T5: Infection And Immunity Flashcards

1
Q

4 types of forensic identification

A

Dental records
Fingerprints
Blood groups
DNA profiling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Uses of DNA profiling

A

Identify fluids/individuals
Paternity testing
Track genetic relationships

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Paternity’s testing process

A

DNA band sequence
23 bands (13 loci, 2 chromosomes)
Half align with mother half align with father

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

DNA profiling gene used

A

Intron non coding block
Short tandem repeat
2-50bps
Same locus of homologous chromosomes
Different no. Repeats
Different combination of bps
13 loci used

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

DNA splicing

A

mRNA —> mature mRNA
Only exons left

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

DNA profiling process

A

DNA sample (blood/skin/semen)
STRs extracted using restriction enzymes/amplified with PCR
Fragments separated using gel electrophoresis
Fragments stained
13 loci bands compared

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

DNA gel electrophoresis process

A

DNA in gel well (agarose)
Voltage applied
-DNA—> anode
Smaller fragments?no. Repeats faster
Comparison ladder
Compare base pairs
Use X-ray, fluorescence, DNA stain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Polymerase chain reaction

A

Amplify DNA sequence, make millions of copies from a small sample
25-30 cycles
DNA sample, free DNA nucleotides, DNA primers, DNA polymerase
Desaturated at 95C, H bonds broken, DNA —> ss
Annealing, 55
C, 26 primers bind
Elongation, 70*C, DNA synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Virus structure (5)

A

Some
Receptor proteins
Lipid envelope
Enzymes
All
Protein coat
Nucleic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Bacterial cell wall types

A

Gram +
Cell membrane, thick peptidoglycan
Gram -
Cell membrane, thin peptidoglycan, outer membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Compare and contrast viruses and bacteria

A

V, B
Size: 20-200nm, >1mm
Genetic material: RNA/dsDNA/ssDNA, dsDNA
Membranes: lipid envelope, membrane bound
Need a host cell, can live independently

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name 5 ways of determine time of death

A

Body temp
Degree of muscle contraction
Extent of decomposition
Forensic entomology
Stages of successio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Body temperature TOD

A

Normal 36.5-37.5
Respiration stops
Temperature becomes ambient
Factors (size, position, clothing, wind speed, ambient temp, humidity, air vs water)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Muscle contraction TOD

A

Rigor mortis
ATP need myosin to make actin
Stop respiration
Muscles dont have ATP, fix
Starts 2-4hrs
Finishes 6-8hrs
Starts in face goes down
Muscle fibres breakdown last
Warm, not stiff
Warm, stiff
Cold stiff
Cold not stiff

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Extent of decomposition TOD

A

Bacteria/fungi metabolise tissue
Enzymes digest tissue
Lysosomes rupture
Breakdown cells w enzymes
Anaerobic conditions
Gas forms blisters and bloating
Colour change greenish
Putrefaction, decomp and breakdown, more liquid in corpse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Forensic entomology TOD

A

Bacterial decomp
Attract insects
Pioneer species lay eggs due to smell/moisture
Maggots feed on tissue
3-4 waves
Increase no. Species
Food source runs out
Succession

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Name 4 infection barriers

A

Skin keratin
Skin flora
Gut flora
Stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How is skin keratin an infection barrier

A

Tough
Waterproof
Prevent pathogen netry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How is skin flora an infection barrier

A

Bacteria
Adapted to living on skin
Outcompete pathogens

20
Q

How is gut flora an infection barrier

A

Intensities
Large bacteria population
Outcompete pathogens

21
Q

How is the stomach an infection barrier

A

HCl secreted from parietal cells in stomach lining
pH 2 kills most pathogens

22
Q

Name 4 non specific immune responses

A

Inflammatory
Lysozyme action
Phagocytosis
Interferons

23
Q

Inflammatory response

A

Damaged mast cells release histamine
Histamine dilates arterioles
Increase capillary permeability
Increase no. WBC going to area

