Human Physiology Flashcards

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1
Q

annotate digestive system

A
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2
Q

mouth

A

ingestion and chewing (saliva)

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3
Q

mouth

A

ingestion and chewing (salvia)

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4
Q

stomach

A

killing pathogens in food and protein digestion

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5
Q

gall bladder

A

stores bile (fluid that aids digestion)

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6
Q

liver

A

secretes bile

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7
Q

pancreas

A

secretes digestive enzymes

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8
Q

small intestine (structure and function)

A

digestion and absorption

  • layers of folded tissue
  • serosa — an outer coat
  • longitudinal muscle layers
  • circular muscles layer
  • sub-mucosa — a tissue layer containing blood and lymph vessels
  • mucosa — the lining of the small intestine, with the epithelium that absorbs nutrients on its inner surface
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9
Q

large intestine

A

absorption of water

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10
Q

anus

A

egestion of feces

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11
Q

peristalsis and digestion in small intestine (enzymes secreted)

A

Waves of contraction of longitudinal muscle, called peristalsis:

  • moves food along the intestine
  • prevents backflow of food towards the mouth
  • (together with horizontal muscles) mixes food with enzymes in the small intestine

Enzymes digest most macromolecules in food into monomers in the small intestine (e.g. proteins, starch, glycogen, lipids and nucleic acids). Cellulose remains undigested. The pancreas secretes three types of enzyme into the lumen of the small intestine:

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12
Q

digestion of starch

A

There are two types of molecules in starch: amylose and amylopectin.

Amylase breaks 1,4 bonds in chains of four or more glucose monomers, so it can digest amylose into maltose but not glucose. Because of the specificity of its active site, amylase cannot break the 1,6 bonds in amylopectin. Fragments of the amylopectin molecule containing a 1,6 bond that amylase cannot digest are called dextrins.

Digestion of starch is completed by enzymes in the membranes of microvilli on vilus epithelium cells: maltase and dextrinase digest maltose and dextrins into glucose. Also, in the membranes of the microvilli are protein pumps that cause the absorption of the glucose produced by digesting starch.

Blood carrying glucose and other products of digestion flows though villus capillaries to venules in the submucosa of the wall of the small intestine. The blood in these venules is carried via the hepatic portal vein to the liver, where excess glucose can be absorbed by liver cells and converted to glycogen for storage.

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13
Q

villi and epithelium (structure and function)

A

Villi increase the surface area of epithelium over which nutrient absorption is carried out.

epithelium = single layer of cells, either microvilli or globet cells that secrete mucus forming the inner lining of the mucosa

inside the villi = blood capillaries and lymphatic system (lacteal)

The rate of absorption depends on the surface area of this epithelium. (The adult small intestine is ca 7 meters long and 25-30 millimeters wide. Villi absorb mineral ions and vitamins and also monomers formed by digestion such as glucose.)

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14
Q

methods of absorption + the nutrients using the specific transport

A

simple diffusion: hydrophobic nutrients such as fatty acids and monoglycerides

facilitated diffusion (channel proteins): hydrophilic nutrients such as fructose

active transport: mineral ions such as sodium, calcium and iron

endocytosis (pinocytosis): triglycerides and cholesterol in lipoprotein particels

More complex transport methods include how glucose is absorbed by sodium co-transporter proteins, which move a molecule of glucose together with a sodium ion across the membrane together into the epithelium cells. The sodium gradient is generated by active transport of sodium out of the epithelium cell by a protein pump. (The glucose can be moved against its concentration gradient because the sodium ion is moving down its concentration gradient.)

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15
Q

Modeling absorption with dialysis tubing

A

Cola drink contains a mixture of substances which can be used to model digested and undigested foods in the intestine. The water outside the bag is tested at intervals to see if substances in the cola have diffused through the dialysis tubing.

The expected result is that glucose and phosphoric acid, which have small-sized particles, diffuse through the tubing but caramel, which consists of larger polymers of sugar, does not.

