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FY > Semester 1 Biology > Flashcards

Semester 1 Biology Flashcards

1
Q

What is a hydrophobic region

A

Interaction between non-polar section of the protein,
tend to exclude water and are side chains

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2
Q

How do disulfide bridges form

A

As a result of an oxidation reaction between 2 cysteine molecules (covalent bonds between sulfur)

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3
Q

Compare and contrast the shape and function of Fibrous and Globular proteins, give examples of each.

A

Fibrous
-Parallel polypeptide chain with cross-links
-Form rope-like fibres or sheets providing strength and flexibility
-Insoluble
E.G keratin in nails and collagen in bones

Globular
-Highly folded polypeptide to produce a complex specific tertiary structure
-Spherical shape
-Soluble
E.G enzymes, antibodies, receptors and hormones

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4
Q

What will happen to Fibrous and Globular proteins when they become denatures

A

Fibrous-loses structural strength
Gloubular-Become insoluble and inactive

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5
Q

4 shapes of bacteria

A

Cocci (spherical)
Bacilli (rod shaped)
Spirilla (spiral shaped)
Vibrio (curved shaped)

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6
Q

Pilli

A

Helps with motility

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7
Q

Capsule

A

-Consists of polysacharides/polypeptide
-Protects against phagocytosis and antibodies
-Prevents dehydration

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8
Q

How does binary fission occur

A

-Cell elongation, circular DNA replicates attaches to mesosomes
-Septum is synthesised to divide the wall
-Septum grows across cell, divides genetic material. 2 daughter cells formed
-2 daughter cells separate and cycle begins again

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9
Q

Mesosome

A

-Infoldings of cell surface membrane, has enzymes involved in respiration
-Plays a role in cell division, aid the separation of DNA in new cells,

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10
Q

Define generation time

A

Time taken for a bacterial population to double in numbers

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11
Q

Lag phase

A

-Little cell division occurs, cells may increase in size
-Cells synthesise RNA, proteins and enzymes

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12
Q

Log/exponential phase

A

-Cells show maximum division (double exponentially)
-Nutrient levels, temperature and pH are at optimal levels
-No factor limiting
-Primary metabolites are formed and excreted during log phase of microorganims

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13
Q

Stationary phase

A

-No increase in population, number of cells produced is equal to number dying
-Level of nutrients decrease, limiting growth, temp/pH has become unfavourable
-Increase in metabolic waste will limit growth
-Secondary metabolites that are not essential for growth and reproduction are produced & excreted here

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14
Q

Death phase

A

-Unfavourable conditions (temp,pH, toxins) increase the death rate above reproduction rate
-Autolysis of cells may occur (self digestion)

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15
Q

Define obligate aerobes

A

Microbes that only grow with oxygen present

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16
Q

Define obligate anaerobes

A

Microbes that only grow in anaerobic conditiones

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17
Q

Define Facultative anaerobes

A

Can respire aerobically when oxygen levels are high and anaerobically when oxygen levels are low

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18
Q

Define aerotolerant aerobes

A

Grow well in anaerobic conditions but can tolerate and grow in presence of oxygen

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19
Q

Define microaerophiles

A

Grow in aerobic conditions but require low conc of oxygen

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20
Q

Halophiles adaptations
(grow in high salt concs)

A

-Maintain high conc of salt in cytoplasm to prevent water moving out of cells by osmosis
-Folding of protein to tolerate high salt conc, allows functioning of enzymes

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21
Q

Alkalinophiles adaptations
(grow optimally at pH above 9)

A

-Have membrane lipids and cell walls that resist dissociation by alkali
-Their proteins and enzymes are adapted to work optimally at this pH

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22
Q

Acidophiles adaptations
(grow optimally below pH 5)

A

-Acid-resistant cell walls and membranes
-Active pumping of excess protons

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23
Q

Barophile adaptations
(grow at high hydrostatic pressure)

A

-Folded in a way that minimises pressure-related effects on their enzymes
-Lipid bilayer of cell membrane becomes more tightly packed at high pressure forms rigid structure that shields inside of cell

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24
Q

Thermophiles adaptations
(optimum temp above 45 deg
Hyperthermophiles above 80 deg)

A

-More saturated fatty acids on lipid membranes, provide membrane stability
-Have more chemical bonds to maintain protein shape

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25
Q

Psychrophile adaptation
(optimum temp 15 deg or lower)

A

-Cold adapted enzymes that are active at low temps
-Have antifreeze proteins that bind to ice crystals preventing them from piercing cell membrane

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26
Q

Define total cell count

A

Total number of cells present, living and dead

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27
Q

Define viable count

A

Only living cells, cells that are capable of dividing

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28
Q

Which methods are used to calc total cell count

A

-Haemocytometry
-Turbidimetry

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29
Q

Why can turbidimetry be used to measure the growth of a culture of microorganisms

