Topic 6: Human Physiology Flashcards

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1
Q

What are the 2 major groups of organs that classify the digestive system?

A

The alimentary canal consists of organs through which food actually passes (oesophagus, stomach, small & large intestine)

The accessory organs aid in digestion but do not actually transfer food (salivary glands, pancreas, liver, gall bladder)

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2
Q

Digestive Organs in the Alimentary Canal:

A

Oesophagus
* A hollow tube connecting the oral cavity to the stomach (separated from the trachea by the epiglottis)
* Food is mixed with saliva and then is moved in a bolus via the action of peristalsis

Stomach
* A temporary storage tank where food is mixed by churning and protein digestion begins
* It is lined by gastric pits that release digestive juices, which create an acidic environment (pH ~2)

Small Intestine
* A long, highly folded tube where usable food substances (nutrients) are absorbed
* Consists of three sections – the duodenum, jejunum and ileum

Large Intestine
* The final section of the alimentary canal, where water and dissolved minerals (i.e. ions) are absorbed
* Consists of the ascending / transverse / descending / sigmoidal colon, as well as the rectum

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3
Q

Digestive organs part of the accessory organs:

A

Salivary Glands
* Release saliva to moisten food and contains enzymes (e.g. amylase) to initiate starch breakdown
* Salivary glands include the parotid gland, submandibular gland and sublingual gland

Pancreas
* Produces a broad spectrum of enzymes that are released into the small intestine via the duodenum
* Also secretes certain hormones (insulin, glucagon), which regulate blood sugar concentrations

Liver
* Takes the raw materials absorbed by the small intestine and uses them to make key chemicals
* Its role includes detoxification, storage, metabolism, bile production and haemoglobin breakdown

Gall Bladder
* The gall bladder stores the bile produced by the liver (bile salts are used to emulsify fats)
* Bile stored in the gall bladder is released into the small intestine via the common bile duct

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4
Q

Explain mechanical digestion?

A

Chewing (Mouth):
Food is initially broken down in the mouth by the grinding action of teeth (chewing or mastication).
The tongue pushes the food towards the back of the throat, where it travels down the esophagus as a bolus.
The epiglottis prevents the bolus from entering the trachea, while the uvula prevents the bolus from entering the nasal cavity

Churning (Stomach):
The stomach lining contains muscles which physically squeeze and mix the food with strong digestive juices (‘churning’)
Food is digested within the stomach for several hours and is turned into a creamy paste called chyme
Eventually the chyme enters the small intestine (duodenum) where absorption will occur

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5
Q

What is the movement of food called:

A

Peristalsis
is the principal mechanism of movement in the oesophagus, although it also occurs in both the stomach and gut

Continuous segments of longitudinal smooth muscle rhythmically contract and relax

Food is moved unidirectionally along the alimentary canal in a caudal direction (mouth to anus)

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6
Q

What is segmentation?

A

Segmentation
involves the contraction and relaxation of non-adjacent segments of circular smooth muscle in the intestines
Segmentation contractions move chyme in both directions, allowing for a greater mixing of food with digestive juices
While segmentation helps to physically digest food particles, its bidirectional propulsion of chyme can slow overall movement

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7
Q

Chemical agents that help break down food in chemical digestion:

A

Stomach Acids: The stomach contains gastric glands which release digestive acids to create a low pH environment (pH ~2)
The acidic environment functions to denature proteins and other macromolecules, aiding in their overall digestion
The stomach epithelium contains a mucous membrane which prevents the acids from damaging the gastric lining
The pancreas releases alkaline compounds (e.g. bicarbonate ions), which neutralise the acids as they enter the intestine

Bile: The liver produces a fluid called bile which is stored and concentrated within the gall bladder prior to release into the intestine
Bile contains bile salts which interact with fat globules and divide them into smaller droplets (emulsification)
The emulsification of fats increases the total surface area available for enzyme activity (lipase)

Enzymes
Enzymes are biological catalysts which speed up the rate of a chemical reaction (i.e. digestion) by lowering activation energy
Enzymes allow digestive processes to therefore occur at body temperatures and at sufficient speeds for survival requirements
Enzymes are specific for a substrate and so can allow digestion of certain molecules to occur independently in distinct locations

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8
Q

Macromolecules and their roles in digestion:

A

Carbohydrates: Carbohydrate digestion begins in the mouth with the release of amylase from the salivary glands (amylase = starch digestion)
Amylase is also secreted by the pancreas in order to continue carbohydrate digestion within the small intestine
Enzymes for disaccharide hydrolysis are often immobilised on the epithelial lining of the small intestine, near channel proteins
Humans do not possess an enzyme capable of digesting cellulose (cellulase) and hence it passes through the body undigested

Proteins: Protein digestion begins in the stomach with the release of proteases that function optimally in an acidic pH (e.g. pepsin = pH 2)
Smaller polypeptide chains enter the small intestine where they are broken down by endopeptidases released by the pancreas
These endopeptidases work optimally in neutral environments (pH ~ 7) as the pancreas neutralises the acids in the intestine

Lipids: Lipid breakdown occurs in the intestines, beginning with emulsification of fat globules by bile released from the gall bladder
The smaller fat droplets are then digested by lipases released from the pancreas

Nucleic Acids: The pancreas also releases nucleases which digest nucleic acids (DNA, RNA) into smaller nucleosides

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9
Q

Function of small and large intestines:

A

The small intestine absorbs usable food substances (i.e. nutrients – monosaccharides, amino acids, fatty acids, vitamins, etc.)

