Topic 6 - Human Physiology Flashcards

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1
Q

order of events in the digestive system

A

ingestion –> digestion –> absorption –> transport

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2
Q

digestion

A
  • enzyme-facilitated chemical process
  • series of chemical reactions breaking down food
  • into smaller and smaller molecular forms
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3
Q

product of digestion of proteins

A

amino acids

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4
Q

product of digestion of lipids

A
  • fatty acids

- glycerol

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5
Q

product of digestion of carbohydrates

A

monosaccharides

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6
Q

product of digestion of nucleic acids

A

nucleotides

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7
Q

importance of enzymes in digestion

A
  • enzymes are protein molecules that catalyse reactions
  • they lower the activation energy of reactions they catalyse
  • input of energy is typically in the form of heat
  • humans maintain a stable temp of 37°C
  • this is enough to maintain good molecular movement by itself
  • but with enzymes it provides enough activation energy for enzyme-catalysed metabolic reactions
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8
Q

why are digestion reactions all similar

A

because they’re all the same type of reactions (hydrolysis)

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9
Q

what keeps food moving continuously down the alimentary canal

A
  • NOT gravity; food material often has to move against gravity
  • the alimentary canal is made up of smooth muscles controlled by the autonomic nervous system (ANS)
  • the action is involuntary and we are unaware of the movement
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10
Q

layers of muscle in the alimentary canal (inner to outer)

A
  • lumen
  • mucosa
  • circular muscle
  • longitudinal muscle
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11
Q

peristalsis

A
  • churning movement
  • used in the stomach to mix food with digestive secretions (including enzymes)
  • for the rest of the alimentary canal, peristalsis involves a contraction just behind the food mass to keep it moving
  • as well as to help it mix with enzymes
  • peristalsis is fast in the oesophagus but slows dramatically in the intestines
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12
Q

role of pancreas in digestion

A

produces 3 enzymes involved in digestion:

  • lipase
  • amylase
  • endopeptidase
  • produced in the form of pancreatic juice
  • secreted into the first portion of the small intestine through the pancreatic duct
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13
Q

digestion of starch

A
  • begins in the mouth with salivary amylase
  • which hydrolyses starch into maltose
  • enzyme activity ceases in the stomach due to highly acidic conditions
  • thus starch remains largely undigested when it reaches the small intestine
  • small intestine is slightly alkaline (optimum pH for pancreatic amylase)
  • as peristalsis moves starch through the small intestine, it’s being continuously hydrolysed
  • another intestinal enzyme (maltase) breaks down maltose into 2 glucose molecules
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14
Q

mucosa

A

cells in the inner lining of e.g. small intestine

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15
Q

maltase

A
  • immobilized enzyme (bound to plasma membranes of epithelial cells in the small intestine lumen)
  • produced by mucosa cells
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16
Q

lacteal

A
  • small vessel of the lymphatic system

- present in villi

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17
Q

adaptations of the small intestine for efficient absorption

A
  • small intestine mucosa has many small projections (villi)
  • each villus is composed of cells whose primary job is to selectively absorb molecules found in the lumen
  • actual absorption occurs through cells in an epithelial layer in direct contact with the nutrients
  • the epithelial cells have tiny membrane projections (microvilli)
  • both the villi and the microvilli greatly extend the surface area for absorption
  • each villus contains a capillary bed for nutrient absorption and transport of digested monomers
  • a lacteal is also present to absorb some of the nutrients
  • larger monomers are absorbed into the lacteal while most of the smaller monomers are absorbed into the capillary bed
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18
Q

transport mechanisms used by villi epithelial cells

A

Passive mechanisms:

  • simple diffusion
  • facilitated diffusion

Active mechanisms:

  • membrane pumps
  • endocytosis
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19
Q

arteries

A
  • blood vessels taking blood away from the heart that has not yet reached a capillary
  • thick + smooth muscle layer used by the autonomic nervous system (ANS) to change the lumen of the blood vessels
  • also made up of elastic fibres to help maintain the high blood pressure achieved by the contractions of the ventricles
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20
Q

how arteries work in maintaining blood pressure

A
  • when blood is pumped into an artery, the elastic fibres stretch
  • allows the blood vessel to accommodate the increased pressure
  • When the contraction is over, the elastic fibres provide another source of pressure as they return to their original position
  • this helps maintain the blood pressure between pump cycles
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21
Q

veins

A

blood vessels that collect blood from capillaries and return it to the heart

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22
Q

succession of blood vessels in the circulatory system

A

large artery –> smaller artery branches –> arteriole –> capillary bed –> venule –> larger veins –> largest vein –> heart

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23
Q

arteriole

A

the smallest artery

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24
Q

why does blood lose pressure by the time it gets to the veins?

A
  • by the time blood makes it to the capillary beds they’ve already lost a lot of pressure
  • blood cells make their way through capillaries one cell at a time
  • chemical exchanges occur in capillary beds as artery and vein walls are too thick to facilitate transport efficiently
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25
Q

how veins work in maintaining blood pressure

A
  • thin walls and larger lumen than arteries
  • many internal passive ‘one-way flow’ valves
  • this helps keep blood moving consistently towards the heart
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26
Q

components of the heart

A
  • 2 thin-walled, muscular chambers (atria)

- 2 thick-walled, muscular pumps (ventricles)

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27
Q

the heart as a double-sided pump

A
  • septum separates the two sides of the heart
  • the right side sends blood to pulmonary circulation
  • the left side sends blood to systemic circulation
  • both sides have similar pressures and volumes of blood at the same time
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28
Q

myogenic muscle contraction

A

spontaneous contracting and relaxing of muscles without any control by the nervous system

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29
Q

why must heart rate be controlled?

A
  • heart is primarily made up of (cardiac) muscle
  • cardiac muscles undergo myogenic muscle contraction
  • despite that, they do need to be controlled
  • in order to make the timing of contractions unified and useful
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30
Q

SA node

A

AKA sinoatrial node

  • mass of specialized tissue with properties of both muscle and nervous system cells
  • acts as pacemaker
  • by sending out an ‘electrical’ signal to initiate the contraction of both atria

e.g. for a person with a resting heart rate of 72 bpm, the signal from the SA node is sent out every 0.8 secs

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31
Q

AV node

A

AKA atrioventricular node

  • mass of specialized tissue
  • receives the signal from SA node, delays for 0.1 secs, and then sends out another ‘electrical’ signal
  • second signal goes to the ventricles and results in their contraction
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32
Q

how do the SA & AV nodes work in tandem

A
  • SA sends out ‘electrical’ signal to initiate the contraction of both atria
  • AV node receives the signal from SA node, delays for 0.1 secs, and then sends out another ‘electrical’ signal
  • explains why both atria, and then later both ventricles, contract in synchrony
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33
Q

why does heart rate increase during increased body activity?

A
  • to compensate for the increased demand for oxygen

- as well as the need to get rid of the increased levels of CO2 accumulating in the bloodstream

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34
Q

how is heart rate regulated?

A
  • the increased CO2 concentrations are detected by the medulla (in the brain stem)
  • the medulla sends a signal through the cardiac nerve to the SA node
  • to increase heart rate to an appropriate level
  • medulla also detects when CO2 concentrations in the bloodstream begin to decrease after activity
  • medulla sends a signal through the vagus nerve to the SA node
  • to decrease heart rate to its myogenic (resting) heart rate
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35
Q

influence of chemicals on heart rate

A

e. g. adrenaline
- adrenal glands secrete adrenaline during periods of high stress/excitement
- adrenaline causes SA node to fire more frequently than usual
- thus heart rate increases, sometimes dramatically so

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36
Q

diastole

A

term used to describe a chamber of the heart that isn’t contracting

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37
Q

systole

A

term used to describe a chamber of the heart that’s contracting

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38
Q

describe when all chambers are at rest

A
  • atrial pressure > ventricular pressure (only slightly though)
  • atrioventricular valves open