A

Transmitted light is proportional to number of cells

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30
Q

Describe end-point inhibition
(negative feedback)

A

-Occurs when end product of metabolic pathway accumulates (acts as an inhibitor)
-Product switches off it’s own production
-Self regulatory, as product is used up its production switched on again

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31
Q

Equation for calculating dilution factor

A

DF=Total volume/Volume added

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32
Q

Give an example of end-point inhibition

A

Glycolysis (respiration)

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33
Q

What are immobilised enzymes

A

-Enzymes that can be trapped in a solid support that can be easily recovered from the reaction mixture
-Enzyme can be reused, reducing the cost of the process

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34
Q

Adavantages of immobilising enzymes

A

-Makes the enzyme more stable by restricting its ability to change shape and denature
-Allows for continuous production as reactants pass over enzyme and product is collected
-Enzymes don’t become contaminated with product, held in a matrix

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35
Q

Examples of physical bonding (immobilising enzymes)

A

-Adsorbed onto insoluble matrix e.g collagen
-Held inside a gel e.g silica gel [gel entrapment]
-Held within semi-permeable membrane e.g polymer microspheres
-Trapped in micro capsule [microencapsulation] e.g in alginate beads

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36
Q

Example of chemical bonding (immobilising enzymes)

A

-Chemically binding enzyme to support medium but preparation is difficult

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37
Q

Features of Fungi

A

-Eukaryotes
-Filamentous fungi have hyphae that form masses (mycelium)
-Heterotrophic
-Use extracellular digestion

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38
Q

Function of cell wall

A

-Main component:chitin (nitrogen containing polysaccharide)
-Provides strength and rigid structure also allows enzyme secretion + absorption

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39
Q

Features of a cell wall

A

Main component: chitin (nitrogen-containing polysaccharide)
-Provides strength to wall and rigid structure
-Allows enzyme secretion + absorption

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40
Q

State aseptic techniques

A

-Use sterile syringes/ equipment
-Flame top of test tubes/ inoculating loops
-Minimise exposure to air (lift lid of Petri dish slightly)
-Avoid contact of sterile apparatus with skin/work surfaces

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41
Q

Culture media:
Complete/complex media

A

-Used to grow a wide range of microorganisms or when nutritional requirements of microorganisms are unknown
-Contains all nutrients required for growth e.g glucose, amino acids, water, vitamins

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42
Q

Culture media:
Selective/minimal media

A

-Suitable for growth of specific microrganisms
-If inoculated with mixed culture, only species that medium was designed for will grow
-Other microorganisms growth will be suppressed

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43
Q

Examples of sterilisation

A

-Direct heat; inoculating loop, neck of tubes
-Autoclaving (120°) glassware
-Putting things in alcohol and then placing on fire (Burning alcohol)
-Disinfectants (inanimate objects) e.g work surfaces
-Ultrafiltration

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44
Q

Bioassay

A

-Enables effectiveness of a compound (antibiotics) on the growth of microorganisms
-Screen microorganisms to determine if they produce effective antibiotics
-Measures ability to inhibit growth of bacteria on bacterial lawn

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45
Q

Antibiotics

A

Compounds that produce microorganisms that inbit or kill bacteria (not effective again viruses)

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46
Q

How can antibiotics work

A

Bactericidal- actually kill bacteria
Bacteriostatic- inhibit or prevent bacterial growth

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47
Q

Disinfectants

A

Chemical compounds that kill bacteria e.g Dettol
Can also use bioassay techniques to determine effectiveness

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48
Q

State the mechanisms of how antibiotics can work

A

-Inhibiting cell wall synthesis
-Cell membrane disruption
-Inhibiting mRNA translation
-Inhibiting nucleic acid synthesis

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49
Q

Broad spectrum antibiotics

A

Effective against wide range of bacteria, may be initially used in the treatment of undetermined bacterial infections

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50
Q

Narrow spectrum antibiotics

A

Effective against a small specific group of bacteria

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51
Q

Two ways that antibiotic-resistant bacteria can obtain this gene

A

-Spontaneous mutation
-Transfer of resistant genes from other bacteria

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52
Q

Vertical gene transmission (process)

A

-Resistance may arise due to random mutation
-Bacteria containing resistant gene survives when exposed to antibiotic
-These bacteria reproduce and pass their gene onto future generation
-Repeated exposure to antibiotics can lead to more bacteria surviving
-Can increase allelic frequency

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53
Q

Horizontal gene transmission (process)

A

-Conjugation
-Donor cell produces conjugation tube (pilus) that connects two bacterial cells
-Donor cell replicates its plasmid and passes the copy to other bacterium
-Recipient cell receives plasmid which may contain the gene for antibiotic resistance

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54
Q

Does horizontal gene transmission allow the gene to be transmitted to the next generation?