The large intestine absorbs water and dissolved minerals (i.e. ions) from the indigestible food residues

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10
Q

Explain the structure of the small intestine (4 main tissue layers)

A

Serosa – a protective outer covering composed of a layer of cells reinforced by fibrous connective tissue

Muscle layer – outer layer of longitudinal muscle (peristalsis) and inner layer of circular muscle (segmentation)

Submucosa – composed of connective tissue separating the muscle layer from the innermost mucosa

Mucosa – a highly folded inner layer which absorbs material through its surface epithelium from the intestinal lumen

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11
Q

What are the features of villi (Mrslim)

A

Microvilli – Ruffling of epithelial membrane further increases surface area

Rich blood supply – Dense capillary network rapidly transports absorbed products

Single layer epithelium – Minimises diffusion distance between lumen and blood

Lacteals – Absorbs lipids from the intestine into the lymphatic system

Intestinal glands – Exocrine pits (crypts of Lieberkuhn) release digestive juices

Membrane proteins – Facilitates transport of digested materials into epithelial cells

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12
Q

Explain the structure of villus Edithelium

A

Tight Junctions: Occluding associations between the plasma membrane of two adjacent cells, creating an impermeable barrier
They keep digestive fluids separated from tissues and maintain a concentration gradient by ensuring one-way movement

Microvilli: Microvilli borders significantly increase surface area of the plasma membrane (>100×), allowing for more absorption to occur
The membrane will be embedded with immobilised digestive enzymes and channel proteins to assist in material uptake

Mitochondria: Epithelial cells of intestinal villi will possess large numbers of mitochondria to provide ATP for active transport mechanisms
ATP may be required for primary active transport (against gradient), secondary active transport (co-transport) or pinocytosis

Pinocytotic Vesicles: Pinocytosis (‘cell-drinking’) is the non-specific uptake of fluids and dissolved solutes (a quick way to translocate in bulk)
These materials will be ingested via the breaking and reforming of the membrane and hence contained within a vesicle

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13
Q

4 Types of Membrane Transport:

A

Secondary Active Transport: A transport protein couples the active translocation of one molecule to the passive movement of another (co-transport)
Glucose and amino acids are co-transported across the epithelial membrane by the active translocation of sodium ions (Na+)

Facilitated Diffusion: Channel proteins help hydrophilic food molecules pass through the hydrophobic portion of the plasma membrane
Channel proteins are often situated near specific membrane-bound enzymes (creates a localised concentration gradient)
Certain monosaccharides (e.g. fructose), vitamins and some minerals are transported by facilitated diffusion

Osmosis: Water molecules will diffuse across the membrane in response to the movement of ions and hydrophilic monomers (solutes)
The absorption of water and dissolved ions occurs in both the small and large intestine

Simple Diffusion: Hydrophobic materials (e.g. lipids) may freely pass through the hydrophobic portion of the plasma membrane
Once absorbed, lipids will often pass first into the lacteals rather than being transported via the blood

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14
Q

What is bulk transport?

A

Endocytosis: Endocytosis involves the invagination of the plasma membrane to create an internal vesicle containing extracellular material

Vesicle formation requires the breaking and reforming of the phospholipid bilayer and hence is an energy-dependent process

In the intestines, vesicles commonly form around fluid containing dissolved materials (pinocytosis – cell ‘drinking’)

Pinocytosis allows materials to be ingested en masse and hence takes less time than shuttling via membrane proteins

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15
Q

How is starch digested?

A

● Starch is a macromolecule composed of alpha glucose monomers linked together.
● It is too large to be absorbed.
● The breakdown of starch is exothermic but is too slow without enzymes.
● Consists of two molecules:
o Amylose (1,4) unbranched
o Amylopectin (1,6) branched.
● Amylase breaks down any 1,4 bonds in starch.
o Amylose is therefore broken down into maltose and maltotriose.
o Amylase cannot break down 1,6 bonds due to its active site specificity.
o Fragments containing 1,6 bonds are called dextrins.
● Enzymes in microvilli on villi epithelium cells (maltase, glucosidase and dextrinase) digest the three products of amylase digestion (maltose, maltotriose and dextrin) into glucose.
● The glucose is then co-transported with sodium ions into the villus epithelium and into the blood capillaries, where it is sent to the liver via the hepatic portal vein and any excess is turned into glycogen.

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16
Q

What are the 4 chambers of the heart?

A

two atria and two ventricles

The atria act as reserviors, by which blood returning to the heart is collected via veins (and passed on to ventricles)

The ventricles act as pumps, expelling the blood from the heart at high pressure via arteries

The reason why there are two sets of atria and ventricles is because there are two distinct locations for blood transport:
The left side of the heart pumps oxygenated blood around the body (systemic circulation)
The right side of the heart pumps deoxygenated blood to the lungs (pulmonary circulation)

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17
Q

What are arteries and their function?

