Table of Contents
ELEMENT 8 – INFECTION & IMMUNITY .............................................................................. 1
Section 8A: Inflammation & Repair ............................................................................................ 1
8.1: Cell & Tissue Damage 1 .......................................................................................................... 1
8.2: Cell and Tissue Damage II ....................................................................................................... 4
8.3: Acute Inflammation I .............................................................................................................. 6
8.4: Acute Inflammation II ........................................................................................................... 11
8.5: Chronic Inflammation I ......................................................................................................... 15
8.7: Biological Effects of Radiation .............................................................................................. 17
8.8: Healing & Repair ................................................................................................................... 19
Section 8B: Immunology ........................................................................................................... 22
8.9 & 8.10: Innate Immunity I & II ............................................................................................... 22
8.11: Recognition of Antigens...................................................................................................... 29
8.12: Transplantation & HLA/MHC .............................................................................................. 36
8.13 & 8.14: T-cell subsets ........................................................................................................... 38
8.15 & 8.16: Effector Mechanisms: Helpful and Harmful I & II ................................................... 42
8.17: Immunedeficiencies............................................................................................................ 45
8.18: Immune Tolerance and Autoimmunity............................................................................... 47
Section 8C: Microbiology and Infection .................................................................................... 49
8.19: Virus Structure and Classification ....................................................................................... 49
8.26: Normal Microbiota ............................................................................................................. 52
8.20: Virus Replication ................................................................................................................. 55
8.21 & 8.22: History of Microbiology and Bacterial Structures & Virulence Factors ................... 58
8.23: Virus Pathogenesis – Patterns of Infection ......................................................................... 61
8.24: Parasites ............................................................................................................................. 64
8.25: Eukaryotes (Fungi) .............................................................................................................. 68
8.27: Host-Pathogen Interactions ................................................................................................ 69
Section 8D: Control of Infectious Disease ................................................................................. 71
8.28: Dysregulation of the Host Response to Infection ............................................................... 71
8.29: Epidemiology of Infectious Diseases .................................................................................. 72
8.30: Hospital Acquired Infection ................................................................................................ 73
8.31: Modes of Action of Antimicrobials ..................................................................................... 74
8.33: Antibiotic Resistance .......................................................................................................... 76
8.34: Immunisation ...................................................................................................................... 77
8.35: Control of Infection ............................................................................................................ 78
ELEMENT 8 – INFECTION & IMMUNITY
Section 8A: Inflammation & Repair
8.1: Cell & Tissue Damage 1
• What is acute cell injury? Injury to a cell which happens due to a damaging event
,• What is chronic cell injury? Injury to a cell which happened over a period of time and/or recurrently
• How do cells die that suffer from
acute cell injury? Necrosis
• How do cells die that suffer from
chronic cell injury? Apoptosis
• What is necrosis?
Unprogrammed cell death due
to acute cell injury from an
adverse external
environment. The cell swells and
bursts, leading to surrounding
inflammation.
• What is apoptosis?
Programmed cell death due to an
internal event. It is planned and
usually desirable. The cell is
degraded into small
fragments. No inflammation
• What type of things will cause
lethal injury to a cell?
Hypoxia, infection, toxins and
mechanical stresses
• What is hypoxic injury? It’s when
there is a lack of oxygen to the
tissue, leading to ischaemic
necrosis.
• What is the area of ischaemic
necrosis called? An infarct
• Name two common types of infarction. Heart attack, stroke.
• What is the term ‘ischaemic’ generally referring to? Its when there’s a reduction in blood supply to
a tissue, causing a reduction in oxygen and potential subsequent hypoxic injury. For example
ischaemic heart disease is the narrowing of the coronary arteries, meaning you’re more likely to get
a heart attack.
• In what two ways can a myocardial infarct occur? Due to a thrombosis (blockage) or due to
narrowing of the arteries, which causes angina and can cause a heart attack during exercise, when
O2 demand in the heart is high.
• What are the two types of cerebral
infarction?