DESCRIBED USING LEFT SIDE OF HEART

  • blood returns to left atrium via pulmonary veins
  • moves passively to left ventricle via left AV valve
  • pressure in aorta significantly higher than in left ventricle
  • this pressure keeps the left semilunar (SL) valve closed
  • thus preventing backflow
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39
Q

describe when atria are in systole and ventricles are in diastole

A
  • atrium in systole contracts
  • but this doesn’t produce very high pressure
  • due to the walls of the atria being thin
  • thus not capable of producing high pressure
  • but no need for great pressure
  • as majority of blood has already accumulated passively within the ventricle through the open AV valve
  • any remaining blood the atrium is moved to the ventricle by the systole
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40
Q

describe when atria are in diastole and ventricles are in systole

A
  • pressure in ventricle > pressure in atrium
  • AV valve closes to prevent backflow to atrium (this creates ‘lub’ sound heard through stethoscope)
  • at this point pressure in aorta > pressure in ventricle
  • so SL valve remains closed
  • relatively large volume of blood in ventricle, and ventricle is highly muscular
  • allows ventricular pressure to build up considerably as systole continues
  • eventually pressure in ventricle > pressure in aorta
  • SL valve then opens
  • thus allowing the ventricle to pump the blood into the aorta
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41
Q

components of plaque

A
  • lipids
  • cholesterol
  • cell debris
  • calcium
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42
Q

what happens when arteries build plaque?

A

becomes harder & less flexible

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43
Q

endothelium

A

inside lining of an artery

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44
Q

atherosclerosis

A
  • slow build-up of materials in the endothelium
  • collectively called plaque
  • takes a very long time to build up
  • many, many years before it’ll become a serious problem
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45
Q

factors affecting build-up of plaque

A
  • genetics
  • eating habits
  • etc
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46
Q

occlusion

A
  • when plaque build-up has become so substantial

- that the blood vessel can no longer supply even a minimally healthy volume of blood to the tissue it ‘feeds’

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47
Q

dangers of occlusion in coronary arteries

A
  • the heart has 3 major coronary arteries
  • they supply cardiac muscle with oxygen-rich blood
  • these arteries branch directly from the aorta and carry blood that has recently been to the lungs
  • cardiac muscle never stops contracting, with alternating periods of systole and diastole occurring repeatedly throughout your life
  • thus very oxygen-demanding
  • if any of these 3 arteries get blocked, some portion of the heart muscle will be deprived of its oxygen supply
  • this causes a coronary thrombosis or an acute myocardial infarction (AKA heart attack)
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48
Q

pathogen

A

living organism or virus capable of causing a disease

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49
Q

examples of pathogens

A

viruses, bacteria, protozoa, fungi, and worms of various types

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50
Q

how does the skin help protect against pathogens?

A
  • skin has 2 primary layers
  • the lower layer (dermis) is alive and adds strength and structure to the skin
  • the upper layer (epidermis) is made up of dead cells
  • it’s constantly being replaced as dermal cells die and move upward
  • layer of mainly dead cells forms a good barrier against most pathogens because it is not truly alive
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51
Q

how pathogens can breach the barrier of skin

A
  • they can enter through cuts/abrasions
  • which is why it’s important to clean wounds
  • pathogens can also enter the body at a few points
    that are not covered by skin
  • but these points have defenses of their own
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52
Q

how do areas not covered by skin defend against pathogens?

A
  • these entry points have tissue cells that form a mucous membrane
  • goblet cells secrete a lining of sticky mucus
  • the mucus traps incoming pathogens to prevent them from reaching cells they can infect
  • some mucous membrane tissue is lined with cilia
  • the cilia have wave-like movement that moves pathogens trapped in mucus up and out of the tissues
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53
Q

how does blood clotting help defend against infection?