A

The function of arteries is to convey blood at high pressure from the heart ventricles to the tissues of the body and lungs

● Elastic tissue contains elastin fibres.
o These fibres store energy to stretch them.
o The subsequent recoil of the fibres releases the energy and forces the blood down the artery.

● Smooth muscle controls the diameter of the lumen and overall blood flow.
● Both elastic and smooth tissues prevent aneurysm (swelling of artery).
● Blood’s movement through arteries is pulsatile, reflecting each heartbeat.

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18
Q

3 Artery Walls:

A

Have muscle and elastic fibres in their walls.

● Tunica externa – tough outer layer.
● Tunica media – thick layer with smooth/elastic fibres
● Tunica intima – smooth endothelium.

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19
Q

Types of arterial blood pressure?

A

● Smooth and elastic fibres maintain blood pressure between pump cycles.

o Systolic pressure (peak pressure reached in an artery).
▪ Stores potential energy in elastin due to high pressure.
o Diastolic pressure (lowest pressure in arteries).
▪ Elastin fibres squeeze blood in the lumen when pressure in the lumen falls at the end of a heartbeat.

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20
Q

What are capillaries and their functions?

A

The function of capillaries is to exchange materials between the cells in tissues and blood travelling at low pressure (<10mmHg)

● Supply blood to every tissue except cornea and lens.
● Capillary wall consists of a layer of endothelial cells.
o Single cell structure makes it very permeable.
o Permeability does however vary, and depends on the needs of the tissues they perfuse.
● Blood cells are suspended in plasma.
o Some plasma leaks out of capillaries to become tissue fluid that contains oxygen, glucose, etc. but not large protein molecules, which can’t pass out of capillaries.
o Tissue fluid flows between cells so they can absorb nutrients and oxygen and excrete metabolic waste into it.
o Tissue fluid then re-enters the capillaries.

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21
Q

What are veins and their functions?

A

The function of veins is to collect the blood from the tissues and convey it at low pressure to the atria of the heart.

● Much lower pressure (than arteries). Have thinner walls than arteries.
● Have fewer smooth/elastic fibres.
● Much larger lumen, hold more blood.
● Blood flow in veins is increased by contraction of muscles (muscles that are not part of the blood vessel) in any activity.
● Most body parts are linked to more than one vein.
● Non pulsatile flow of blood.

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22
Q

What is the function of valves in veins?

A

● Ensure circulation by preventing backflow.
● Due to low blood pressure in veins, backflow is possible. Hence pocket valves prevent this.
● Flaps of pocket valves catch blood, fill with it, and block the vein’s lumen.
● This increases pressure and past a certain pressure threshold the blood pushes through the flaps and continues flowing towards the heart.
● This allows for unidirectional blood flow.
● Maximizes the use of intermittent pressures by muscular and postural changes.

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23
Q

How to identify blood vessels?

A

Arteries have thick walls and narrow lumens because they transport blood at high pressure

Capillaries have walls that are only a single cell thick because they exchange materials between blood and tissue

Veins have thin walls with wide lumens and valves because they transport blood at low pressure

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24
Q

Describe the process of the heart beating?

A

The sinoatrial node acts as the primary pacemaker – controlling the rate at which the heart beats (i.e. pace ‘making’)

The SA node triggers roughly 60 – 100 cardiac contractions per minute (normal sinus rhythm)
If the SA node fails, a secondary pacemaker (AV node) may maintain cardiac contractions at roughly 40 – 60 bpm
If both fail, a final tertiary pacemaker (Bundle of His) may coordinate contractions at a constant rate of roughly 30 – 40 bpm

The interference of the pacemakers will lead to the irregular and uncoordinated contraction of the heart muscle (fibrillation)

When fibrillation occurs, normal sinus rhythm may be re-established with a controlled electrical current (defibrillation)

The sinoatrial node sends out an electrical impulse that stimulates contraction of the myocardium (heart muscle tissue)
This impulse directly causes the atria to contract and stimulates another node at the junction between the atrium and ventricle
This second node – the atrioventricular node (AV node) – sends signals down the septum via a nerve bundle (Bundle of His)
The Bundle of His innervates nerve fibres (Purkinje fibres) in the ventricular wall, causing ventricular contraction

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25
Q

what kind of contraction does the heart have?

A

The contraction of the heart is myogenic – meaning that the signal for cardiac compression arises within the heart tissue itself

In other words, the signal for a heart beat is initiated by the heart muscle cells (cardiomyocytes) rather than from brain signals

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26
Q

2 ways in which the heart beat is regulated?