A

No
It increases the number of antibiotic-resistant bacteria in a population. Conjugation can occur between diff populations

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55
Q

Transduction

A

-Bacteriophage attaches to cell membrane of bacteria
-Inserts its DNA into host and is integrated into DNA of bacteria
-Bacteriophage DNA replicates and host DNA splits into bacteriophage-size pieces
-New bacteriophage assembled some with this DNA or bacterial DNA
-Bacteriophage w/ bacterial DNA attacks another bacterial cell

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56
Q

Transformation

A

-DNA from lysed bacterial cell is bound to DNA binding protein in host cell wall
-One strand of DNA enters host cell and the other is broken down
-Single strand bound to DNA of host cell
- Host cell is transformed

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57
Q

What are the membrane-bound organelles

A

Lysosome, Nucleus, Golgi body, SER + RER, Mitochondria and Chloroplast

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58
Q

What will bacteria cells always contain

A

Cell wall, cell membrane, circular genomic DNA, Ribosomes, cytoplasm

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59
Q

Densities of organelles in centrifugation

A

Nuclei (heaviest), chloroplast (if plant), mitochondria, ER and ribosomes

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60
Q

Advantages of TEM
and
Limitations of TEM

A

+ Higher resolution than SEM
+ Can see internal structures even molecular sizes e.g. proteins and nucleic acid

-Very thin sections of specimen must be used
-Does not show 3D arrangement of cellular components
-Specimen gradually deteriorates in the electron beam

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61
Q

Principles of TEM

A

-A beam of electrons is transmitted through the specimen
-Specimen must be thin and stained using heavy metal salts
-These substances deflect electrons in the beam, remaining electrons produce a pattern as they pass through the specimen which is converted to an image

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62
Q

Advantages of SEM
and
Limitations of SEM

A

+ Surface of structures are shown
+ Gives a 3D effect
+Much thicker sections can be examined than with a TEM

-Lower resolution than TEM
-Only the surface of an object can be viewed

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63
Q

Principles of SEM

A

-Specimen is coated with a thin film of heavy metal e.g. Gold
-Electron beam is scanned across specimen
-Electrons that are reflected from the surface are collected, produce an image on viewing screen

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64
Q

Structure of Mitochondrion, linked with respiration

A

-Folds of inner membrane are cristae and provide a large SA for the stalked particles they possess
-Stalked particles contain enzymes for ATP production by the ETC (for oxidative phosphorylation)
-Matrix contains enzymes of Krebs cycle (aerobic respiration) Mitochondrial DNA (FOR ITS REPLICATION) AND ribosomes

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65
Q

Ways that ribosomes can appear
Made of 2 subunits

A

-Singularly in cytoplasm
-In chains (polymers)
-Attached to ER

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66
Q

Golgi body structure + function

A

-Has cisternae that are continually being formed at one end and pinched off as vesicles at the other end
-Secretary cells have large Golgi bodies

FUNCTION
-Production of glycoprotein
-Packaging and secretion of protein
-Formation of cell walls in plant cells
-Lipid biosynthesis

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67
Q

Lysosomes

A

-Contain digestive enzymes e.g proteases, nucleases and lipases
-Enzymes must be kept apart from rest of cell or would destroy it
-Enzymes are synthesised for RER and transported to Golgi, which then bud off to form lysosome

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68
Q

Function of lysosome

A

-Digestion of material taken in by endocytosis, can release their enzymes into vesicles and digest material.
Products then absorbed by cytoplasm leaving undigested remains

-Autophagy, unwanted structures within cell are engulfed and digested within lysosome

-Release of enzymes outside cell e.g sperm releasing acrosome to digest path of cells surrounding egg before fertilisation

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69
Q

Define tissue

A

Aggregation of similar cells that perform a specific physiological function

e.g. epithelial, nervous, muscular tissues

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70
Q

Define Organ

A

A structure consisting of different tissues, which have specific physiological functions
e.g stomach has role of digestion

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71
Q

Structure of Palisade mesophyll cells

A

-Numerous chloroplasts
-Relatively thins walls to allow CO2 to diffuse in at faster rate
-Cylindrical (column) with relatively large SA which increase the rate of gaseous diffusion
- Few air spaces in between so maximum light can be absorbed

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72
Q

Types of epithelial tissue
Structure and function of one Epithelial cell

A

-Line inside or outside of organs e.g PCT, small intestines
-3 basic types: squamous, cuboidal and columnar

-Columna epithelial cells have cell membrane folded into microvilli for a large SA
-Numerous mitochondria provide ATP for AT of amino acid and sugars

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73
Q

Stem Cells

A

-Divide by mitosis and differentiate into range of different cells
(once they are specialised cells they cannot undergo mitosis)

74
Q

Plant stem cells

A

-Totipotent so can differentiate into any kind of cell from that organisms

-Used for cloning plants for desireable traits
-Quickly produce mature plants
-Can regenerate whole plants from those that have been GM

75
Q

Embryonic stem cells: Totipotent

A

-Cells which can differentiate into any kind of body cell, including extra-embryonic tissue. Then develop not complete organisms

76
Q

Embryonic stem cells: Pluripotency

A

-Can give rise to all cells of the body but cannot produce the cells of extra-embryonic tissue.

