Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Med Yr2 > Body defence > Flashcards

Body defence Flashcards

1
Q

Aims of inflammation (3)
- C
- D
- H

A
  • Contain and isolate the injurious stimulus
  • Destroy, dilute or wall off the agents and neutralise toxins
  • Heal and repair damage caused
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Acute inflammation: 5 cardinal signs
- H
- R
- S
- P
- L

A
  • Heat: hyperthermia
  • Redness: Hyperaemia
  • Swelling: exudate
  • Pain: neural damage, chemical mediators
  • Loss of function: pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Acute inflammation: pathogenesis (3)

A
  • Vascular changes
  • Cellular events
  • Chemical mediators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Vascular changes due to acute inflammation: vascular calibre
(What happens)

A
  • Rapid transient vasoconstriction of arterioles followed by vasodilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Vascular changes due to acute inflammation: blood flow

A
  • Initial reduction followed by increased blood flow to capillaries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Vascular changes due to acute inflammation: vascular permeability

A
  • Increased permeability of microvasculature
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Inflammatory swelling cause:

A

Oedema due to accumulation of exudate in the interstitium

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

Exudate properties:
- origin
- Protein content
- Sp.gravity

A
  • Inflammatory extravascular fluid
  • Protein rich
  • Sp. Gravity > 1.020
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Non-inflammatory swelling cause:

A

Oedema due to accumulation of transudate in the interstitium

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

Transudate properties:
- Origin
- Protein content
- Sp.Gravity < 1.020

A
  • Ultra filtrate of blood
  • Low protein contents
  • Sp. Gravity < 1.020
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cellular events due to acute inflammation: transmigration and degranulation of leukocytes
- General mission of leucocytes

A
  • Leucocytes need to move from the circulation to the site injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cellular events due to acute inflammation: transmigration and degranulation of leucocytes
- Extravasation

A
  • Endothelial cells and leucocytes express mutually recognising adhesion molecules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cellular events due to acute inflammation: transmigration and degranulation of leucocytes\
- Migration

A
  • Leucocytes move following concentration gradients of chemicals and infl mediators (chemotaxis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cellular events due to acute inflammation: phagocytosis
- General mission of phagocytes

A
  • Phagocytes bind the material to ingest in a multistep process
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Cellular events due to acute inflammation: phagocytosis
- Recognition and attachment

A
  • Using its own receptors or to molecules that have been marked by other cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Cellular events due to acute inflammation: phagocytosis
- Engulfment

A
  • pseudopodia surround the agent producing a vacuole, phagosome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cellular events due to acute inflammation: phagocytosis
- Killing/degradation

A
  • lysosomal granules fuse with the phagosome activating the destruction by releasing lysozyme, proteases, hydrolase (O2 independent) and toxic superoxides (oxygen dependant)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Chemical mediators of acute inflammation: Plasma mediators
- Form
- System examples (3)

A
  • Need to be activated from precursor form
  • Coagulation system
  • Kinin system
  • Complement system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Plasma mediators: Coagulation system
- Activated by
- Produces (3)

A
  • Tissue damage
  • Fibrin
  • Thrombin
  • Factor Xa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Plasma mediators: coagulation system
- Fibrin role

A
  • Helps contain infections
  • Cross links platelets at site of wound
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Plasma mediators: coagulation system
- Thrombin role

A
  • increases leukocyte adhesion and fibroblast proliferation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Plasma mediators: coagulation system
- Factor Xa role

A
  • Increases vascular permeability and leucocyte exudation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Plasma mediators: kinin system
- Activation
- End product
- End product role

A
  • Activated by coagulation factor XII
  • Produces bradykinin
  • Causes vasodilation and triggering pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Plasma mediators: complement system

A
  • 20 components
  • Foreign expression of adhesion molecules on leucocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Complement system component roles
- Membrane attack complex (MAC) C5-9:

A
  • Lysis of microbes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Complement system component roles
- C3b

A
  • Acts as an opsonin (signals for phagocytosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Complement system component roles
- C5a