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16
Q

Harvey and the circulation of blood

A

Until the 17th century the doctrines of Galen, an ancient Greek philosopher, about blood were accepted with little question by doctors. Galen taught that blood is:

  • produced by the liver
  • pumped out by the heart
  • consumed in the other organs.

William Harvey is usually credited with the discovery of the circulation of blood. He demonstrated that blood flow through vessels is unidirectional with valves to prevent back flow and also that the rate of flow through major vessels is far too high for blood to be consumed in the body after being pumped out by the heart. He showed that the heart pumps blood out in arteries and that it returns in veins.

He also predicted the existence of capillaries that linked arteries to veins but where too small to be seen with his contemporary equipment.

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17
Q

The double circulation (pulmonary and systemic ciruclation)

A

pulmonary circulation goes to the lungs

systemic circulation goes to other organs

The heart is a double pump with left and right sides. The right side pumps deoxygenated blood to the lungs via the pulmonary artery. Oxygenated blood returns to the left side of the heart in the pulmonary vein. The left side pumps this blood via the aorta to all organs of the body apart from the lungs. Deoxygenated blood is carried back the right side of the heart in the vena cava.

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18
Q

types and structure of blood vessels

A

arteries convey blood pumped out at high pressure by the ventricles from the heart away. They carry the blood the tissues of the body

capillaries carry blood through tissues. They have permeable walls that allow exchange of materials between the cells of the tissue and the blood in the capillary

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

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19
Q

Cardiac muscle and coronary capillaries

A

The walls of the heart are made of cardiac muscle – it can contract on its own without being stimulated by a nerve (myogenic contraction).

There are many capillaries in the muscular wall of the heart. The blood running through these capillaries is supplied by the coronary arteries, which branch off the aorta, close to the semilunar valve. The blood brought by the coronary arteries brings nutrients and oxygen for aerobic cell respiration, providing energy for cardiac muscle contraction.

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20
Q

annotate

A
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21
Q

cardiac cycle (beating of the heart) + pressures during phases

A
  1. The walls of the atria contract, pushing blood from the artria into the ventricles through the atria-ventricular valves, which are open. The semilunar valves are closed, so the ventricles fill with blood.
  2. The walls of the ventricles contract powerfully and the blood pressure rapidly rises inside them. This first causes the atria-ventricular valves to close, preventing back-flow to the atria and then causes the semilunar valves to open, allowing blood to be pumped out into the arteries. At the same time the artria start to refill by collecting blood from the veins.
  3. The ventricles stop contracting so pressure falls inside them. The semilunar valves close, preventing back-flow from the arteries to the ventricles. When the ventricular pressure drops below the atrial pressure, the atrio-ventricular valves open. Blood entering the atrium from the veins then flows on to start filling the ventricles.

The next cardiac cycle begins when the walls of the atria contract again.

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22
Q

Control of heart rate

and

Changes in the rate

A

Sinoatrial (SA) node — one region of specialized cardiac muscle cells in the wall of the right atrium acts as the pacemaker of the heart by initiating each contraction. The node sends out an electrical signal that stimulates the contraction as it is propagated first through the walls of the atria and then through the walls of the ventricles.

Change in heart rates (messages) can be carried to the SA node by nerves and hormones.

  • Impulses brought from the medulla of the brain by two nerves can cause the SA node to change the heart rate. One nerve speeds up the rate and the other slows it down.
  • The hormone adrenalin (epinephrine) increases the heart rate to help prepare the body for vigorous physical activity.
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23
Q

Coronary artery disease (description and causes)

A

Coronary arteries are arteries surrounding the heart.

Is caused by fatty plaque building ip in the inner lining of coronary arteries, which become occluded (narrowed). As this becomes more severe, blood flow to cardiac muscle is restricted, causing chest pain. Minerals often become deposited in the plaque making it hard and rough. Various factors have been shown by surveys to be associated with coronary artery disease and are likely causes of it:

  • high blood cholesterol levels
  • smoking
  • high blood pressure (hypertension)
  • high blood sugar levels (diabetes)
  • genetic factors (thus a family history of the disease)
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24
Q

Barries to infection (and defences if the barriers are trespassed)

A

A pathogen is an organism or virus that causes disease.

