy and then dilate to provide a birth canal

233
Q

vagina

A

stimulate the penis to cause ejaculation and provide a birth canal

234
Q

vulva

A

protect internal parts of the female reproductive system

235
Q

what is the menstrual cycle controlled by?

A

negative and positive feedback mechanisms involving ovarian and pituitary hormones

236
Q

state the two phases of the menstrual cycle

A

follicular phase
luteal phase

237
Q

follicular phase

A
  • a group of follicles is developing in the ovary
  • in each follicle an egg is stimulated to grow
  • at the same time the lining of the uterus (endometrium) is repaired and starts to thicken
  • the most developed follicle breaks open, releasing its eggs into the oviduct
  • the other follicles degenerate
238
Q

luteal phase

A
  • the wall of the follicle that released an egg becomes the corpus luteum
  • continued development of the endometrium prepares it for the implantation of an embryo
  • if fertilisation does not occur the corpus lute in the ovary breaks down
  • the thickening of the endometrium in the uterus also breaks down and is shed during menstruation
239
Q

FSH and LH

A

protein hormones produced by the pituitary gland that bind to FSH and LH receptors in the membranes of follicle cells

240
Q

estrogen and progesterone

A

ovarian hormones produced by the wall of the follicle and corpus lute. they are absorbed by many cells in the female body, where they influence gene expression and therefore development

241
Q

FSH function

A

rises to a peak towards the end of the menstrual cycle
- stimulates the development of follicles, each containing an oocyte and follicular fluid
- stimulates the secretion of oestrogen by the follicle wall

242
Q

Estrogen function

A

rises to a peak towards the end of the follicular phase
- stimulates repair and thickening of the endometrium after menstruation and an increase in FSH receptors that make the follicles more receptive to FSH, boosting oestrogen production (positive feedback)
- at high levels, oestrogen inhibits FSH secretion (negative feedback) and stimulates LH secretion

243
Q

LH function

A

rises to a sudden and sharp peak towards the end of the follicular phase
- stimulates the completion of meiosis in the oocyte and partial digestion of the follicle wall allowing it to burst open at ovulation
- LH promotes development of wall of follicle after ovulation into corpus luteum, which secretes oestrogen (positive feedback) and progesterone

244
Q

progesterone function

A

rise at the start of the luteal phase, reach a peak and then drop back to a low level by the end of this phase
- promotes thickening and maintenance of endometrium
- inhibits FSH and LH secretion by pituitary gland

245
Q

draw a diagram showing the various stages of the menstrual cycle and hormones

A

p337

246
Q

describe ivf

A
  1. down-regulation: woman takes a drug each day (usually nasal spray) to stop her pituitary gland secreting FSH or LH. secretion of oestrogen and progesterone therefore also stops. menstrual cycle suspended and doctors can control timing and amount of egg production in woman’s ovaries
  2. superovulation- intramuscular injections of FSH and LH given daily for ~10 days, to stimulate follicles to develop. FSH injections are of higher concentration than usual so far more follicles develop than usual.
  3. injection of HCG- stimulates follicles to mature
  4. micropipette mounted on an ultrasound scanner is passed through uterus wall to wash eggs out of the follicles
  5. each egg is mixed with 50-100,000 sperm cells in sterile conditions in a shallow dish, which is then incubated at 37’C until the next day
  6. if fertilisation occurs then one or more embryos are placed in the uterus when they are ~48 hours old
  7. extra progesterone usually given as a tablet placed inside vagina, to ensure uterus lining is maintained