A
  • Powerful chemotactic agent (stimulates cell migration)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Complement system: Anaphylatoxins
- 2 examples
- Effects

A
  • C3a and C5a
  • Increase vascular permeability and cause vasodilation via histamine release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Chemical mediators of acute inflammation: Vasoactive amines (2)

A
  • Histamine
  • Serotonin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Vasoactive amines of acute inflammation: histamine
- Produced by
- Released in response to (2)
- Effects

A
  • Mast cells, basophils, platelets
  • Physical injury and immune reactions
  • Dilation of arterioles, increases vascular permeability of venules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Vasoactive amines of acute inflammation: serotonin
- Produced by
- effects

A
  • Platelets and enterochromaffin cells
  • Similar actions to histamine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Cell mediators of acute inflammation: arachidonic acid metabolites
- Causes

A

-Prostaglandins
- Arteriolar dilation
- Pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Cell mediators of acute inflammation: Cytokines and chemokines
- Effects (2)

A
  • Increased vascular permeability
  • Chemotaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Cell mediators of acute inflammation: Nitric oxide
- Effect

A
  • Vasodilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Cell mediators of acute inflammation: Platelet activating factor
- Effects (3)

A
  • Platelet aggregation
  • Increased vascular permeability
  • Activation of leucocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Cell mediators of acute inflammation: lysosoaml constituents of leukocytes and O2 derived free radicals
- Effect

A
  • Phagocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Cell mediators of acute inflammation: Neuropeptides
- Effect

A
  • Pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Acute inflammation - Systemic effects: fever
- Caused by (3)
- Method

A
  • IL1, IL6 and TNF
  • Release of prostaglandins affectioning the hypothalamic thermostat higher
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Acute inflammation - systemic effects: Malaise/lethargy/sleepiness
- Caused by

A
  • Cytokines affecting the brain to reduce behaviour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Acute inflammation - Systemic effects: Pain
- Caused by (2)

A
  • Prostaglandins
  • Bradykinin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Acute inflammation - Systemic effects: Leucocytosis

A
  • Colony stimulating factors stimulate release of leucocytes from the marrow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Acute inflammation - Systemic effects: Tissue damage
- Causes (3)

A
  • Neutrophil and Macrophage lysosomal enzymes
  • Oxygen metabolites
  • Nitric oxide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Acute inflammation - systemic effects: other (2)

A
  • Swelling in a confined space (e.g. brain)
  • Hyperexia, shock and death due to too many cytokines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Acute inflammation morphology: Serous inflammation

A
  • Exudation of transudate into space caused by tissue damage (skin blister) in in body cavities (effusion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Acute inflammation morphology: Fibrinous inflammation

A
  • Fibrinogen exits the blood and accumulates a fibrin in extracellular space
  • Due to increased vascular permeability/procoagulant stimuli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Acute inflammation morphology: Purulent inflammation

A
  • Production of pus, comprising of neutrophils, dead or alive, cellular debris and oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Exudate, pus, abscess and empyema definition

A
  • Exudate is a fluid with a protein content similar to plasma
  • Pus is an inflammatory exudate rich in white blood cells, living and dead plus or minus microorganisms
  • Abscess is a localised collection of pus surrounded by fibrous
    tissue.
  • Empyema: pus formation in existing body cavity (pleura, joints,
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Chronic inflammation pathogenesis: (3)

A
  • Persistent infection by organisms with low toxicity, triggering delayed hypersensitivity
  • Prolonged exposure to non degradable toxic agents. Exogenous (asbestos), Endogenous (plasma lipids)
  • Autoimmune diseases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Chronic inflammation: macrophage accumulation persistence
- Caused by

A
  • Continuous recruitment from circulation
  • Local proliferation
  • Immobilisation of peripheral macrophages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Chronic inflammation: morphology
Can cause

A
  • Healing due to fibrous tissue replacement
  • Tissue destruction and necrosis
  • Chronic non specific inflammation (granulation tissue)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Chronic inflammation: Granulation tissue (non specific)