24
Q

Lysozyme action

A

Enzymes breaks down bacteria cell walls in tears saliva nd breast milk

25
Q

Phagocytosis (6)

A

Macrophages
Neutrophils
Triple lobe nucelus
Pseudopodia engulf bacterium
Phagocytosis vesicle
Lysosome releases digestive enzymes

26
Q

Interferons

A

Interfere with viral replication in host cells
Bind to infected CSM receptors
Reduce rate of virus binding

27
Q

Compare non/specific immune response

A

Specific
Distinguish non/self
Specific
Diverse
Immunological memory

28
Q

Activation of T cells process

A

Macrophage engulfs antigen
MHC + antigen protein —> APC
T helper cell has comp CD4 receptors
Clones T helper cells and makes T memory cells

29
Q

Activation of B cells process

A

Cloned T helper cells fuse with APC B cells with comp receptors
Release cytokines and B memory cells
Cytokines and B effector cells differentiate into plasma cells that makes antibodies for the antigens

30
Q

Primary response

A

Antibodies from plasma cells bind and label antigens
Macrophages engulf the pathogen
Lysosomes fuse to phagocyte membrane
Release enzymes and digest pathogen

31
Q

Secondary response process

A

Infected cell —> APC
cloned T helper cells bind to APC with comp receptors
Cytokines clone memory cells and T killer cells
T killer cells bind to other infected cells with antigens
T killer cells release any es that am,e pores than ions enter the cell through
Water enters the cell via osmosis
Water lysis
Stray pathogens are engulfed by macrophages

32
Q

Describe the stages of a virus hijacking a host cell

A

Virus attaches to host cell
Inserts Nucleic acid
Acid replicates
Protein coat synthesised
New virus particles formed
Virus particles released via lysis

33
Q

HIV infection process

A

Glycoprotein on membrane binds to T helper CD4
Envelope + T helper membrane fuse
RNA —> cell —> chromosome
Transcriptase and integrase
Tt
Infect T helper cells
Weaker immune system

34
Q

TB infection process

A

Granuloma/turburcule, anaerobic tissue of macrophages and bacteria
Bacteria multiply
Destroy lung tissue (decrease SA/ROGE
Suppress T helper/killer/antibodies
Cough blood
Fever/fatigue

35
Q

Post transcriptal changes

A

Differential splicing
Pre mRNA removes introns by splicosomes
Exons spliced together —> mRNA
Some/all exons removed/reordered
1 gene —> multiple proteins
Tt

36
Q

Name 2 types of immunity

A

Active
Passive

37
Q

Active immunity

A

Ag exposure
Lag phase
Protein made
Memory cells, long term protection
Nat: infection
Art: vaccine

38
Q

Passive immunity

A

External Ab source
No immune response
Immediat
Short term
No memory cells
Nat: maternal Ab
Art: Ab shot

39
Q

2 types of antibiotics

A

Bactreiostatic: prevent multiplication
Bacterioscidal: kill bacteria

40
Q

Evolutionary antibiotic race

A

New treatment/antibiotic/vaccine = selection pressure
Evolve resistance
Escape vaccine
Thrive/reproduce/pass in allele

41
Q

Antibiotic hospital immunity cause

A

Mor antibiotics
More resistance
More mutation

42
Q

Antibiotic hospital immunity solutions

A

Restrict location/frequency of use, reduces selection pressure of antibiotics
Improve hygiene, prevents infection spread
Isolate/screen/report cases, identify risk for/prevent transmission

43
Q

Methods of HIV transfer

A

Blood
Sexual fluids
Needle sharing
Mother to foetus

44
Q

Ways in which antibodies effect antigens

A

Mark for phagocytosis
Soluble toxins are made insoluble and inactive
Clump microorganisms for phagocytes to engulf
Lysis, break open bacteria cell walls

45
Q

Benefits of secondary immune response

A

Shorter lag period
More rapid effector cell reproduction
Greater production of antibodies/T killer cells