Primary defenses are barriers:

  • Skin; sebaceous glands in the skin secrete lactic acid and fatty acids, which make the skin acidic. This prevents, very effectively, the growth of most pathogenic bacteria.
  • Mucous membranes (“Schleimhaut”) are soft areas of skin that are kept moist with mucus, found in the nose, trachea, vagina and urethra. Many bacteria are killed by lysozyme, an enzyme in the mucus, or get caught in the sticky mucus in the trachea; cilia then push the mucus and bacteria up and out of the trachea.

When pathogens enter the body:

two types of white blood cells fight infections: phagocytes and lymphocytes.

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25
Q

When pathogens enter the body:

A

two types of white blood cells fight infections:

phagocytes and lymphocytes.

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26
Q

Phagocytes

A

Phagocytes ingest pathogens by endocytosis. The enzyme lysosome then kills and digests the pathogens. This ingestion can occur in blood but also at the immediate site of infection in tissue. Large number of phagocytes at a site form pus.

Phagocytes give humans non-specific immunity to diseases, because a phagocyte does not distinguish between pathogens — it ingests any pathogen if stimulated to do so.

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27
Q

blood clotting

A

When skin is cut and blood escapes from blood vessels, a semi-solid blood clot is formed from liquid blood to seal up the cut and prevent entry of pathogens.

Platelets are _small cell fragments t_hat circulate with red and white blood cells in blood plasma. The clotting process begins with the release of clotting factors either from damaged tissue cells or from platelets. These clotting factors sett off numerous cascade-reactions (“domino”) in which the product of each reaction is the catalyst of the next reaction.

This system helps to ensure that clotting only happens when it is needed and also makes it a very rapid process. In the last reaction, fibrinogen, a soluble plasma protein, is altered by the removal of sections of peptide that have many negative chargers. This allows remaining polypeptide to bind to others, forming long protein fibers called fibrin. Fibrin forms a mesh of fibers across wounds. Blood cells are caught in the mesh and soon form a semi-solid clot. If exposed to air the clot dries to form a protective scab, which remains until the wound has healed and new skins has regrown.

The last rapid reactions:

  • prothrombin is converted to thrombin by prothrombin activator
  • fibrinogen is converted to fibrin by thrombin
28
Q

Blood clots in coronary arteries

A

If the deposits of plaque in coronary arteries rupture, blood clots form (coronary thrombosis), which may completely block the artery. Consequentially, an area of cardiac muscle receives no oxygen and stops beating in a coordinated way — a heart attack. Uncoordinated contraction of cardiac muscle is fibrillation. This may be fatal, or the heart starts beating again.

29
Q

stages in production of antibodies

A
  1. Lymphocytes make antibodies, stimulated by antigens (foreign substances).
  2. Lymphocytes can only make one type of antibody, so many different lymphocyte types are needed. They stick some of the antibodies that they can make on their cell membrane, with the antigen-combining site projecting outwards.
  3. Pathogen binds to antibodies.
  4. Lymphocyte becomes active and produces many identical plasma cells by mitosis.
  5. Large production of the same antibodies begins, which, when bound to pathogens, stimulates destruction — specific immunity.
  6. After infection is cleared, some memory cells persists, while the rest disappears.
30
Q

HIV

A

The human immunodeficiency virus (HIV) destroys lymphocytes gradually. Hence, less antibodies are produced, known as AIDS (acquired immunodeficiency syndrome). This can lead to death from untreated infections, that would normally be controlled easily.

Transmission via body fluids (does not survive long outside body nor passes through skin): blood and tears (sex, cuts, hypodermic needles, etc.), placenta (from mother to baby), breastfeeding.