A

Nerve Signalling: The pacemaker is under autonomic (involuntary) control from the brain, specifically the medulla oblongata (brain stem)
- Two nerves connected to the medulla regulate heart rate by either speeding it up or slowing it down:
- The sympathetic nerve releases the neurotransmitter noradrenaline (a.k.a. norepinephrine) to increase heart rate
- The parasympathetic nerve (vagus nerve) releases the neurotransmitter acetylcholine to decrease heart rate

Hormonal Signalling: Hormones are chemical messengers released into the bloodstream that act specifically on distant target sites (like the heart)
- Heart rate can undergo a sustained increase in response to hormonal signalling in order to prepare for vigorous physical activity
- The hormone adrenaline (a.k.a. epinephrine) is released from the adrenal glands (located above the kidneys)
Adrenaline increases heart rate by activating the same chemical pathways as the neurotransmitter noradrenaline

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27
Q

Explain the cardiac cycle (2 periods):

A

It is comprised of a period of contraction (systole) and relaxation (diastole):

Systole: Blood returning to the heart will flow into the atria and ventricles as the pressure in them is lower (due to low volume of blood)
-When ventricles are ~70% full, atria will contract (atrial systole), increasing pressure in the atria and forcing blood into ventricles
-As ventricles contract, ventricular pressure exceeds atrial pressure and AV valves close to prevent back flow (first heart sound)
-With both sets of heart valves closed, pressure rapidly builds in the contracting ventricles (isovolumetric contraction)
-When ventricular pressure exceeds blood pressure in the aorta, the aortic valve opens and blood is released into the aorta

Diastole: As blood exits the ventricle and travels down the aorta, ventricular pressure falls
-When ventricular pressure drops below aortic pressure, the aortic valve closes to prevent back flow (second heart sound)
-When the ventricular pressure drops below the atrial pressure, the AV valve opens and blood can flow from atria to ventricle
-Throughout the cycle, aortic pressure remains quite high as muscle and elastic fibres in the artery wall maintain blood pressure

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28
Q

What are the risks of coronary heart disease (coronary artery becomes blocked) ? ( a goddess)

A

Age – Blood vessels become less flexible with advancing age
Genetics – Having hypertension predispose individuals to developing CHD
Obesity – Being overweight places an additional strain on the heart
Diseases – Certain diseases increase the risk of CHD (e.g. diabetes)
Diet – Diets rich in saturated fats, salts and alcohol increases the risk
Exercise – Sedentary lifestyles increase the risk of developing CHD
Sex – Males are at a greater risk due to lower oestrogen levels
Smoking – Nicotine causes vasoconstriction, raising blood pressure

29
Q

What are our surface barriers against diseases?

A

● Skin and mucous membranes form a primary defence against pathogens that cause infectious disease.
o Tough outer layer provides physical barrier.
o Sebaceous glands, associated with hair follicles, secrete sebum, moisture and lowers pH.
▪ Inhibits growth of bacteria.

● Mucous membranes are found in nasal passages, penis, and vagina.
o Secrete sticky solution of glycoproteins, which acts as a physical barrier by trapping pathogens. Goblet cells in the esophagus do this.
o Enzyme lysozyme gives anti-bacterial properties.

30
Q

Explain the blood clotting process:

A

-Clotting factors cause platelets to become sticky and adhere to the damaged region to form a solid plug

-Additionally, clotting factors trigger the conversion of the inactive prothrombin into the activated enzyme thrombin

-Thrombin in turn catalyses the conversion of the soluble plasma protein fibrinogen into an insolube fibrous form called fibrin

-The fibrin strands form a mesh of fibres around the platelet plug and traps blood cells to form a temporary clot

-When the damaged region is completely repaired, an enzyme (plasmin) is activated to dissolve the clot

31
Q

Explain Coronary Thrombosis:

A

Coronary thrombosis is the formation of a clot within the blood vessels that supply and sustain the heart tissue (coronary arteries)

Occlusion of a coronary artery by a blood clot may lead to an acute myocardial infarction (heart attack)

● Blood clot is called a thrombus in medical terms.
● Blood clot in the coronary arteries can result in heart being deprived of molecules required for respiration.
o Cardiac muscles are unable to contract properly with the shortage of ATP and become irregular and uncoordinated.
o Results in fibrillation.
● Occlusion in the coronary arteries occurs when an atheroma develops, hardening the artery and damaging them.
● Lesions occur when the atheroma ruptures.
● These ruptures trigger the clotting process and results in fibrillation.
● Caused by smoking, high blood cholesterol concentration, and high blood pressure.

32
Q

What are phagocytes?

A

● White blood cells that give non-specific immunity.
● After skin and mucous membranes, the WBC gives a secondary line of defence.
● They engulf pathogens by endocytosis and digest them with enzymes from lysosomes.
● Infection of wounds results in pus – large amount of phagocytes aggregating at the infected site.

33
Q

What are lymphocytes?

A

The adaptive immune system is coordinated by lymphocytes (a class of leukocyte) and results in the production of antibodies

B lymphocytes (B cells) are antibody-producing cells that recognise and target a particular pathogen fragment (antigen)
Helper T lymphocytes (TH cells) are regulator cells that release chemicals (cytokines) to activate specific B lymphocytes

When phagocytic leukocytes engulf a pathogen, some will present the digested fragments (antigens) on their surface

These antigen-presenting cells (dendritic cells) migrate to the lymph nodes and activate specific helper T lymphocytes
The helper T cells then release cytokines to activate the particular B cell capable of producing antibodies specific to the antigen
The activated B cell will divide and differentiate to form short-lived plasma cells that produce high amounts of specific antibody
Antibodies will target their specific antigen, enhancing the capacity of the immune system to recognise and destroy the pathogen
A small proportion of activated B cell (and activated TH cell) will develop into memory cells to provide long-lasting immunity

34
Q

What is an antigen vs antibody?