-Are able to differentiate into all cells that arise from, the primary germ layers: ectoderm, endoderm and mesoderm. All animal cells are derived from these germ layers

77
Q

Adult stem cells: Multipotency

A

-Found in mature mammals can differentiate into a limited number of types of cells

78
Q

What does cholesterol do to Phospholipid membrane

A

Decreases the permeability of the cell membrane

79
Q

Receptor proteins

A

-Have specific tertiary structures that allow specific hormones to attach. NOT an enzyme

E.g insulin binds to its specific receptor allowing the cell to respond

80
Q

Diffusion

A

Net movement of molecules from a high conc to a low conc down a CG until molecules are equally distributed

Passive process

81
Q

FD, properties of carrier proteins

A

Change shape as they move molecules across membrane

82
Q

FD, properties of channel proteins

A

Have a fixed shape and transport ions
Charge determines what will bind, opposites attract

83
Q

Factors that affect AT (same as factors affecting respiration)

A

-Lowering of temp
-Lack of O2
-Metabolic and respiratory inhibitors e.g cynide

84
Q

The process of active transport and adaptation of cell

A

-Enzyme ATPase hydrolyses ATP, releasing energy
-Energy used to attach molecule to carrier protein and provide energy for carrier to change shape to move molecule across membrane
-Cells involved in AT have lots of mitochondria to provide ATP required via respiration

85
Q

Define water potential

A

Potential (tendency) of water molecules to leave a solution by osmosis

86
Q

Hypotonic (Hypo- too little)

A

Has low conc of solute molecules and a high conc of water molecules

87
Q

Hypertonic (Hyper-too much)

A

Has high conc of solute molecules and low conc of water molecules

88
Q

Isotonic

A

-When osmosis stops, water movement equal in both directions

89
Q

Cell turgor

A

-As water enters the cell, vacuole enlarges, and then vacuole cytoplasm and cell membrane exert an outward turgor pressure on cell wall
-Essential in providing support in many plants

90
Q

Pinocytosis (cell drinking) type of endocytosis

A

-Material taken up in liquid form, forms small vesicles
-Can be known as micropinocytosis as vesicles are micro pinocytotic

91
Q

Phagocytosis (cell drinking) type of endocytosis

A

-Material taken up in solid form, using phagocytic cells (have been specialised)

92
Q

How do pathogens produce disesase

A

-Damaging host tissue, reproducing inside cells
-Producing toxins

93
Q

Factors affecting pathogenicity

A

-Attachment and entry
-Type of toxins
-Infectivity
-Invasiveness

94
Q

Pathogenicity: attachment and entry

A

-Ligands and glycoproteins of bacterial cell wall attach to protein receptors in host cell membrane
-Enzyme produced by pathogen may damage the cell wall of host cell, causing entry of pathogen
Or endocytosis

95
Q

Pathogenicity: types of toxins

A

-Exotoxins that are proteins secreted/leaked from bacteria. These cause the symptoms of the disease NOT the bacteria
[released in small amounts but have widespread effect]

-Endotoxins are lipopolysaccharides present in bacterial cell wall. can be released when cell wall of bacterium breaks up after death
[released in large amounts but have small effect]

96
Q

Pathogenicity: Infectivity + EXAMPLE

A

Number of bacteria needed to cause the infection, varies widely from one type to another

e.g. Salmonella needs a large number of bacteria to cause food poisoning and typhoid fever only requires a small amount

97
Q

Pathogenicity: invasiveness

A

Ability of the bacteria to spread, usually in hosts blood and lymph system

98
Q

Transmission of disease

A

-Airborne/ droplets
-Foodborne
-Waterborne
-Contact, skin 2 skin, clothing 2 skin
-Sexual intercourse
-Vector-borne

99
Q

Transmission of Cholera

A

-Transmitted by ingestion of water (rarely food) that has been contaminated with faecal matter containing pathogen

~Drinking water that’s not properly purified
~Untreated sewage leaks into water courses
~Food is eaten that has been contaminated by those preparing and serving it

100
Q

Course of infection of Cholera

A

-Produces a toxin that acts on epithelial cells of small intestines, this changes membrane permeability

-Receptor has specific tertiary structure and toxin is complementary to binding site on receptor
-Attachment of toxin causes ion channels to open, causing Cl- ions to diffuse into lumen of intestine
-This raises water potential of epithelial cells and lowers water potential of lumen
-So water moves from cells + blood into lumen by osmosis= watery faeces/diarrhoea