31
Q

antibiotics (viruses)

A

Antibiotics are chemicals produced by microorganisms, to kill or control the growth of other organisms. They block the processes of the cells, but only in prokaryotes.

Viruses lack a metabolism and only rely on a host. It is therefore not possible to block these processes without also harming host cells.

Most bacterial diseases can be treated, but some have multiple resistance as a result of over-use accelerating the natural selection of bacteria and viruses; we are running out of antibiotics.

32
Q

penicillin

A

Developed by Florey and Chain in 1930s, tested only shortly mice and right after on humans (who were on the verge of death).

To be safe, one should first test medicine on animals, then in small and then larger doses on healthy, informed humans. Only then should the drug be tested on sick patients with a large sample size to avoid side effects.

33
Q

ventilation and gas exchange

A

Because cell respiration happens, oxygen is needed and carbon dioxide must be released.

Ventilation brings fresh air to the alveoli of human lungs and removes the stale air.

Gas exchange, swapping one gas for another, happens by diffusion in the alveoli, so it depends on concentration gradients of oxygen and carbon dioxide between the air in alveoli and blood flowing in adjacent capillaries.

34
Q

annotate ventilation system

A
35
Q

monitoring ventilation rates and tidal volume in humans

A

Ventilation rate: the number of inhalations / exhalations per minute

  1. Observed by simple observation in a minute.

or

  1. An inflatable chest belt around the thorax, sensors measure expansion; both rate and relative size of ventilation.

Tidal volume: volume of air taken in / out with each inhalation /exhalation

  1. Breathing out into a spirometer so the volume can be measured.
36
Q

muscles used in ventilation

A

Antagonistic muscles are required for inspiration and expiration because muscles only work when they contract, forcing air in and out of the lungs.

Inhaling

  • The external intercostal muscles contract, moving the ribcage up and out.
  • The diaphragm contracts, becoming flatter and moving down.
  • The muscle moments increase the volume of the thorax.
  • The pressure inside the thorax therefore drops below atmospheric pressure.
  • Air flows into the lungs from outside the body until the pressure inside the lungs rises to atmospheric pressure.

Exhaling

  • The internal intercostal muscles contract, moving the ribcage down and in.
  • The abdominal muscles contract, pushing the diaphragm up into a dome shape.
  • The muscle movements decrease the volume of the thorax.
  • The pressure inside the thorax therefore rises above atmospheric pressure.
  • Air flows out from the lungs to outside the body until the pressure inside the lung falls to atmospheric pressure.
37
Q

Adaptions of an alveolus for gas exchange (pneumocytes)

A
  • permeable to oxygen and carbon dioxide
  • a large surface area for diffusion
  • thin, so distance for diffusion is small
  • moist, oxygen can dissolve
  • as the lung contains hundreds of millions of alveoli, a huge surface area is available

Type 1 pneumocytes

Extremely thin (single layer) and permeable alveolar cells that are adapted to carry out quick gas exchange.

Type 2 pneumocytes

Secrete a fluid to keep the inner alveolus wall surface moist and allow gases to dissolve. The fluid also contains a natural detergent (“cleaner” - surfactant), to prevent the sides of the alveoli from sticking together by reducing surface tension.

Blood capillaries

A dense network of capillaries with low oxygen and high carbon dioxide blood concentrations.

38
Q

causes and consequences of lung cancer

how are correlations found?

A

Epidemiology is the study of the incidence and cause of disease. Surveys may uncover correlations, which does not prove causation. The main causes of lung cancer are:

  • smoking tobacco and passive smoking
  • air pollution (diesel exhaust fumes, nitrogen oxides, etc.)
  • radon gas (leaking from rocks, especially granite)
  • asbestos and silica (when the dust is inhaled)

Consequences:

difficulties with breathing, persistent coughing (with blood), vernal fatigue, chest pain, appetite loss, weight loss and many more…

39
Q

emphysema

A

The main cause of emphysema are smoking and air pollution. The cilia that line the airways and expel mucus are damaged, so mucus builds up in the lungs, causing infections. Toxins in cigarette smoke and polluted air cause inflammation and damage to the white blood cells that fight infections. A protease (trypsin) is released from inflamed cells and damaged white blood cells. This enzyme digests elastic fibers in the lungs and eventually causes complete breakdown of alveolus walls. Microscopic alveoli are replaced by progressively larger air sacs with thicker, less permeable walls.