A

Antigen: An antigen is a substance that the body recognises as foreign and that will elicit an immune response

Antibody: An antibody is a protein produced by B lymphocytes (and plasma cells) that is specific to a given antigen

35
Q

Explain antibody production

A

● Lymphocytes produce antibodies providing specific immunity.
● Proteins on the surface of the pathogen (antigens) are recognized as foreign bodies and trigger a specific immune response.
● Antibodies bind to the antigen.
● Each lymphocyte produces one type of antibody.
● Few of these, but the antigens on the pathogens stimulate cell divisions that produce the appropriate type of antibody.
● Plasma cells, clones of the antibody producing lymphocytes, then secrete antibodies to control the pathogen.

36
Q

Explain how antibiotics work?

A

● Antibiotics block metabolic processes in prokaryotic cells, resulting in their death
o These metabolic processes are not present in viruses (they don’t have metabolic processes as they rely on the host cells to carry out their metabolic processes for them. This is why antibiotics don’t affect viruses.
● Does not affect human cells.
● Block DNA replication, transcription, translation, ribosomal function and cell wall formation.

37
Q

What diseases can’t be treated by antibiotics?

A

Viruses and antibiotics:
● Viral diseases cannot be treated using antibiotics because they lack a metabolism.
● Live off the chemical processes of a host cell.
● Do not synthesise proteins and depend on a host for ATP synthesis.
● Using antibiotics to treat viral infections are redundant, and contribute to the overuse of antibiotics, which contributes to antibiotic resistance.
● Antivirals can target viral enzymes (neuraminidase and hemagglutinin) without affecting host cells.

38
Q

Explain resistance to antibiotics?

A

● Bacteria have evolved with genes that confer resistance to antibiotics.
● Natural selection results in resistance. Some strains have developed such as MRSA - methicillin resistant staphylococcus aureus.
● Doctors must prescribe antibiotics for serious bacterial infections only.
● Antibiotics courses must be completed.
● High standards of hygiene in hospitals.
● Animal feeds should not contain antibiotics.

39
Q

What is HIV, what does it do and how, how is it transmitted?

A

● HIV invades and destroys helper T cells and as a result antibodies cannot be produced.
● HIV positive if body begins making antibodies against HIV
● Retrovirus uses reverse transcriptase to make DNA copies of its genes.
o Antiretroviral drugs can slow destruction of T helper cells.
o Results in weak immune system due to acquired immune deficiency syndrome (AIDS).
o Occurs due to sex or sharing of hypodermic needles.

40
Q

What is ventilation?

A

● Maintains concentration gradients of oxygen and carbon dioxide between air in alveoli and blood flowing in adjacent capillaries.
● Gas exchange happens by diffusion between air in alveoli and blood in capillaries.
● Air in alveoli has higher oxygen concentration than in blood capillaries.
● Ventilation is the maintenance of this concentration gradient by supplying the alveoli with fresh air.

41
Q

Ventilation rate

A

● Number of times air is drawn in/expelled in a minute.
● Tidal volume: volume of air drawn in and expelled with each inhalation or exhalation.

42
Q

Type 1 and 2 pneumocytes

A

Type 1:
● Number of times air is drawn in/expelled in a minute.
● Tidal volume: volume of air drawn in and expelled with each inhalation or exhalation.

Type 2:
● Type II pneumocytes secrete a solution containing surfactant.
● Creates moist surface inside the alveoli to prevent the sides from sticking together; this reduces surface tension.
● The fluid also dissolves oxygen, which can then diffuse to the blood in the alveolar capillaries.
● Pulmonary surfactant: contained within fluid released by Type II pneumocytes.
o Monolayer on the surface of the moisture lining the alveoli; hydrophilic heads face the moisture and hydrophobic tails face the air.
o Reduces surface tension and prevents water from adhering to the sides of the alveoli during exhalation.

43
Q

Role of alveoli

A

site of gas exchange

44
Q

How does ventilation/breathing occur

A

● Air is carried to the lungs in the trachea and bronchi and then to the bronchioles, which have alveoli.
● Rings of cartilage in trachea keep it open even when pressure is low or surrounding tissue pressure is high.