101
Q

Symptoms of Cholera

A

Diarrhoea, dehydration, stomach cramps, vomiting and fever

102
Q

Treatment of Cholera

A

-Oral rehydration solution (ORS), contains water, Na+, Cl- and glucose
-Ions and glucose taken up by co transport protein
-Water potential of epithelial cell is reduced and is lower than that of the lumen
-Water from ORS moves from lumen to cell by osmosis
-Water moves into blood and patient is rehydrated

103
Q

Virus

A

-Intracellular parasite

-Damage host cells following entry and replication of virus
-Toxins produced in process of replication

104
Q

Structural features of virus

A

-DNA/RNA
-Capsid (subunits called capsomere)
-Enzymes
-Lipid envelope (some)
-Glycoprotein, represent antigens that antibodies may possess

105
Q

Symptoms of Influenza

A

-Incubation period~ 2 days
-Headaches, sore throats, backaches, joint pain, shivering, sweating (symps can last for 7 days)
-Coughing may continue due to epithelial damage to trachea and bronchi

106
Q

Transmission of Influenza

A

-Droplets during coughing and sneezing, enter respiratory passages
-Overcrowding and poor ventilation enhance spread

107
Q

Influenza: course of infection

A

-Virus attack generally localised on epithelial lining of respiratory passage
-Individual remains infective for more than 6 days

108
Q

Replication of Influenza

A

-Virus particles enter epithelial cells, molecules in outer coat of virus bind to receptor molecules in CM of epithelial cells

-Virus coat removed releasing viral RNA and RNA polymerase
-Viral RNA enters hosts nucleus and controls protein synthesis in cell
-RNA polymerase activated and synthesises viral mRNA strands
-Viral proteins + lipids formed in cytoplasm and assembled into viral coats
-Viral RNA and coats assembled into new virus particles
-Lysis of cell occurs, releases viral particles which infect other cells

109
Q

Difficulty of treating viruses

A

-Are intracellular, drugs don’t penetrate cells so they are difficult to treat
-Antibiotics may be given to treat secondary infections

110
Q

Coronavirus symptoms

A

-Continuous cough, high temp, change in sense of taste/smell, lack of energy, headaches , stuffy/runny nose

111
Q

Transmission of Coronvirus

A

-Zoonotic (transmitted between animals and people and between people)
-Spreads through close contact of people with virus, even if they don’t show symptoms
-Small droplets released when someone breathes, speaks, coughs or sneezes
-Catch virus if droplets breathed in or touched
-Risk of transmission highest indoors + crowded places

112
Q

Replication of Coronavirus

A

-In humans able to attach to epithelial cell receptors (of respiratory tract) by having complementary glycoproteins
-Release RNA genome into host cells cytoplasm
-RNA genome acts like mRNA so directly translated by ribosomes into new viral particles

113
Q

HIV course of infection
Stages of infection

A

-4 phases,
1)asymptomatic (no symptoms)
2)Antibody positve phase, period between infection and onset of clinical signs
3)Aids-related complex (ARC) , may contract opportunistic bacterial, viral and fungal infection. Loss of weight and reduction in T cells
-4th stage: opportunistic infections of organs, development of secondary cancers, HIV wasting syndrome. May die from pneumonia if immune system collapses

114
Q

Structural features of HIV

A

-AIDs caused by infection of HIV
-Has RNA AND reverse transcriptase that produces DNA in host
-Has nucleocapsid, inner and outer protein capsid
-Nucleopcapsid had glycoprotein on surface allowing it to attach to host cell helper t cell

115
Q

Transmission of HIV

A

-Transmitted by introduction of blood, semen or vaginal secretions from an infected individual into bloodstream of another individual

-Sexual transmission
-Blood transfusions of infected blood
-Sharing of needles (drug users)
-Mother to baby via placenta

116
Q

Replication of HIV

A

-Viruses attach to CD4 helper T cells by glycoproteins binding to receptor sites
-Viral RNA + reverse transcriptase release and enter T cell
-Reverse transcriptase converts viral RNA into cDNA, using viral RNA as template
-cDNA enters nucleus attaches to host DNA, replicates

-Viral DNA can remain inactive (latent) up to 10 yrs
-Once activated viral DNA controls synthesis of viral proteins and RNA within T cell
-HIV particles assembled and T cell destroyed. Virus infects other T cells as it reproduces T helper cells in blood decrease
-T cells stimulate B cells (antibodies) to combat infection
-Immune response breaks down, individual suffers from opportunistic infections e.g pneumonia, kaposi’s

117
Q

How does HIV cause AIDs (simple terms)

A

-A pathogen is identified in body
-T lymphocytes are HIV infected so produce more HIV
-HIV released as T cells die
-HIV infect more helper T cells so NO IMMUNE REPSONSE
-So no destruction of pathogen
-Opportunistic infection