A
  • small blood vessels like capillaries, arterioles, and venules are normally located in the skin
  • if broken, pathogens then have a way to gain entry into he body
  • our bodies have evolved a set of responses to create a clot that ‘seals’ the damaged blood vessels
  • this prevents excessive blood loss and helps prevent pathogens from entering
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54
Q

plasma proteins

A
  • proteins present in blood plasma
  • they perform a variety of purposes
  • some are involved in clotting
  • they remain inactive until called to action
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55
Q

examples of clotting proteins

A
  • prothrombin

- fibrinogen

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56
Q

platelets

A
  • cell fragments
  • they form in bone marrow (along with RBCs and WBCs) but don’t remain as entire cells
  • platelets are formed when a very large cell breaks down into many fragments
  • each of the fragments becomes a platelet
  • they don’t have a nucleus
  • cellular life span is short (8-10 days)
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57
Q

clotting process when a blood vessel is damaged

A
  • damaged cells of the blood vessel release chemicals stimulating platelets to adhere to the damaged area
  • damaged tissue and platelets release clotting factors that convert prothrombin into thrombin
  • thrombin (enzyme) catalyses conversion of soluble fibrinogen into (relatively) insoluble fibrin
  • fibrin is a fibrous protein forming a meshlike network
  • fibrin helps to stabilize the platelet plug
  • more cellular debris become trapped in the brin mesh
  • a stable clot forms eventually
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58
Q

immune response

A

reaction of the immune system that occurs when a pathogen enters the body

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59
Q

primary immune response

A
  • first encounter with a particular type of pathogen

- tends to take 1 week+ to be successful

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60
Q

secondary immune response

A
  • second/third/etc encounter
  • quicker and more intense
  • the ability to perform these immune responses signify ‘immunity’
61
Q

WBCs

A

AKA leucocytes

  • they help us fight off pathogens in our bodies
  • provides us with immunity for pathogens we encounter more than once
62
Q

macrophage

A

AKA phagocytes

  • large leucocyte
  • can change their cellular shape to surround invading cells via phagocytosis
  • can easily change their shape
  • so can be transported fairly easily through small vessels
63
Q

how do macrophages work to identify pathogens?

A
  • can recognize whether a cell it encounters is a natural part of the body or not
  • this recognition is based on the protein molecules that make up part of the surface of all cells and viruses
  • if the macrophage identifies the cell as foreign, it engulfs the cell via phagocytosis
64
Q

non-specific immunity

A
  • phagocytes don’t make distinctions between foreign materials
  • they simply attack anything that isn’t identified as a natural part of the body

e.g. phagocytes contain many lysosome organelles to chemically digest whatever was engulfed

65
Q

binding site

A

where an antibody attaches itself to an antigen

66
Q

antibodies

A
  • Y-shaped protein molecules
  • produced by the body
  • in response to a specific type of pathogen
  • each type of antibody is different because each is produced in response to a different pathogen
67
Q

antigens

A
  • foreign proteins
  • each pathogen is made up of either cells with cell membranes or a protein coat called a capsid (virus-specific)
  • antigens are found on that outer surface
  • if a WBC comes into contact with them, they trigger an immune response
68
Q

function of antibodies

A
  • at the end of each Y fork is a binding site

- by binding to the antigen, the antibody is also attached to the pathogen

69
Q

lymphocytes

A
  • leucocytes producing antibodies
  • each type of lymphocyte can produce only one type of antibody
  • so a huge number of different types are needed
  • each lymphocyte puts some of the antibody it makes into its cell surface membrane
  • with the binding site pointing out
70
Q

process of primary immune response

A
  1. A specific antigen type is identified
  2. When a pathogen enters the body, its antigens bind to the antibodies in the cell surface membrane of a specific type of lymphocyte
  3. That specific type of lymphocyte divides repeatedly by mitosis to rapidly increase their quantity
  4. They all begin antibody production.
  5. The newly released antibodies circulate in the bloodstream and eventually find their antigen match
  6. Using various mechanisms, the antibodies help eliminate the pathogen.
  7. Some of the cloned antibody-producing plasma cells remain in the bloodstream to provide immunity against a second infection by the same pathogen (memory cells)
  8. Memory lymphocytes respond quickly if the same antigen is encountered again (secondary immune response)
71
Q

HIV

A

human immunodeficiency virus

  • primarily infects lymphocytes
  • thus a person infected with HIV will experience a severe drop in lymphocyte population
  • eventually they lose the ability to produce adequate antibodies
  • takes many years before an infected loses his/her specific immune response capability
  • but when it occurs the person acquires immune deficiency syndrome (AIDS)
  • when AIDS symptoms do begin, the infected person can no longer fight off pathogens due to this syndrome
  • thus secondary infections are more likely to kill an AIDS patient than the disease itself
72
Q

how is HIV transmitted?