1. Ischaemic – narrowing of the vessels
means brain tissue doesn’t get enough
oxygen
2. Haemorrhagic – a bleed means that the
tissue itself isn’t getting enough blood
and therefore oxygen
• How can you tell the difference without
a scan? You can’t
• How does this pose problems and deaths?
Ischaemic strokes are more common, so some first responders give blood thinners as standard, in
the hope of unblocking the blockage. This is appropriate for ischaemic strokes, but if it’s
haemorrhagic, giving blood thinners will make the bleed worse and kill the patient faster. It’s hard to
know what to do.
,• What is infective injury? When bacteria or another foreign pathogen causes the damage.
• What types of infective injuries are there?
1. Direct toxic injury – when toxins released by the pathogen causes the damage (e.g.
necrotising fasciitis = flesh eating bacteria. The bacteria release toxins which kill cells)
2. Immunological injury – an indirect injury caused by the hosts response to the micro-
organism (e.g. tuberculosis. The body creates granulomas to compartmentalise the
infection, but this causes tissue inside to become hypoxic and die
• What is toxic shock? When toxins escape the infected cells and cause widespread activation of T
cells in the body
• What is toxic injury? When external toxins like poisons or nerve gases kill the cells.
• How does the nerve gas sarin work? Inhibits acetylcholinesterase so [acetylcholine] stays high and
the muscles are paralysed
• What can mechanical injury be caused by? Extreme cold
(frostbite), extreme heat (burns) or physical damage
• How are burns and frostbites catergorised? According to
how deep they have penetrated: 1st/superficial, 2nd/partial
thickness or 3rd degree/full thickness. In full thickness
damage, blood circulation is disrupted so you can get
ischemic injuries in other parts of the body/limb as well.
• What is the final common path of injury in all forms of
lethal cell injury? Oxidative injury by free radicals such as
hydroxyl (OH-) and superoxide (O2-). These radicals damage
unsaturated bonds of cell membrane proteins and lipids,
allowing water in by osmosis à cell swells and bursts. The free
radicals cant be removed by the ETC because its not
functioning properly.
• What three functions do we use to help define death of a
cell?
1. Boundary functions – for osmotic stability. Free
radicals destroy bonds of the membrane molecules.
2. Energy metabolism – membrane function is
dependent on ATP production. When Na+/K+ pumps
stop working, osmotic gradients change. When
calcium pumps stop working you get erroneous
activation/inhibition of various enzymes such as
kinases and phospholipases.
3. Protein synthesis – cell function impaired when
protein synthesis stops
• What three techniques can be used to assess cell death?
1. Dye exclusion – this tests membrane function, as healthy cells won’t uptake dyes like Trypan
Blue, whereas dead ones will.
2. Radiolabelling newly synthesised proteins
3. Morphology – dead cells become swollen and lose their nuclei and cytoplasmic detail
• What are the four types of necrosis and how do they differ?
Type Description
, Coagulation Most common form. Cytoplasmic protein
are denatures and cells become swollen
‘tombstones’. Cytoplasmic detail disappears.
Liquefaction Proteolytic enzymes digest necrotic cells
into a fluid. Happens in brain tissue
Caseous Necrotic tissue becomes a firm, dry material.
Happens in TB patients due to the
granulomas
Gangrenous This is when necrotic tissue has been
secondarily infected with saprophytic
bacteria, which feed on dead and decaying
matter. These bacteria release their own
toxins, which begin to infect and kill
surrounding healthy cells. Amputation
required.
Fat When lipase enzymes start to digest fat
necrotic cells, resulting in chalky white
deposits
8.2: Cell and Tissue Damage II
• What are the differences between necrosis and apoptosis?