118
Q

Structural Features of Ebola Virus

A

-Glycoprotein
-Nucleoprotein
-Transcription Factor VP30
-Polymerase cofactor VP35
-Polymerase (L)
-Matrix
-VP24

119
Q

Structural features of bacteriophage

A

-DNA or RNA
-Head
-Collar
-Tail
-Long Tail fibres
-Base plate

120
Q

Possible cycles for when bacteriophage attaches to host cell

A

-Virulent phages, often follow the lytic pathway resulting in the lysis of prokaryotic cell

-Temperate Phages enter a state (lysogeny), where viral DNA is incorporated into DNA of prokaryote host. Remains dormant but is replicated every time the host cell divides

121
Q

Define Parasite

A

An organism that lives in or on living tissue of a host organism at expense of that host

122
Q

Transmission of Malaria

A

-Mosquito(vector) picks up Plasmodium from infected human when it feeds. Females feed on human blood to obtain protein required to develop their eggs
-Plasmodium reproduces in gut of females, produces thousands of plasmodium which move to salivary glands of female
-When mosquito feeds again on healthy individual plasmodium pass into blood along with anticoagulant in saliva
-Travel to liver, enter cells + multiply
-Leave liver and enter RBCs of the infected person, multiply further
-Once multiplied they cause cells to burst, releasing more plasmodium for further infection. Coincide with malaria symptoms

123
Q

Treatment of malaria

A

-Vaccination
-Avoid being bitten, cover arms + legs, insect repellent, mosquito nets
-Use insecticides
-Antimalarial drugs prior to and after travel

[Parasite remain in bloodstream for 30 mins so immune system cant react]

124
Q

Describe and explain one adaptation of the malaria parasite which causes it to be unaffected by the body immune system

A

Lives inside host cell so avoids attack by host, production of antibodies slow

125
Q

State infectious pathogens

A

Bacteria, viruses and fungi

126
Q

Transmission

A

When a pathogen is transferred from one individual to another

127
Q

Non-specific defence mechanism

A

Act against all types of micro organisms, prevent them from gaining access to living cells

128
Q

Non-specific defence mechanism: skin

A

-Outer layer of epidermis consists of dead ,tough cells (non-hospitable environment) containing indigestible Keratin that provide resistance to bacterial invasion

-Secretion from sebaceous glands have antiseptic properties against some bacteria

-Commensal bacteria compete more successfully than pathogenic bateria

129
Q

Non-specific defence mechanism: Tears

A

Contain lysozyme which breaks down cell walls of bacteria

130
Q

Non-specific defence mechanism: Saliva

A

Also has lysozyme. Chewing stimulates salivation increasing amount of lysozyme present in mouth

131
Q

Non-specific defence mechanism: Mucus

A

-Secreted by epithelial cells lining nasal passage and respiratory tract
-Traps bacteria and dust particles entering air passage, also contains lysozyme other antibacterial substances

132
Q

Non-specific defence mechanism: Cillia

A

-Minute hairs on epithelial cells in upper respiratory tract
-Cillia beat which create current moving mucus + trapped particles to pharynx (throat)
-Swallowing carries microbes to stomach, killed off by HCl or enzymes
-Coughing and sneezing also removes trapped particles and microbes

133
Q

What happens if non-specific defence mechanisms are breached

A

Internal mechanisms step in

134
Q

Process of phagocytosis (non-specific mechanism)

A

-Detection, phagocyte (neutrophils + macrophage) detects microbes by chemicals(chemotaxis) they give off + sticks microbes to its surface
-Ingestion, Microbe is engulfed by phagocytes, forms a vesicle
-Phagosome forms, this encloses microbes in a membrane
-Fusion with lysosome, phagosome fuses with lysosome
-Digestion, microbes are broken down by enzymes into chemical constituents
-Dishcharge, indigestible material is discharged from phagocytes
Soluble products are absorbed

135
Q

Role of phagocytic WBCs in preventing spread of microorganisms

A

-Phagocytes destroy micro organism which enter blood, prevent their spread to other parts of body
-Can also act as APCs, using pathogens antigen on their cell surface membranes for T cells

136
Q

B lymphocytes

A

-Involved in antibody-mediated immunity (humoral response)
-Produce specific antibodies (immunoglobulins) when exposed to specific antigen
-Antibody destroys or neutralises antigen

137
Q

T lymphocytes

A

-Mainly involved in cell-mediated immunity e.g attack pathogens + foreign tissue
-Thymus gland activates T lymphocytes
-Have molecules on CSM (receptors) that recognise specific antigens then destroy the foreign cell/tissue [cytotoxic + killer T cells]
-Helper T cells and suppressor T cells, help regulate antibody production in B cells
-T Memory cells