A
  • unprotected sex with an infected
  • sharing a hypodermic needle with an infected
  • possible for HIV+ mother to infect her child during pregnancy/childbirth/breastfeeding
73
Q

how do antibiotics work to combat bacterial infections?

A
  • prokaryotes and eukaryotes have major structural and biological differences
  • antibiotics take advantage of those differences to block some biochemistry needed by bacteria but not by eukaryotic cells
74
Q

why do antibiotics have no effect on viral infections?

A
  • viruses make use of our own body cells’ metabolism to create new viruses
  • so any chemical that inhibits them also damages our own cells
75
Q

ventilation

A
  • the process of filling lungs with air then expelling that air
  • allows diffusion of gas to occur in the lungs
  • each breath in and out maintains conc gradients that encourage diffusion of gases between alveoli and capillary beds
76
Q

alveoli

A
  • small spherical sacs in the lungs
  • site of gas exchange
  • oxygen in alveoli diffuse into the blood stream
  • CO2 in the blood stream diffuses into alveoli
77
Q

how ventilation works

A
  • lung tissue is passive, not muscular
  • so it’s not the lungs themselves but the surrounding musculature that performs movement
  • it’s based on the inverse relationship between pressure and volume
78
Q

mechanism of inspiration

A
    • diaphragm contracts (moves down)
      - rib cage moves up and out
      - external intercostal muscles contract
      - abdominal muscles relax
      - these actions increase volume of thoracic cavity
    • pressure in thoracic cavity drops below atmospheric pressure
      - less pressure on lung tissue (partial vacuum)
    • air flows into lungs from outside the body
      - to counter partial vacuum
79
Q

mechanism of expiration

A
    • diaphragm expands (moves up)
      - rib cage moves down and in
      - due to contraction of internal intercostal and abdominal muscles
    • muscle movements decrease volume of thorax (and therefore thoracic cavity)
      - more pressure on lung tissue
    • air flows out of lungs and exits the body
      - until pressure in lungs falls to atmospheric pressure
80
Q

ventilation rate

A

number of inhalations/exhalations per minute

81
Q

tidal volume

A

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

82
Q

how to monitor ventilation rate in humans

A
  • simple observations
  • placing an inflatable chest belt around the thorax
  • using a differential pressure sensot ro measure pressure variations in the chest belt
  • thus deducing the ventilation rate and relative size of ventilations
83
Q

how to monitor tidal volume in humans

A
  • using a spirometer
  • can be made using a bell jar (with vol.s marked) placed in a pneumatic trough
  • a tube is used to exhale into the bell jar so the expired volume can be measured
84
Q

movement of air in inhalation

A

trachea –> right/left primary bronchi –> smaller bronchi branches –> bronchioles –> alveoli

85
Q

adaptations of alveoli for their function

A
  • made up of a single layer of cells so distance for diffusion is small
  • also permeable to oxygen and CO2
  • large SA for diffusion
  • moist so oxygen can dissolve
86
Q

types of alveolar cells

A
  • type I pneumocytes

- type II pneumocytes

87
Q

type I pneumocytes

A
  • very thin
  • large SA
  • well-designed for diffusion
  • incapable of mitosis for replacement if damaged
88
Q

type II pneumocytes

A
  • cuboidal
  • smaller SA
  • secretes a surfactant solution
  • this reduces the surface tensions of the moist inner surface of alveoli and prevents sides from sticking to each other
  • capable of mitosis for replacement if damaged
89
Q

emphysema

A
  • lung disease
  • primarily caused by smoking
  • gradually turns healthy alveoli into large, irregular structures with gaping holes
  • thus reducing the SA for gas exchange so less oxygen reaches the blood stream
90
Q

lung cancer

A
  • prone to metastasis

- takes over bronchioles and alveoli

91
Q

causes of lung cancer

A
  • smoking (causes 90% of lung cancer cases)
  • passive smoking
  • air pollution
  • radon gas
    asbestos and silica
92
Q

neuron

A
  • cells transmitting nerve impulses

- neuron cells can be unusually long (there are some that extend from the lower spinal cord down to the big toe)