Emphysema is a chronic and progressive disease with severe consequences. As the surface area for gas exchange is reduced, the oxygen saturation of the blood falls and exercise becomes more difficult. The lungs lose their elasticity, making it increasingly difficult to exhale (shortness of breath). Mucus in the lungs causes coughing and wheezing (“schnaufen”).

40
Q

Structure and function of neurons

A

The nervous system is composed of cells called neurons. They carry messages at high speed in the form of electrical impulses. Many neurons are very elongated and carry impulses long distances in a short time.

Myelinated nerve fibers have a myelin sheath with small gaps called nodes of Ranvier, allowing the nerve impulse to jump from node to node. This is know as saltatory conduction and speeds up the transmission along the axon.

41
Q

Synapses (general facts)

A
  • A synapse is a junction between two neurons or a junction between neurons and receptor or effector cells.
  • The plasma membranes of neurons are separated by a narrow fluid-filled gap called the synaptic cleft.
  • Messages are passed across the synapse in form of chemicals called neurotransmitters, which always pass in the same direction from the pre-synaptic neutron to the post-synaptic neuron.
42
Q

functioning of synapsis (outline)

A
  1. A nerve impulse reaches the end of a pre-synaptic neuron.
  2. Depolarization of the pre-synaptic membrane causes vesicles of neurotransmitter to move to the pre-synaptic membrane and fuse with it, releasing the neurotransmitter into the synaptic cleft by exocytosis.
  3. The neurotransmitter diffuses across the synaptic cleft and binds to receptors in the post synaptic membrane.
  4. The receptors are transmitter-gated sodium channels, which open when neurotransmitter binds. Sodium ions diffuse into the post-synaptic neuron. This causes depolarization of the post-synaptic membrane.
  5. The depolarization passes on down the post-synaptic neuron as an action potential.
  6. Neurotransmitter in the synaptic cleft is rapidly broken down, to prevent continuous synaptic transmission.
43
Q

cholinergic synapses

A

Synapses that use acetylcholine as a neurotransmitter.

The acetylcholine is broken down in the synaptic clef by the enzyme cholinesterase, producing acetyl groups and choline. The choline is reabsorbed by the pre-synaptic neuron.

44
Q

Neonicotinoid pesticides

A

They bind to acetylcholine receptors in the post-synaptic membranes of cholinergic synapses in insects. Cholinesterase does not break down these pesticides so they remain bound to the receptors, preventing acetylcholine from binding. They therefore block synaptic transmission, which ultimately kills insects. Unfortunately, honeybees are killed along with insect pests.

45
Q

resting potential

A

The negative voltage across the plasma membrane of a neuron when it is not conducting a nerve impulse.

There are sodium-potassium pumps in the plasma membranes of axons. They pump 3 sodium ions out and 2 potassium ions in, by active transport, establishing concentration gradients. The inside of the neuron developed a net negative charge, compared with the outside, because of the presence of chloride and other negatively charged ions. There is therefore a potential across the membrane, typically -70mV.

46
Q

action potentials

A

The depolarization and repolarization of a neuron, due to facilitated diffusion of ions across the membrane through voltage-gated ion channels.

If the potential across the membrane rises from -70 to -50mV (threshold potential), voltage-gated sodium channels open and sodium ions diffuse in down the concentration gradient. The entry of positively charged sodium ions causes the inside of the neuron to develop a net positive charge compared to the outside — the potential across the membrane is reversed — depolarization.