138
Q

Forms and location of antigens

A

-Proteins or glycoproteins, appear as foreign to organism

-May be present on surface of pathogen,
on cell surface of tissue or organ transplant,
or free molecule e.g toxin

139
Q

Where are antibodies found

A

Plasma, tissue fluid, breast milk, B cell surface

140
Q

What do B cells attach to

A

-Viruses (neutralisation), bacteria, cancer cells (protein toxins), foreign RBCs

141
Q

Structure of antibody

A

=4 polypeptide chains (2 heavy + 2 light)
-Joined together by disulphide bonds (underneath intersection of Y)
-ig/G/M/A/D/E

-Constant region the sequence of AA is same in all molecules of same antibody
-Variable region sequences of AA is diff in diff molecules of same antibody
-Variable regions form 2 antigen binding sites w/ specific tertiary structure
-Antigen binding sites bind to 2 separate antigen molecules , can form a lattice = antibody-antigen complex

142
Q

Functions of antibodies

A

-Agglutination of antigens
-Stimulation of phagocytosis
-Precipitation of soluble toxins
-Preventing pathogens attaching to cell membranes

143
Q

Agglutination

A

-Clumping together of cells possessing antigen (agglutinogen) for antibody(agglutins) to react
-Antibody antigen complex forms an agglutinated mass of cells, which are then destroyed

-Agglutination of donor RBCs occurs when individual is given wrong blood group this can lead to blood clots/death

144
Q

Stimulation of phagocytosis

A

-Antibodies (opsonins) label foreign cells for destruction by phagocytic WBCs by attaching to antigen on surface of microorganism

-Phagocytes have receptors in CSM which match opsonins, enables them to recognise, bind and engulf the bacteria

145
Q

Precipitation of soluble toxins

A

-Similar process to agglutination but on a molecular level
-Antibodies (precipitins) attach to soluble toxins (antigen) causes them to grow together forming a precipitate
-Neutralises action of the toxin molecules which are then destroyed

146
Q

How to prevent the attachment of pathogens

(Immunnology)

A

-Use antibodies that are produced against antigens on surface of micro organism this prevents pathogen attaching to cell membranes
-Antigens (glycoproteins in particular) normally aid the entry of microbe into the host cell

147
Q

Difference between DNA + RNA

A

DNA=2 polynucleotide strands but DNA=single polynucleotide strand

148
Q

Where are phosphodiester bonds formed

A

Covalent bond between phosphate group of one nucleotide and pentose of the next

149
Q

Purines

A

Adenine + Guanine

150
Q

Pyrimidine

A

Thymine + Cytosine

151
Q

Role of double helix in DNA

A

Protects bases
Makes molecules more stable

152
Q

Role of H bonds in DNA

A

-Gives stability
-Prevent code from being disrupted
-Allows chain to unzip easily for replication and transcription

153
Q

Role of sequence of bases in DNA

A

Provides genetic code for protein synthesis

154
Q

Role of complementary base pairing in DNA

A

Enables info to be replicated accurately

155
Q

Production of antibodies in humoral response

A

-Body has large number of different B cells, each type produces a diff specific antibody
-B cells secrete small amount of specific antibody onto CSM
-Macrophage becomes APC after phagocytosis
-If specific antigen attaches to B cell, these divide by mitosis, results in large pop of identical plasma cells
-Helper T cells stimulate B cells to divide
-Antibodies bind specifically to antigens, form an antibody antigen complex, antigen/source is destroyed or neutalised

Extra info
Primary response is slow requires 72hrs so disease symptoms may arise
-Following exposure some B cells develop into memory cells which divide into plasma cells. Which produce antibodies upon secondary infection=immunity
-T cells regulate this process, Helper T cells stimulate B cells to divide and suppressor T cells inhibit this process

156
Q

Cellular response

A

-Cytotoxic T cells uses its receptor to attach to antigen and secretes chemicals to destroy pathogen/ foreign cell
-Helper T cells stimulate B cells to divide and produce antibodies
-Memory T cells that remain in blood and produce a quicker response upon secondary infection with same pathogen

Extra info:
-Vast number of T cells, each one responds to different antigen
-Antigen presented as APC to T cell
-Stimulates T cell to divide by mitosis and form clones w/ same receptors, then develop into different type of type of cells

157
Q

Give an example of Antigenic variation

A

-Influenza has high mutation rate (as do other micro organisms)
-So individuals will not have immunity to new strains as not recognised by B cells and other antibodies

158
Q

Passive immunity/ artificial active immunity

A

-Vaccine that contains antigen is injected
-Stimulates an immune response, B cells release antibodies. some divide to form memory B cells, T cells divide to form memory T cells
-Boosters can be given to give a more effective response

159
Q

Natural passive immunity

A

-Preformed antibodies obtained across placenta and through breast milk
-Short-term protection as no production of own antibodies and memory B cells