45
Q

Pressure and breathing

A

-When the pressure in the chest is less than the atmospheric pressure, air will move into the lungs (inspiration)
-When the pressure in the chest is greater than the atmospheric pressure, air will move out of the lungs (expiration)

46
Q

Inspiration vs expiration

A

Muscles that increase the volume of the chest cause inspiration (as chest pressure is less than atmospheric pressure)

The muscles responsible for inspiration are the diaphragm and external intercostals (plus some accessory muscles):
-Diaphragm muscles contract, causing the diaphragm to flatten and increase the volume of the thoracic cavity
-External intercostals contract, pulling ribs upwards and outwards (expanding chest)
-Additional muscle groups may help pull the ribs up and out (e.g. sternocleidomastoid and pectoralis minor)

Muscles the decrease the volume of the chest cause expiration (as chest pressure is greater than atmospheric pressure)

The muscles responsible for expiration are the abdominal muscles and internal intercostals (plus some accessory muscles):
-Diaphragm muscles relax, causing the diaphragm to curve upwards and reduce the volume of the thoracic cavity
-Internal intercostal muscles contract, pulling ribs inwards and downwards (reducing breadth of chest)
-Abdominal muscles contract and push the diaphragm upwards during forced exhalation
-Additional muscle groups may help pull the ribs downwards (e.g. quadratas lumborum)

47
Q

What are the causes of lung cancer?

A

● Smoking: Tobacco smoke contains mutagenic chemicals.
● Passive smoking: non-smokers inhale tobacco smoke exhaled by smokers.
● Air pollution: diesel exhaust fumes, nitrogen oxides.
● Radon gas: radioactive gas that leaks out of certain rocks.
● Asbestos: contained in dust and other particles that can be inhaled.
● Silica.

48
Q

What is emphysema

A

● Results in larger air sacs with thicker walls.
● Longer diffusion pathways lead to more inefficient gas exchange.
● Less surface area for gas exchange.
● Ventilation is therefore more difficult because lungs are less elastic.
● Cilia that line the airways and get rid of mucus are damaged and stop functioning. Mucus builds up as a result and causes infections. White blood cells that combat these infections are damaged (inflamed and damaged) by toxins in cigarette smoke, causing these WBCs and surrounding cells to release trypsin, which breaks down the elastic fibres in the lungs.
● Results in low oxygen saturation in the blood.

49
Q

What are neurons?

A

specialised cells that function to transmit electrical impulses within the nervous system

● Neurons transmit electrical impulses. A nerve impulse is an electrical signal.
● Cell body (cytoplasm + nucleus) and nerve fibres, along which impulses travel.
● Dendrite: short branched nerve fibres.
● Axons: Elongated nerve fibres.

50
Q

What does myelination from myelinated nerve fibres allow for?

A

myelinations allows for saltatory conduction.

● Basic structure of a nerve fibre:
o Fibre is cylindrical in shape.
o Plasma membrane surrounds cytoplasm.
o One micrometre diameter.
o Conducts nerve impulses at a speed of 1 meter per second.
● Myelination is the formation of many layers of phospholipid bilayers, created by Schwann cells.
o Each time a Schwann cell goes around the nerve fibre, a double layer of phospholipid bilayer is deposited.
● Node of Ranvier is the gap between two myelinations.
o Nerve impulses jump from one node to the next – saltatory conduction.
o Much quicker than continuous conduction.
o Rate of 100 meters per second.

51
Q

What is resting potential and how is it maintained?

A

A resting potential is the difference in charge across the membrane when a neuron is not firing

In a typical resting potential, the inside of the neuron is more negative relative to the outside (approximately –70 mV)

The maintenance of a resting potential is an active process (i.e. ATP dependent) that is controlled by sodium-potassium pumps

-The sodium-potassium pump is a transmembrane protein that actively exchanges sodium and potassium ions (antiport):
-It expels 3 Na+ ions for every 2 K+ ions admitted (additionally, some K+ ions will then leak back out of the cell)
-This creates an electrochemical gradient whereby the cell interior is relatively negative compared to the extracellular environment (as there are more positively charged ions outside of the cell and more negatively charged ions inside the cell)
-The exchange of sodium and potassium ions requires the hydrolysis of ATP (it is an energy-dependent process)

52
Q

What is action potential and how is it maintained?

A

● Consists of depolarization and repolarization of the neuron.
● Depolarization is the change from negative to positive charge and repolarisation is the change from positive to negative charge.
● Depolarization: Opening of sodium channels allowing sodium ions to diffuse into the neuron. This raises membrane potential to +30mV.
● Repolarization: closing of the Sodium voltage gated channels and the subsequent opening of the potassium voltage gated channels.
o Potassium ions then diffuse out down their concentration gradient.
o Membrane potential falls below resting potential -90mV.
● Refractory period: restoration of resting potential. This is hyperpolarization, where the potential changes from -90mV to -70mV by the action of the sodium potassium pump.

53
Q

What is the propagation of action potential (nerve impulse):

A

● Occurs because the ion movements that depolarise one part of the neuron trigger depolarization in the neighbouring part of the neuron (local currents of Na+ ions moving diffusing to other areas of the axoplasm).
● Impulse propagation is unidirectional and moves along the axon.
● Refractory period prevents backwards propagation.

54
Q

What is myelination:

A

The main purpose of the myelin sheath is to increase the speed of electrical transmissions via saltatory conduction.