93
Q

spinal nerves

A
  • emerge directly from spinal cord

- mixed nerves (some sensory, some motor)

94
Q

cranial nerves

A

emerge from brain stem

95
Q

synaptic terminal buttons

A
  • swollen membraneous areas
  • located at the end of an axon
  • contains many vesicles filled with neurotransmitters
  • releases neurotransmitters to chemically transmit impulses
96
Q

action potential

A

AKA impulse

  • messages transmitted by nerves
  • self-propagating wave of ion movements in and out of the neurone membrane
  • can occur anywhere on a motor neuron
  • measured the same way as electricity but the two are very different
97
Q

difference between action potential and electricity

A
  • electricity is the flow of electrons along a conductor

- action potential is the diffusion of ions in and out of neuron axons

98
Q

resting potential

A
  • period in which an area of a neurone can send an action potential, but isn’t actually sending one
  • this area of the neuron is polarized
99
Q

requirements to achieve resting potential

A
  • a net positive charge outside the axon membrane (positive in relation to the inside)
  • a net negative charge inside the axon membrane
  • thus achieving a conc. gradient of both Na+ and K+ ions
100
Q

how is resting potential created?

A
  • via active transport (sodium-potassium pumps)
  • Na+ transported out of cell (intercellular fluid)
  • K+ transported into cell (cytoplasm)
  • also due to presence of -tive organic ions permanently located in cytoplasm
101
Q

depolarization

A
  • nearly instantaneous event
  • occurs in 1 area of an axon
  • Na+ diffuse in down the conc gradient
  • results in inside of neuron becoming positive (temporarily) in relation to outside
  • due to presence of both K+ and Na+ in neuron
  • thus reversing the potential across the membrane
102
Q

effect of depolarization on action potential

A
  • initiates the next area of the axon to open up the channels for sodium
  • allows action potential to continue down the axon
  • so in essence, action potential is the depolarization and repolarization of a neuron
103
Q

receptor neurone

A
  • neurone modified to begin sequence of events
  • by transducing (converting) a physical stimulus into the first action potential (e.g. for retinal receptors it’s a minimum light intensity detected)
104
Q

self-propagation of action potential

A
  • can only be done if a minimum threshold is reached
  • this begins at the first receptor neurone
  • there’s no such thing as strong/weak impulse, all that matters is that the stimulus reaches the minimum threshold
  • chain sequence of events
  • each successive area of the neurone membrane reaches its threshold and causes the next area of the membrane to also reach its threshold
105
Q

repolarization

A
  • nearly instantaneous event
  • occurs in 1 area of an axon
  • reversal of membrane polarity causes potassium channels to open
  • K+ diffuses out down the conc gradient
  • so only Na+ present
  • causes inside of neuron to become negative compared to outside
106
Q

myelin sheath

A
  • series of Schwann cells
  • wrapped around axon multiple times
  • creates multiple layers of the same cell membrane
  • Schwann cells are spaced evenly along any one axon
  • with small gaps (nodes of Ranvier)
107
Q

saltatory conduction

A
  • action potential of myelinated axons skips from one node of Ranvier to the next
  • as impulse progresses along the axon towards the synaptic terminals
  • so Na+/K+ ion movements only needed at nodes of Ranvier
108
Q

why is the sodium-potassium pump not required in myelinated axons

A
  • myelin sheath acts as an insulator, preventing charge leakage through the membrane
  • cytoplasm within the axon is electrically conductive
  • allows electrical potential to skip from one node of Ranvier to the next
109
Q

advantages of myelinated axons over non-myelinated axons

A
  • impulse travels much faster in myelinated neurons
  • as saltatory conduction by the Schwann cells allows areas of the membrane to be skipped
  • this renders Na/K pump actions unnecessary except for nodes of Ranvier
  • thus less energy expended for the transmission of impulses
  • as only nodes of Ranvier needs Na/K pump to re-establish resting potential
110
Q