160
Q

Artificial passive immunity

A

-Involves injection of preformed specific antibodies usually following exposure to particular virulent antigens e.g rabies, snake venom
-Provides short-term protection

161
Q

Ways to reduce rejection if transplant

A

-Ensure tissue of the recipient + donor are genetically similar
-Irradiation of areas producing WBC e.g bone marrow to reduce number of T cells
-immunosuppressive drugs to reduce number of T lymphocytes

-Recipient must be kept in sterile conditions after operation due to risk of infection

162
Q

Define transplant

A

Replacement of diseased organs by healthy ones

163
Q

Agglutinogen(antigen) and agglutin (antibody) on different blood groups

A

BG. Antigen. Antibody.
A. A b
B B a
AB. A+B -
O. None. a+b

164
Q

Rhesus positive/negative individuals

A

-Rhesus positive individuals have antigen D on surface of RBC membrane but rhesus negative individuals do not

165
Q

Haemolytic disease

A

-When rhesus negative mother recieves rhesus positive blood from her child
-Develops rhesus antibodies against rhesus-positive blood cells, first child not affected
-Memory B cells remain in mother
-During second rhesus-positive pregnancy antibodies pass through placenta and cause lysis of rhesus positive RBCs in foetus
-Child born with severe anaemia

166
Q

Prevention for haemolytic disease

A

-Rhesuse negative mothers are injected with rhesuse antibodies (anti-D) soon after birth
-Anitbodies will destroy fetal rhesuse positive RBCs in mother before she becomes sensitised and develops an immune response
-Must be repeated after every rhesus positive pregnancy

167
Q

Monoclonal antibodies

A

-Identical antibodies w/ same tertiary structure
-Have same antigen binding site
-B cell fused with cancer cell

168
Q

Uses of monoclonal antibodies

A

-Target medication to specific cell types
-Medical diagnosis
~Detect presence of specific antibodies (Indirect ELISA) or antigens( direct ELISA)

169
Q

Direct ELISA test

Normal Elisa test

A

-Monoclonal antibody coated well
-Antigen binds to antibody
-Second monoclonal antibody,w/ enzyme binds to immobilised antigen
-Substrate added which causes colour change

-Washing of the well between each stage (especially the final washing) is important in preventing false positives

170
Q

Indirect ELISA test

A

-Antigen coated well
-Specific antibody binds to antigen
-Enzyme-linked antibody binds to specific antibody
-Substrate added which causes colour change

171
Q

What does rate of colour formation tell you in the ELISA test

A

-Rate of colour formation is proportional to the amount of antigen or antibody present depending on the test

172
Q

Evidence for SCR (method)

A

-Cells of E.Coli were grown on a medium, in which14N was replaced with 15N
-Cells were allowed to divide, bacteria then transferred into medium with 14N (normal isotope), allowed to divide
-Samples of bacteria taken after each generation, DNA was extracted and spun in centrifuge
-DNA containing heavy isotope 15N is slightly heavier than DNA containing 14N

173
Q

The results for SCR method

A

-1st generation, each DNA molecule contains 1 strand of 15N (heavy) and 1 strand of 14N (light)

-2nd generation, 50% of cells contain 14N
the other half contain hybrid DNA

-3rd generation, 25% contain hybrid DNA
75% contain DNA with 14N

174
Q

Define discontinuous replication

A

The synthesis of a new strand of a replicating DNA molecule, by a series of shorter fragments that are subsequently joined together.

175
Q

Define continuous replication in DNA replication

A

-DNA polymerase can only add nucleotides in the 5’ to 3’ direction as it synthesises a complementary strand
-So synthesis proceeds immediately along the leading strand

176
Q

Bases in RNA

A

-Uracil replaces Thymine
-Also Guanine, Cytosine and Uracil

177
Q

Regulation of transcription (gene tech)

A

-Transcription factors move from cytoplasm into nucleus
-TF binds to promoter region on DNA
-Allows RNA polymerase to transcribe the gene

If inhibitor blocked promoter region gene expression is prevented

178
Q

Regulation of translation

A

-Can be prevented by breaking down mRNA before the ribosomes translate it
-Small double stranded RNA molecules (siRNA) carry this out

-Enzyme cuts RNA into fragments forming siRNA
-One strand combines with restriction endonuclease enzyme, becomes integrated into its active site
-siRNA binds via complementary base pairing
-This signals restriction endonucleases enzyme to cut mRNA at the position which siRNA binds
-mRNA is now unable to be translated into a polypeptide

179
Q

Define epigenetics

A

Involves inheritable changes in gene expressions without changes to their DNA base sequences

179
Q

Acetylation

A

Unwinds DNA to histones, can be transcribed easier
(Active acetylation)

180
Q

Methylations

A

Winds DNA closer to histones, so less likely to be transcribed

FY (4 decks)

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