The reversal of membrane polarity causes potassium channels to open, allowing potassium ions to diffuse out down the concentration gradient. The exit of positively charged potassium ions causes the inside of the neuron to develop a net negative charge again compared with the outside — the potential across the membrane is restored — repolarisation.

47
Q

definition of a nerve impulse and the propagation (transmission) of an impulse

A

A nerve impulse is an action potential that travels along the axon of a neuron from one end to the other.

  • There is an action potential whenever a part of the axon reaches the threshold potential of -50mV. An action potential in one part of the axon triggers an action potential in the next part, that was previously in the resting potential — propagation of the nerve impulse.
  • Local currents: the diffusion of sodium ions along the axon, both inside and outside the membrane.
48
Q

osciloscope traces

A

The changes in membrane potential in axons during an action potential can be measured using electrodes, displayed on an oscilloscope.

  1. The axon membrane rises from resting to threshold potential, either due to local currents or to the bind of a neurotransmitter at a synapse — stimulus.
  2. Membrane depolarizes due to voltage-gated sodium channels opening.
  3. Membrane repolarises due to voltage-gated potassium channels opening.
  4. Membrane returns to the resting potential due to the active pumping of Na+ ions out and K+ ions in to the axon.
49
Q

memory and learning

A

Higher functions of the brain including memory and learning are currently only partly understood. The emergent property enables the powerful computing. They have traditionally been investigated by psychologists but increasingly the techniques of molecular biology, biophysics, medicine, computer science and biochemistry are used as investigative tools (#collaboration of science fields).

Exemplary research

The Centre for Neural Circuits and Behavior (Oxford University) specializes in research techniques known as optogenetics. Neurons are genetically engineered to emit light and respond to light. This allows patterns of activity in the neurons of living brain tissue to be studied.

50
Q

adipose tissue

A

fat storage cells

51
Q

Blood glucose concentration and the hormones secreted to regulate it

A
  • Concentration usually 4-8 millimoles per dm3 of blood
  • Cells in the pancreas monitor the concentration and secrete the hormones:
  • insulin to lower glucose level, secreted by beta cells (stimulates liver and muscle cells to absorb glucose and convert it to glycogen; granules of glycogen are stored in these cells; other cells are stimulated to absorb glucose and use it in cell respiration instead of fat)
  • glucagon to higher glucose level, secreted by alpha cells (stimulates liver cells to break down glycogen into glucose and release the glucose)
52
Q

diabetes mellitus (type I and II)

A

Rise or fall beyond normal limits of glucose levels.

Type I

  • onset usually during childhood
  • immune system destroys beta cells in the pancreas so the amount of insulin secreted becomes insufficient
  • consequence: frequent blood measurements and insulin injections (often before meals)
  • diet cannot by itself control this type of diabetes

Type II

  • onset usually after childhood
  • target cells become insensitive to insulin, so insulin injects are not an effective treatment (usually)
  • low carbohydrate diets can control the condition
  • rich fat and low fibre food, lack of exercise and genetic factors that affect fat metabolism increase the risk of type II
53
Q

thyroxin (composition, where is it secreted and why)

A

hormone regulating: metabolic rate & body temperature

  • targets almost all cells.
  • Higher metabolic rates support more protein synthesis and growth and it increases the generation of body heat.
  • Thyroxin is implicated in heat generation by shivering and uncoupled cell respiration in brown adipose tissue (BAT) — secreting more thyroxin.
  • It also causes constriction of vessels that carry blood from the core to the skin, reducing heat loss.
  • Secreted by the thyroid gland in the neck.
  • It has an unusual chemical structure as it contains four atoms of iodine.
  • Prolonged deficiency of iodine in the diet therefore prevents the synthesis of thyroxin.
54
Q

leptin (where is it screted, why and whats the effect)

A

Leptin is secreted by cells in adipose tissue (fat storage cells) and acts on the hypothalamus of the brain to inhibit appetite.

Leptin binds to receptors in the membrane of these cells. If adipose tissue increases, blood leptin concentrations rise, causing long-term appetite inhibition and thereby reduce food intake.