synapse

A
  • junction between neurons
  • where communication between neurons occur
  • communication between neurons is always chemical
  • both neurons align such that the dendrites of one touch the synaptic terminals of the other
111
Q

presynaptic neuron

A
  • the neuron communicating the message

- releases neurotransmitters from its synaptic terminal buttons

112
Q

postsynaptic neuron

A
  • the neuron receiving the message

- receives neurotransmitters via receptors in dendrites

113
Q

process of synaptic transmission

A
  1. Action potential results in Ca2+ diffusing into the terminal buttons
  2. Vesicles in terminal buttons fuse with the plasma membrane and release neurotransmitters via exocytosis
  3. Neurotransmitters diffuse across synaptic gap/cleft
  4. They bind with receptor proteins on the postsynaptic neurone membrane
  5. Binding results in postsynaptic neuron’s ion channels opening for Na+ ions to diffuse in
  6. This initiates the action potential movement down the postsynaptic neurone as it is now depolarized and the action potential is self-propagating
  7. The neurotransmitter is degraded using enzyme(s) and released from the receptor protein
  8. The ion channel closes to sodium ions
  9. Neurotransmitter fragments diffuse back across the synaptic gap to be reassembled in the terminal buttons (reuptake) for reuse
114
Q

effect of chemicals on synaptic transmission

A
  • neonicotinoid is an insecticide binding to postsynaptic receptors in place of the neurotransmitter acetylcholine
  • action potential is not propagated when neonicotinoid binds
  • as neonicotinoids are not broken down by acteylcholinesterase, the receptor becomes permanently blocked
  • this leads to paralysis and eventually death of the insect
115
Q

examples of hormones

A
  • thyroxin
  • leptin
  • melatonin
  • insulin
  • oestrogen
116
Q

thyroxin

A

secreted by: thyroid gland

composition: an amino acid + iodine
- 2 types: T3 and T4 (numbers correspond to number of I atoms in the molecule)
- T3 is the active form; T4 is normally converted to T3 upon reaching the target cell
target: any cell in the body
function: regulates DNA transcription and body temp
effect: ↑ mRNA produced = ↑ proteins produced = ↑ metabolism = ↑ body temp

117
Q

leptin

A

produced by: adipose tissue (↑ fat stored = ↑ leptin)

target: hypothalamus
function: inhibits appetite after enough food is ingested
effect: ↓ appetite = ↓ food intake
- obese people may have been desensitized to leptin’s effects

118
Q

melatonin

A

secreted by: pineal gland

  • secretion is stimulated when signals are sent by suprachiasmatic nuclei (SCN) in the hypothalamus
    function: regulates circadian rhythm
    effect: feelings of sleepiness
  • production is stimulated by darkness
  • secretion never actually stops, just becomes very little in daytime
119
Q

insulin

A

secreted by: pancreatic beta cells
target: all body cells (primarily hepatocytes and muscle cells)
function: reduce blood glucose levels
effect 1 (regular body cells): ↑ opening of protein channels = ↑ facilitated diffusion of glucose into all body cells = ↓ blood glucose levels
effect 2 (muscle cells/hepatocytes): ↑ opening of protein channels = ↑ facilitated diffusion of glucose = glucose molecules converted to glycogen = glycogen stored in cytoplasm of muscle cells/hepatocytes as granules = ↓ blood glucose levels

120
Q

glucagon

A

secreted by: pancreatic alpha cells

target: hepatocytes and muscle cells
function: increase blood glucose levels
effect: stimulates the hydrolysis of glycogen in muscle cells and hepatocytes = glucose released into bloodstream = ↑ blood glucose levels