Feature Necrosis Apoptosis
Histology Sheets of cells dying together, Single cells dying, tissue is intact
tissue is disrupted
Cytology Cell swells and intracellular Cell shrinks and contract, and nucleus
features disintegrate and cytoplasm condense à forms
apoptotic bodies
Ultrastructure Membrane ruptures, Membrane and mitochondria stay in
mitochondria and ER swell and tact
ribosomes detach
Circumstances Never physiological, always due Programmed death or due to chronic
to cell injury injury
Effects Inflammation and tissue No inflammation, tissue is intact
destruction
ELEMENT 8 – INFECTION & IMMUNITY .............................................................................. 1
Section 8A: Inflammation & Repair ............................................................................................ 1
8.1: Cell & Tissue Damage 1 .......................................................................................................... 1
8.2: Cell and Tissue Damage II ....................................................................................................... 4
8.3: Acute Inflammation I .............................................................................................................. 6
8.4: Acute Inflammation II ........................................................................................................... 11
8.5: Chronic Inflammation I ......................................................................................................... 15
8.7: Biological Effects of Radiation .............................................................................................. 17
8.8: Healing & Repair ................................................................................................................... 19
Section 8B: Immunology ........................................................................................................... 22
8.9 & 8.10: Innate Immunity I & II ............................................................................................... 22
8.11: Recognition of Antigens...................................................................................................... 29
8.12: Transplantation & HLA/MHC .............................................................................................. 36
8.13 & 8.14: T-cell subsets ........................................................................................................... 38
8.15 & 8.16: Effector Mechanisms: Helpful and Harmful I & II ................................................... 42
8.17: Immunedeficiencies............................................................................................................ 45
8.18: Immune Tolerance and Autoimmunity............................................................................... 47
Section 8C: Microbiology and Infection .................................................................................... 49
8.19: Virus Structure and Classification ....................................................................................... 49
8.26: Normal Microbiota ............................................................................................................. 52
8.20: Virus Replication ................................................................................................................. 55
8.21 & 8.22: History of Microbiology and Bacterial Structures & Virulence Factors ................... 58
8.23: Virus Pathogenesis – Patterns of Infection ......................................................................... 61
8.24: Parasites ............................................................................................................................. 64
8.25: Eukaryotes (Fungi) .............................................................................................................. 68
8.27: Host-Pathogen Interactions ................................................................................................ 69
Section 8D: Control of Infectious Disease ................................................................................. 71
8.28: Dysregulation of the Host Response to Infection ............................................................... 71
8.29: Epidemiology of Infectious Diseases .................................................................................. 72
8.30: Hospital Acquired Infection ................................................................................................ 73
8.31: Modes of Action of Antimicrobials ..................................................................................... 74
8.33: Antibiotic Resistance .......................................................................................................... 76
8.34: Immunisation ...................................................................................................................... 77
8.35: Control of Infection ............................................................................................................ 78
ELEMENT 8 – INFECTION & IMMUNITY
Section 8A: Inflammation & Repair
8.1: Cell & Tissue Damage 1
• What is acute cell injury? Injury to a cell which happens due to a damaging event
,• What is chronic cell injury? Injury to a cell which happened over a period of time and/or recurrently
• How do cells die that suffer from
acute cell injury? Necrosis
• How do cells die that suffer from
chronic cell injury? Apoptosis
• What is necrosis?
Unprogrammed cell death due
to acute cell injury from an
adverse external
environment. The cell swells and
bursts, leading to surrounding
inflammation.
• What is apoptosis?
Programmed cell death due to an
internal event. It is planned and
usually desirable. The cell is
degraded into small
fragments. No inflammation
• What type of things will cause
lethal injury to a cell?
Hypoxia, infection, toxins and
mechanical stresses
• What is hypoxic injury? It’s when
there is a lack of oxygen to the
tissue, leading to ischaemic
necrosis.
• What is the area of ischaemic
necrosis called? An infarct
• Name two common types of infarction. Heart attack, stroke.
• What is the term ‘ischaemic’ generally referring to? Its when there’s a reduction in blood supply to
a tissue, causing a reduction in oxygen and potential subsequent hypoxic injury. For example
ischaemic heart disease is the narrowing of the coronary arteries, meaning you’re more likely to get
a heart attack.
• In what two ways can a myocardial infarct occur? Due to a thrombosis (blockage) or due to
narrowing of the arteries, which causes angina and can cause a heart attack during exercise, when
O2 demand in the heart is high.
• What are the two types of cerebral
infarction?