Myelination
Not all neurons within the nervous system are insulated with a myelin sheath

The advantage of myelination is that it improves the speed of electrical transmission via saltatory conduction
The disadvantage of myelination is that it takes up significant space within an enclosed environment

55
Q

Explain Chemical Transfer Across a Synapse

A

-When an action potential reaches the axon terminal, it triggers the opening of voltage-gated calcium channels

-Calcium ions (Ca2+) diffuse into the cell and promote the fusion of vesicles (containing neurotransmitter) with the cell membrane

-The neurotransmitters are released from the axon terminal by exocytosis and cross the synaptic cleft

-Neurotransmitters bind to specific receptors on the post-synaptic membrane and open ligand-gated ion channels

-The opening of ion channels generates an electrical impulse in the post-synaptic neuron, propagating the pre-synaptic signal

-The neurotransmitters released into the synapse are either recycled (by reuptake pumps) or degraded (by enzymatic activity)

56
Q

What is the purpose of the myelin sheath?

A

The main purpose of the myelin sheath is to increase the speed of electrical transmissions via saltatory conduction

-Along unmyelinated neurons, action potentials propagate sequentially along the axon in a continuous wave of depolarisation
-In myelinated neurons, the action potentials ‘hop’ between the gaps in the myelin sheath called the nodes of Ranvier
-This results in an increase in the speed of electrical conduction by a factor of up to 100-fold

57
Q

What is Acetylcholine:

A

● Used as a neurotransmitter.
● Produced by combining choline with an acetyl group.
● Loaded into vesicles and released into the synaptic cleft during synaptic transmission.
● Bind the specific receptors on postsynaptic membrane.
● Acetylcholinesterase rapidly breaks acetylcholine into acetyl and choline.
● Choline is then reabsorbed into the presynaptic neuron.

58
Q

What are Neonicotinoids?

A

● Block synaptic transmission at cholinergic synapses in insects by binding of neonicotinoid pesticides to acetylcholine receptors.
● Acetylcholinesterase does not break down neonicotinoids, so the binding is irreversible.
● Synaptic transmission is therefore prevented.
● Not very effective on humans, however concerns regarding honeybees have been raised.

59
Q

What is the threshold potential

A

● Nerve impulses follow an all-or-nothing principle.
● If the threshold potential is reached then an action potential is triggered, if not then it isn’t.
● If threshold potential is reached there will always be full depolarization.
● If the threshold potential is not reached in postsynaptic membrane, sodium potassium pumps pump out the sodium ions that have entered
the postsynaptic neuron.
o The postsynaptic membrane returns to the resting potential.
● Most postsynaptic neurons in the brain have synapses with many presynaptic neurons.
● Many of these release neurotransmitters at the same time so the threshold potential will be reached.

60
Q

How do insulin and glucagon control blood glucose concentration?

A

When blood glucose levels are high (e.g. after feeding):
-Insulin is released from beta (β) cells of the pancreas and cause a decrease in blood glucose concentration
-This may involve stimulating glycogen synthesis in the liver (glycogenesis), promoting glucose uptake by the liver and adipose tissue, or increasing the rate of glucose breakdown (by increasing cell respiration rates)

When blood glucose levels are low (e.g. after exercise):
-Glucagon is released from alpha (α) cells of the pancreas and cause an increase in blood glucose concentration
-This may involve stimulating glycogen breakdown in the liver (glycogenolysis), promoting glucose release by the liver and adipose tissue, or decreasing the rate of glucose breakdown (by reducing cell respiration rates)

61
Q

Explain diabetes and the 2 types as well as treatments:

A

● Consistently elevated blood glucose levels. Damages tissues; decreases reabsorption of water from urine, resulting in dehydration.
● Type I: early onset.
o Inability to produce insulin. Autoimmune disease arising from the destruction of beta cells.

● Type II: late onset.
o Inability to process/respond to insulin due to deficiency of insulin receptors or glucose transporters.
o Caused by sugary or fatty diets, lack of exercise and genetic factors.

● Treatments:
o Type I: Constant blood sugar tests and insulin injections. Done before a meal to prevent spikes in blood sugar. Implanted devices that release insulin into blood as necessary. Stem cells can become
fully functional beta cells.
o Type II: Adjusting diet to reduce peaks and troughs of blood glucose. Small frequent amounts of food. No sugary foods; only low glycaemic carbs (slow digesting). Exercise and weight loss.

62
Q

What is thyroxin and its uses?

A

● Secreted by thyroid gland to regulate metabolic rate and control body temperature.
● Contains four atoms of iodine. Iodine is therefore important to the diet.
● Targets all body cells.
● Most metabolically active cells (liver, brain and muscle) are main targets.
● High metabolic rates = more protein synthesis and growth. Increases body heat generation.
● Cooling triggers increased thyroxin secretion.
● Thyroxin deficiency:
o Lack of energy, forgetfulness and depression, weight gain, constipation.

● Tries to maintain normal body temperature by regulating metabolic
processes of the body → negative feedback.
o Less thyroxin secreted when body temp is too high= reduced metabolic rate, reduced respiration and vasodilation of skin arterioles.
o More thyroxin secreted when body temp is too low = increased metabolic rate, increased respiration and vasoconstriction of skin arterioles.