A
  • Vascularised fibrous tissue that replaces the fibrin clot.
  • Contains blood vessels, fibroblasts and macrophages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Chronic inflammation: Granuloma (specific)
- Types (2)
- Role

A
  • Non necrotising and necrotising granulomas
  • Granulomas destroy or isolate pathogens/foreign material, but may cause tissue damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Healing and repair: multistep process

A
  • Regeneration: growth of cells and tissues to replace lost structures
  • Scar formation: laying down of fibrous tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Healing and repair: causes for variation in results (4)

A
  • Nature of the trauma
  • Severity
  • Duration of the damage (acute vs chronic)
  • Tissue type
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Cell renewal:
- proliferation
- differentiation

A
  • Proliferation: will replace lost cells
  • Differentiation: will replace complex architectural structures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Variation in cells ability to proliferate: Labile cells

A
  • Cells that continuously regenerate (epidermis)
  • Good capacity to proliferate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Variation in cells ability to proliferate: Stable cells

A
  • Cells that multiply only when needed (hepatocytes)
  • Slow proliferation rate unless necessary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Variation in cells ability to proliferate: permanent cells

A
  • Cells that do not multiply (neurons, cardiac muscle)
  • No effective regeneration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Repair of wounds by deposition of fibro-connective tissue:

A
  • New blood vessels form at wound site (angiogenesis)
  • Migration and proliferation of fibroblasts (myofibroblasts)
  • Synthesise extracellular matrix proteins (collagen) for mechanical support, regulation of cellular functions and wound strength
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Healing by primary intention: (4)

A
  1. Wound edges joined by fibrin plug
  2. Regrowth of basal layer off epidermis
  3. Lysis of fibrin and re-epitheliaslisation
  4. restoration to intact skin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Healing by secondary intention: (4)

A
  1. Large defect filled by fibrin clot
  2. New blood vessels and fibroblasts (granulation tissue) grow from dermis
  3. Granulation tissue fibroblasts restore integrity by laying down collagen
  4. Collagen matures, allowing regrowth of epidermis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Healing by first intention effects: (3)

A

*Induction of an acute inflammatory
process by wounding/damage
*Granulation tissue
* Migration and proliferation of both
parenchymal and connective tissue
cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Healing by secondary intention effects: (6)

A
  • Inflammatory reaction is more intense (more debris and exudate)
  • Larger amount of granulation tissue is formed* Synthesis of extracellular matrix proteins * Remodelling of connective tissue and
    parenchymal components
  • Collagenisation and acquisition of wound strength
  • Wound contraction (by myofibroblasts)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

The requirements of the immune system: (2)

A
  • Protective: the most effective means to destroy pathogens
  • Preservative: immune mediated protection without disrupting normal physiological functions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Autoimmunity:

A

failure to distinguish self from non-self cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Immunopathology:

A

Tissue damage caused by excessive immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Allergy:

A

mounting an immune response to an environmental material

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Immune deficiency:

A

Lack of functional immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Innate immune system: skin
- Physical barrier characteristics (3)
. Layers
. Epithelium type
. Further??

A
  • Multi-layered
  • Stratified squamous epithelium
  • Dead cornified, non-nucleated cells bound in keratin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Innate immune system: skin
- Chemical barrier
. Conditions
. Sweat secretions
. Sebaceous gland secretion

A
  • Lacking water
  • Lactic acid, alcohol, Lysozymes
  • Free fatty acids, wax
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Innate immune system: skin
- Microbiological

A
  • Commensals (normal flora) reduce nutrients and produce more fatty acids, compete with pathogens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Innate immunity: alimentary tract
- Physical barrier

A
  • Peristalsis by the oesophagus
  • Desquamation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Innate immunity: alimentary tract
- Chemical barrier (4)

A
  • Stomach acid (pH 2.0)
  • Gastric enzymes
  • pancreatic enzymes
  • Bile salts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Innate immune response outcomes:
- At best
- At worst

A
  • eradicates the infection
  • Delays infection until an adaptive immune response is generated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Cellular innate immune defence: Macrophages
- Role