55
Q

Testing of leptin on patients with clinical obesity and reasons for the failure of control the disease.

A

Tests on humans, in contrast to mice, were not successful in reducing body mass because the obese already had exceptionally high blood leptin concentrations and have become resistant even at high concentrations. Appetite is therefore not inhibited and food intake is excessive — more adipose tissue develops.

A very small proportion of cases of obesity in humans are due to mutations in the genes for leptin synthesis or its various receptors on target cells. Trials in people with such obesity have shown 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 and consequently most of those offered this treatment have refused it. Also leptin has been shown to affect the development and functioning of the reproductive system, so injections are not suitable in children and young adults. All in all leptin has not fulfilled its early promise as a means of solving the human obesity problem, as it worked successfully on mice.

56
Q

melatonin

A

Melatonin is secreted by the pineal gland to control circadian rhythms.

Humans are adapted to live in a 24-hour cycle and have rhythms in behaviour that fit this cycle. These are known as circadian rhythms and can continue even in the absence of light fluctuations as it is an internal system.

Circadian rhythms in humans depend on two groups of cells in the hypothalamus called the suprachiasmatic nuclei (SCN). In the brain they control the secretion of the hormone melatonin by the pineal gland. Melatonin secretion increases in the evening and drops at dawn and as the hormone is rapidly removed from the blood by the liver, blood concentrations rise and fall rapidly in response to these changes in secretion.

The most obvious effect of melatonin is the sleep-wake cycle. High melatonin levels cause feelings of drowsiness and promote sleep through the night. Falling melatonin levels encourage waking at the end of the night. Experiments have shown that melatonin contributes to the night-time drop in core body temperature, as blocking the rise in melatonin levels reduces it and giving melatonin artificially during the day causes a drop in core temperature. Melatonin receptors have been discovered in the kidney, suggesting that decreased urine production at night may be another effect of this hormone. Light cues detected by the eye pass impulses to cells in the SCN, adjusting, if necessary, the rhythm by a few minutes each day.

Jet lag is caused by SCN and pineal gland continuing to set a circadian rhythm to suit the timing of the departure. It lasts only a few days as the light impulses adjust to the new regime. Melatonin is used to try to prevent or reduce jet lag by taking it orally at the time when sleep should ideally occur. Trials have found that to be effective.

Until a baby is about three months old it does not develop a regular day-night rhythm of melatonin secretion. Also, melatonin declines with age, explaining the more irregular sleep patterns as we grow older.

57
Q

annotate (with function) female reproductive system

A
58
Q

annotate (with function) male reproductive system

A
59
Q

Sex determination in males

A

A gene on the Y chromosome causes embryonic gonads to develop as testes and secrete testosterone.

SRY codes for TDF (testis determine factor), a gene regulation protein. By bindig to specific DNA sites TDF stimulates the expression of genes for testis.

Testosterone, secreted by developing testes, causes prenatal (before birth) development of male genitalia (penis, sperm duct and prostate gland) and both sperm production and development of male secondary sexual characteristics during puberty.

Testes develop from the embryonic gonads in about the eighth week of pregnancy, at the time when the embryo is becoming a fetus and is about 30mm long. Before that everyone is female.

During puberty secretion of testosterone increases, stimulating sperm production (primary sexual characteristics) and secondary sexual characteristics (growth of penis and testes, pubic hair, deepening voice).

60
Q

Sex determination in females

A

Oestrogen (estrogen) causes prenatal development of female reproductive organs (oviduct, uterus and vagina) and female secondary sexual characteristics during puberty.

Progesterone prepares the uterus during the menstrual cycle for the implantation of an embryo and has important roles in supporting a pregnancy

If the gene SRY is not present in an embryo because there is no Y chromosome, the embryonic gonads develop into ovaries. At first oestrogen and progesterone are secreted by the mother’s ovaries and later by the placenta.

During puberty the secretion of those two female hormones increases, causing the development of secondary sexual characteristics (bigger breasts, pubic hair, etc.).