63
Q

What is leptin and its uses?

A

● Secreted by cells in adipose tissue and acts on the hypothalamus of the brain to inhibit appetite.
● Blood leptin concentrations are controlled by: food intake and adipose tissue amount in the body.
● Targets group of cells in the hypothalamus that control appetite. Binds onto them.
● As adipose tissue increases, leptin concentrations rise, inhibiting appetite.
● Obese mice had two copies of a recessive allele, ob. Those with homozygous recessive could not produce leptin.
● In obese humans, however, cells seem to have developed resistance to leptin. Increased leptin levels, therefore, have no/reduced effect on appetite restriction.

64
Q

What is melatonin and its uses?

A

● Is secreted by the pineal gland to control circadian rhythms.
● Circadian rhythms are controlled by suprachiasmatic nuclei cells (SCN) in the hypothalamus.
● Control secretion of melatonin from the pineal gland.
● Secretion increases in the evening and decreases at dawn.
● Melatonin release results in falling core body temperature.
● Melatonin receptors in the kidney lead to decreased urine production at night.
● Ganglion cells that detect whether it is light or dark and pass impulses to the SCN, which allows it to adjust to the 24hr day and night cycle.
● Jet lag:
o SCN and pineal gland continue to set a circadian rhythm for the point of departure rather than destination.
o Impulses sent by ganglion help regulate body to point of destination.
o Melatonin tablets prevents onset of jetlag by promoting deeper sleep etc.

65
Q

Explain sex determination in males:

A

● Gene on Y chromosome causes embryonic gonads to develop as testes and secrete testosterone.
● In the presence of the SRY gene, which codes for the TDF, testes develop.
● This gene is only found on the Y chromosome.
● TDF is not produced in girls, as they don’t have Y-chromosomes.
● TDF stimulates expression of genes for testis development.

66
Q

What is testosterone and what does it do?

A

● Causes prenatal development of male genitals and both sperm production and development of male secondary sexual characteristics during puberty.
o Testes develop in the 8 th week.
o Until the 15 th week, testosterone-secreting cells produce testosterone, during which genitalia develop.
o At puberty, primary sexual characteristics (sperm) develop.
o Testosterone causes onset of secondary sexual characteristics during puberty: enlargement of penis, pubic hair, deepening of voice.

67
Q

Explain sex determination in females:

A

● Oestrogen and progesterone cause prenatal development of female reproductive organs and female secondary sexual characteristics during puberty.
● SRY gene is not present so embryonic gonads develop as ovaries.
● Oestrogen and progesterone are secreted by the mother’s ovaries and then placenta.
● In the absence of fetal testosterone, the maternal oestrogen and progesterone will contribute to the development of ovaries.
● Oestrogen causes the prenatal development of female reproductive organs such as the fallopian tubes, uterus and vagina.
● Puberty causes the development of breasts and growth of pubic and underarm hair.
o Also results in increased oestrogen and progesterone production.
o Positive feedback, as raised levels of oestrogen during puberty cause development of female secondary sexual characteristics.

68
Q

Explain the process of the menstrual cycle:

A

● Is controlled by negative and positive feedback mechanisms involving ovarian and pituitary hormones.
● Follicular phase: follicles develop in ovary.
o An egg is stimulated to grow in each follicle. Endometrium is repaired and thickens.
o Most developed follicle breaks open, egg is released into oviduct, and other follicles degenerate.

● Luteal phase: Corpus luteum formed from wall of follicle that released ovum.
o Endometrium continues to develop for implantation. If fertilisation doesn’t occur, corpus luteum breaks down. Endometrium also sheds.

● Towards the end of the menstrual cycle, FSH rises to a peak and follicle development is stimulated.
o Secretion of oestrogen from follicle wall is also stimulated.
● Oestrogen peaks at the end of a follicular phase and stimulates the repair and thickening of the endometrium.
o Also increases FSH receptors, making follicles more receptive to FSH and further stimulating the secretion of oestrogen (positive feedback). At high levels, oestrogen then inhibits FSH.
● LH rises suddenly at the end of follicular phase and stimulates:
o Completion of meiosis I in the oocyte and;
o Partial digestion of follicle wall so it can burst open at ovulation.
o Assists development of follicular wall into corpus luteum post- ovulation.
o This (Corpus Luteum) secretes more oestrogen and progesterone.
● Progesterone levels rise at the beginning of the luteal phase and drop back down by the end of the phase.
o Promotes thickening and maintenance of the endometrium and inhibits FSH and LH secretion by the pituitary gland.

69
Q

Explain IVF, invitrofertilization

A

● Drugs are taken to stop FSH and LH secretion.
o Allows external control of menstrual cycle.
o Intramuscular injections of FSH and LH are administered for 10 days to stimulate follicle development.
o High concentration of FSH results in around 12 developed follicles
(superovulation).

● HCG is then administered to stimulate maturation of follicles.
o Each egg is then mixed with 100000 sperm cells and incubated for 37˚C.

● After fertilization, eggs are placed in the uterus.
o Progesterone tablet placed in the vagina to ensure uterus lining is maintained.