A
  • Kill intracellular pathogens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Cellular innate immune defence: Neutrophils
- Role

A
  • kill rapidly dividing bacteria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Cellular innate immune defence: Eosinophils
- Role

A
  • Kills parasites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Cellular innate immune defence: Basophils
- Role

A
  • Trigger allergic reactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Cellular innate immune defence: Mast calls
- Role

A
  • Trigger inflammatory response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Cellular innate immune defence: Natural killer cells
- Role

A
  • Kills virus infected cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Cellular innate immune defence: Dendritic cells
- Role

A
  • Activate adaptive immune response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Non-cellular innate immune defence: Complement

A
  • Opsonises pathogens with layer of marker molecules, marking them for phagocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Non-cellular innate immune defence: Acute phase proteins

A
  • Similar to complement and and activates complement system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Non-cellular innate immune defence: Interferons (3 steps)

A
  • Interferons are induced in viral infected cells and secreted
  • Interferons bind to adjacent cells, signal transduction pathways are activated and interferon-inducible gene products are expressed
  • This induces an antiviral state (cell can no longer support viral reproduction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Macrophages:
- Sentinel
- Pseudopodia
- Migration
- Phagocytosis
- Size

A
  • Sentinels (signal) of danger/infection
  • Pseudopodia: temporary arm-like projections to grab pathogens
  • Migration: exist in the blood stream inactive, activated when entering tissue
  • Phagocytosis: engulf and destroy pathogens, dead neutrophils and tissue debris
  • Size: largest phagocytes, long lived
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Neutrophils:
- Abundance
- Migration (Diapedesis):
- Lifespan

A
  • 70% of WBCs
  • Diapedesis: neutrophils squeeze out of blood vessels towards the site of damage (chemotaxis) via amoeboid movement
  • Lifespan: a few days / self-destruct after phagocytosing 5-25 objects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Natural Killer cells:
- Lifespan
- Action

A
  • Very short lived (7-8 hours)
  • NK cells attack virus infected cells via surface membrane changes:
    . Pore insertion (perforin)
    . Apoptosis (granzymes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

The relationship between the innate immunity and adaptive immunity:

A

The adaptive immune response enhances the efficiency of some determinants of the innate immune response. It provides memory which enhances the speed of secondary exposure (response)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

B-lymphocytes: role

A
  • Produce antibodies and present antigens to T-lymphocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

T-lymphocytes: role

A
  • Help co-ordinate the immune response and kill infected cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Clonal expansion:

A
  • A pool of diverse naive lymphocytes sits in the lymph nodes
  • When an antigen binds to its complimentary receptor on a lymphocyte, a clonal expansion of this lymphocyte occurs (massive increase in number)
  • Some clones fight infection, some remain in the memory pool
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Isotope switching after activation:

A
  • All newly formed B cells express monomeric IgM and IgD at the cell surface as receptors
  • Following activation, B cells undergo isotope switching to produce different types of antibodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Primary adaptive immune response to an antigen:
- Lag phase
- Effect on serum
- Secretion contents
- Long term effect

A
  • B cells undergo clonal selection in response to an antigen, proliferate and differentiate into plasma cells
  • Exponential increase in serum antibody levels, peaks at 7-10 days, then declines
  • Initially all IgM secretion but some IgG is produced later in the response
  • Formation of memory B cells
94
Q

Secondary adaptive immune response to an antigen:

A
  • Mediated by memory B cells formed in primary response
  • Shorter lag phase and higher antibody production than primary response
  • Antibody affinity for the antigen is higher than in the primary response
  • Includes various secondary antigens, not just IgG
95
Q

B lymphocyte recognition of antigens: (3)

A
  • B lymphocytes express immunoglobulin molecules on their surface
  • Antigens bind to theses immunoglobulin molecules, cross-linking them
  • This triggers signals that activate the B cell
96
Q

Effector B-cells (plasma cells): role

A
  • Secrete a soluble form of immunoglobulin (antibodies)
97
Q

Immunoglobulin:
- definition
- structure

A
  • The basic structure of an antibody
  • two identical heavy (long) chains and two identical light (short) chains, bound by disulphide bonds
98
Q