1. Ischaemic – narrowing of the vessels
means brain tissue doesn’t get enough
oxygen
2. Haemorrhagic – a bleed means that the
tissue itself isn’t getting enough blood
and therefore oxygen
• How can you tell the difference without
a scan? You can’t
• How does this pose problems and deaths?
Ischaemic strokes are more common, so some first responders give blood thinners as standard, in
the hope of unblocking the blockage. This is appropriate for ischaemic strokes, but if it’s
haemorrhagic, giving blood thinners will make the bleed worse and kill the patient faster. It’s hard to
know what to do.
,• What is infective injury? When bacteria or another foreign pathogen causes the damage.
• What types of infective injuries are there?
1. Direct toxic injury – when toxins released by the pathogen causes the damage (e.g.
necrotising fasciitis = flesh eating bacteria. The bacteria release toxins which kill cells)
2. Immunological injury – an indirect injury caused by the hosts response to the micro-
organism (e.g. tuberculosis. The body creates granulomas to compartmentalise the
infection, but this causes tissue inside to become hypoxic and die
• What is toxic shock? When toxins escape the infected cells and cause widespread activation of T
cells in the body
• What is toxic injury? When external toxins like poisons or nerve gases kill the cells.
• How does the nerve gas sarin work? Inhibits acetylcholinesterase so [acetylcholine] stays high and
the muscles are paralysed
• What can mechanical injury be caused by? Extreme cold
(frostbite), extreme heat (burns) or physical damage
• How are burns and frostbites catergorised? According to
how deep they have penetrated: 1st/superficial, 2nd/partial
thickness or 3rd degree/full thickness. In full thickness
damage, blood circulation is disrupted so you can get
ischemic injuries in other parts of the body/limb as well.
• What is the final common path of injury in all forms of
lethal cell injury? Oxidative injury by free radicals such as
hydroxyl (OH-) and superoxide (O2-). These radicals damage
unsaturated bonds of cell membrane proteins and lipids,
allowing water in by osmosis à cell swells and bursts. The free
radicals cant be removed by the ETC because its not
functioning properly.
• What three functions do we use to help define death of a
cell?
1. Boundary functions – for osmotic stability. Free
radicals destroy bonds of the membrane molecules.
2. Energy metabolism – membrane function is
dependent on ATP production. When Na+/K+ pumps
stop working, osmotic gradients change. When
calcium pumps stop working you get erroneous
activation/inhibition of various enzymes such as
kinases and phospholipases.
3. Protein synthesis – cell function impaired when
protein synthesis stops
• What three techniques can be used to assess cell death?
1. Dye exclusion – this tests membrane function, as healthy cells won’t uptake dyes like Trypan
Blue, whereas dead ones will.
2. Radiolabelling newly synthesised proteins
3. Morphology – dead cells become swollen and lose their nuclei and cytoplasmic detail
• What are the four types of necrosis and how do they differ?
Type Description
, Coagulation Most common form. Cytoplasmic protein
are denatures and cells become swollen
‘tombstones’. Cytoplasmic detail disappears.
Liquefaction Proteolytic enzymes digest necrotic cells
into a fluid. Happens in brain tissue
Caseous Necrotic tissue becomes a firm, dry material.
Happens in TB patients due to the
granulomas
Gangrenous This is when necrotic tissue has been
secondarily infected with saprophytic
bacteria, which feed on dead and decaying
matter. These bacteria release their own
toxins, which begin to infect and kill
surrounding healthy cells. Amputation
required.
Fat When lipase enzymes start to digest fat
necrotic cells, resulting in chalky white
deposits
8.2: Cell and Tissue Damage II
• What are the differences between necrosis and apoptosis?
Feature Necrosis Apoptosis
Histology Sheets of cells dying together, Single cells dying, tissue is intact
tissue is disrupted
Cytology Cell swells and intracellular Cell shrinks and contract, and nucleus
features disintegrate and cytoplasm condense à forms
apoptotic bodies
Ultrastructure Membrane ruptures, Membrane and mitochondria stay in
mitochondria and ER swell and tact
ribosomes detach
Circumstances Never physiological, always due Programmed death or due to chronic
to cell injury injury
Effects Inflammation and tissue No inflammation, tissue is intact
destruction