121
Q

regulation of blood glucose in a nutshell

A
  • blood glucose levels are regulated by the liver
  • hepatic portal vein takes blood to the liver
  • hepatocytes (liver cells) process blood so that its levels are reasonable
  • their activity is stimulated by insulin and glucagon
  • insulin and glucagon work antagonistically
122
Q

diabetes

A
  • disease characterized by hyperglycaemia (high blood glucose content)
  • has 2 types
123
Q

type I diabetes

A
  • autoimmune disease
  • immune system attacks and destroys pancreatic beta cells
  • so not enough insulin is produced
  • 10% of all diabetics
124
Q

cause of type II diabetes

A
  • body cell receptors don’t respond properly to insulin (insulin resistant)
  • pancreatic secretion of insulin also decreases over time
  • associated with genetics, obesity, lack of exercise and advanced age
  • 90% of all diabetics
125
Q

effect of diabetes

A
  • sufficient glucose in their blood, but not in their body cells where it is needed
  • bc insulin is what stimulates the facilitated diffusion of glucose into cells
  • in other words, facilitated diffusion of glucose does not occur without insulin (type I) or a proper response to it (type II)
126
Q

treating type I diabetes

A

insulin injections at appropriate times

127
Q

treating type II diabetes

A

controlling diet

128
Q

dangers of not treating diabetes

A
  • damage to the retina (could lead to blindness)
  • kidney failure
  • nerve damage
  • increased risk of cardiovascular disease
  • poor wound healing (could lead to gangrene)
129
Q

how are sex organs developed in the foetus?

A
  • male and female reproductive structures have common
    origins in a pre-8-week-old embryo (i.e. they are homologous)
  • a gene called SRY located in Y chromosome determines sex
  • if present, it codes a protein called TDF (testis determining factor)
  • this causes testes development and high testosterone production
  • no Ys = alleles interacting on both X chromosomes stimulate further production of oestrogen and progesterone (they were already being produced regardless of gender)
130
Q

stages of fertilization

A

zygote – embryo – fetus – baby

131
Q

where does fertilization occur?

A

only in the fallopian tube, before the egg sticks on the lining

132
Q

what happens if the zygote remains in the fallopian tube?

A
  • the fallopian tube will eventually explode

- it’s a medical emergency called ectopic pregnancy

133
Q

functions of testosterone

A
  • stimulates initial development of male gonad (happens in early embryo stage after 15 weeks)
  • stimulates secondary sexual development (puberty), including urge for sex, increased muscle, growth of height and penis, deepened vocal cord
  • maintains sex drive and production of sperms
134
Q

male reproductive anatomy

A
  • testis
  • epididymis
  • scrotum
  • vas deferens
  • seminal vesicle
  • prostate gland
  • penis
  • urethra
135
Q

testis

A
  • male gonads

- sperm are produced here in small tubes called seminiferous tubules

136
Q

epididymis

A

area where sperm mature

137
Q

scrotum

A
  • sacs that hold the testes outside the body cavity

- this allows sperm production and maturation to occur below body temp

138
Q

vas deferens

A
  • muscular tube

- carries mature sperm from epididymis to urethra during ejaculation

139
Q

seminal vesicles

A
  • small glands

- produce and add seminal fluid to semen

140
Q

prostate gland

A

produces most of the seminal fluid (including carbohydrates for the sperm)

141
Q

penis

A
  • becomes erect due to blood engorgement

- this facilitates ejaculation

142
Q

urethra

A

tube by which the semen leaves the penis after all the glands have added fluids

143
Q

female reproductive anatomy

A
  • ovaries
  • fallopian tubes/oviducts
  • uterus
  • endometrium
  • cervix
  • vagina
144
Q

ovaries

A
  • female gonads
  • produce oestrogen and ovum (in the form of secondary oocytes)
  • when the ovum is released, the area where ovulation occurs grows into the corpus luteum, stimulating the temporary production of progesterone
145
Q

fallopian tubes/oviducts

A

ducts that carry the ovum to the uterus

146
Q

uterus

A

muscular structure where the early embryo implants and

develops if a pregnancy occurs

147
Q

endometrium

A

highly vascular inner lining of the uterus

148
Q

cervix

A
  • lower portion of the uterus
  • has an opening to the vagina to allows sperm to enter for fertilization
  • provides a pathway for childbirth
149
Q

vagina

A
  • muscular tube leading from external genitals to cervix

- semen is ejaculated here during sexual intercourse