61
Q

what are all kind of hormone are all the sex determining hormones?

A

steroids

62
Q

menstrual cycle (when does it occur, regulatory hormones, phases, oocyte, follicle, ovulation, edometrium, corpus luteum)

A
  • Between puberty and the menopause, women who are not pregnant experience the menstrual cycle.
  • Regulatory hormones: FSH and LH (produced by the pituitary gland) and estrogen and progesterone (produced by the ovary).
  • During each menstrual cycle and oocyte (egg) matures inside a fluid-filled sac in the ovary called a follicle, during the follicular phase (first half of the cycle).
  • The follicle is released when the follicle bursts open during ovulation, making it available for fertilization by a sperm. The ones that don’t burst degenerate.
  • The second half of the cycle is called the luteal phase because the wall of the follicle that released an egg becomes a body called the corpus luteum.
  • Continued development of the endometrium in the uterus prepares it for the implantation of an embryo.
  • If fertilisation does not occur the corpus luteum in the ovary breaks down. The thick endometrium also breaks down and is shed during menstruation.
63
Q

feedback control used in menstruation

A

Negative feedback has a stabilizing effect because a change in levels always causes the opposite change.

Positive feedback tends to lead to sudden rises or falls, because a rise causes father rises and a fall causes further falls.

64
Q

outline of menstruation

A
  • FSH rises to a peak towards the end of the menstrual cycle and stimulates the development of follicles, each containing an oocyte and follicular fluid. FSH also stimulates secretion of oestrogen by the follicle wall.
  • Oestrogen rises to a peak towards the end of the follicular phase. It stimulates the 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). When it reaches high levels oestrogen inhibits the secretion of FSH (negative feedback) and stimulates LH secretion.
  • LH rises to a sudden and sharp peak towards the end of the follicular phase. It stimulates the completion of meiosis in the oocyte and partial digestion of the follicle wall allowing it to burst open at ovulation. LH also promotes the development of the wall of the follicle after ovulation into the corpus luteum which secretes oestrogen (positive feedback) and progesterone.
  • Progesterone levels 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. Progesterone promotes the thickening and maintenance of the endometrium. It also inhibits FSH and LH secretion by the pituitary gland (negative feedback).
65
Q

in vitro fertilisation (IVF) - outline and purpose

A

to overcome fertility problems in either the male or female parents

1. Down-regulation

Woman takes drug each day, usually nasal spray, to stop pituitary gland secreting FSH and LH. Secretion of estrogen and progesterone therefore also stops. This suspends the normal menstrual cycle and allows doctors to control the timing and amount of egg production in the ovaries.

2. Artificial doses of hormones — superovulation

Daily intramuscular injections of FSH and LH are given for about ten days, stimulating follicle development. The FSH injections give a much higher concentration than during a normal menstrual cycle, so far more follicles develop than usual.

3. Egg retrieval and fertilisation

Follicles are stimulated to mature by a hormone injection of hCG, normally secreted by the embryo. A micropipette mounted on an ultrasound scanner is passed through the uterus wall to wash eggs out of the follicles. Each egg is mixed with 100,000 sperm cells in sterile conditions in a dish, which is then incubated at 37° until the next day.

4. Establishing a pregnancy

If fertilisation is successful, then one or more embryos are placed in the uterus (about 48 hours old). Because the women has not gone through a normal menstrual cycle, extra progesterone is needed to ensure thick uterus lining. Normal pregnancy continues.

66
Q

William Harvey and the discovery of sexual reproduction

A
  • Initially believed in “seed and soil” theory by Aristotle: males produce seeds, forming an egg when mixed with menstrual blood; egg develops into fetus in female.
  • Tested the theory by dissecting a female deer during mating season; expected to find eggs developing in the uterus immediately after mating, but only found signs of fetuses after two or more months; proved Aristotle’s theory false.
  • Falsely concluded due to inefficient apparatus (no effective microscope): offspring is not result of mating.