Immunoglobulin: heavy chain structure

A
  • One variable region, multiple constant regions
99
Q

Immunoglobulin: light chain structure

A
  • One variable region, one constant region
100
Q

Immunoglobulin:
-Fab
- Fc

A
  • Fragment for antibody binding, acts as the specific “key” for antigens
  • Fragment crystallisable, binds to effector cells, triggering function
101
Q

Antibody types: Dimeric IgA
- Location

A
  • found in mucous, saliva, tears and breast milk
102
Q

Antibody types: IgD

A
  • It is part of the B cell
  • Activates basophils and mast cells
103
Q

Antibody types: IgE

A
  • Protects against parasitic worms, also causes allergic reactions
104
Q

Antibody types: IgG
- Location
- Role

A
  • Secreted by plasma cells in the blood
  • Able to cross the placenta into the fetus, providing protection for the neonate
105
Q

Antibody types: IgM
- Location (2)
- Role
- Structure

A
  • Can be attached to the surface of a B cell or secreted into the blood
  • Responsible for early stages of immunity
  • Pentamer
106
Q

Antibody functions: Neutralisation

A
  • Antibodies bind to a virus, toxin or bacteria, blocking them from binding to cells
107
Q

Antibody functions: Opsonisation

A
  • Antibodies bind to a bacteria, they then bind their Fc receptors to a macrophage cell for phagocytosis
108
Q

Antibody functions: ADCC

A
  • Antibody dependant cellular cytotoxicity: antibodies bind to antigens on target cell. Fc receptors on NK cells recognise the antibody, taget cell is destroyed
109
Q

Antibody functions: Activation of the complement cascade

A
  • IgG or IgM bind to antigens on bacterial surface. C1q binds to the antibodies, causing a cascade of other proteins to bind, punching a hole in the bacteria
110
Q

Antibody functions: triggering mast call activation: IgE binds to mast cell

A
  • IgE binds to mast cells, triggering degranulation, releasing histamines and serotonin (allergy)
111
Q

Antibody functions: eosinophil activation

A
  • Triggers parasite destruction
112
Q

T cell:
- Role
- Locations
-Recognition

A
  • Provide a cellular defence
  • Produced in the bone marrow and mature in the thymus, then enter circulation
  • Can only recognise short linear amino acid sequences of peptides
113
Q

Dendritic cells:
- Role

A
  • Dendritic cells act as APCs (antigen presenting cells). They take up bacterial antigens at the skin and transport the antigens (whilst processing them) to draining lymph nodes, where they present them to T and B cells
114
Q

Antigen recognition by naive T cells:

A
  • The T cell receptor (TCR) does not bind with the full soluble antigen
  • It recognises peptide fragments of antigens that are processed and presented by major histamine complex (MHC) molecules
115
Q

Major histamine complex:

A
  • A molecule on the surface of APCs, the part of a APC that presents the peptide fragment of a processed antigen
116
Q

Expression of MHC class 1and 2 molecules:
- Class 1
- Class 2

A
  • All nucleated cells (except neurones, sperm, some placenta cells) express MHC class 1
  • Only antigen presenting cells (Dendritic cells, B cells and macrophages) express class 2 MHC molecules
117
Q

Endogenous antigens:

A
  • Synthesised within the antigen presenting cells, can be self or non-self (e.g. virus proteins)
  • Presented by class 1 MHC
118
Q

Exogenous antigens:

A
  • Synthesised outside fo the antigen presenting cell and internalised; can be self or non-self (e.g. bacteria, toxins)
  • Presented by class 2 MHC
119
Q

Endogenous antigen-class I pathway: (5)

A
  • Cell infected by virus or bacteria or a cancer cell
  • Newly made foreign/self proteins expressed within cytoplasm
  • Proteins modified and broken down into peptides by proteosomes
  • Peptides transported via to ER, complexed with MHC class I proteins, inserted into membrane
  • Recognised by CD8+ cytotoxic T cells, activating killer T cells
120
Q

Exogenous Antigen class II pathway: (4)

A
  • Extracellular antigens are taken up by endocytosis by APCs
  • They are degraded into peptides in a phagosome
  • Phagosomes fuse with MHC class II, containing lysosome vesicles, complex with peptides inserted into membrane
  • Recognised by CD4+ helper T cells, activating helper T cells
121
Q

APCs deliver three signals to naive T cells:

A
  1. Activation: Interaction of TCR with peptide - MHC complex
  2. Survival: provided by co-stimulation
  3. Differentiation: provided by cytokines
122
Q

CD4+ T helper cell (Th) differentiation: Th1 cells
- Helps fight:
- Produces:

A
  • intracellular bacteria, viruses, cancer
  • IFN-gamma by activating T-bet gene
123
Q

CD4+ T helper cell (Th) differentiation: Th2 cells
- Fights against:
- Produces:

A
  • Extracellular bacteria, parasites, toxins, allergens
  • IL-4 by activating GATA3 gene
124
Q

CD4+ T helper cell (Th) differentiation: Th1 cells
- Action

A
  • Travels to infected tissue where macrophages present bacterium antigens
  • The Th1 cell binds to the antigens and activates the macrophage, killing the bacteria
125
Q

CD4+ T helper cell (Th) differentiation: Th2 cells
- Action

A
  • interact with antigen specific B cells in lymphoid tissue.
  • Th2 activates the B cell, which then produces antitoxin antibodies
126
Q

CD4+ T helper cell (Th) cell differentiation: Cytotoxic CD8+ cells
- Role
- Signals required

A
  • selective killers of target cells at the sites of infection , generated against endogenous antigens (viruses)
  • Armed effector CD8+ cells without co stimulation
127
Q

Importance of viruses: (4)

A
  • Greater impact in poorer countries
  • They infect every living thing
  • Climate effect
  • 8% of human genome contains ancient viral DNA
128
Q

Healthcare impact of viruses in the UK:
- Direct:
- Indirect:
- Costs:

A
  • Direct: acute illness, chronic illness, redirected resources, death
  • Indirect: loss of function, loss of earnings, economic productivity, healthcare costs
  • Costs: NHS costs, economic £370 billion spent, NHS backlog
129
Q

Basic virology: general features of a virus
- Replication requirements
- Size
- Transmission
- Energy production

A
  • Dependant on living cells for replication (obligate intracellular pathogen)
  • Sub-microscopic: 10-300nm in size
  • Have either RNA or DNA genomes surrounded by a protein coat
  • Progeny virus particles transport the genome to a new host cell where the infectious cycle begins again
  • Metabolically inert and lack genes coding for energy production
130
Q

Virus transmission:
- Direct (3)
- Indirect (4)
- Fluids (6)

A
  • Direct: contact, droplets, aerosol
  • Indirect: vehicle born, fomites, vectors, airborne
  • Fluids: Respiratory secretions, urine, faeces, vomit, blood, semen
131
Q

Viral lifecycle strategies: (5)

A
  • Short lived illness, highly infectious: measles
    • Infectious before illness develops: hepatitis A
    • Asymptomatic/ subclinical infection: almost all
    • Latency and reactivation: herpesviruses
      • Persistent infections: HIV, HPV, HCV
132
Q

Lymphadenopathy:

A

a disease of the lymph nodes, in which they are an abnormal size or consistency (infection, inflammation, cancer)

133
Q

Neural spread of a virus:

A

Herpes Simplex Virus (HSV) is highly neuroinvasive for peripheral nervous system, rarely enters CNS but I it does it has high neurovirulence (poor outcome)

134
Q

Intra-host viral spread: bloodstream/lymphatic system

A
  • Direct entry via capillaries
  • Endothelial cell replication
  • Injection / inoculation
135
Q

Viraemia:
- Definition
- location (2)

A
  • Presence of virus in the blood
  • Virus may be free in the blood or contained within infected cells
  • Virus has access to almost all organs
136
Q

Intra-host viral spread: nervous system (2)

A
  • Usually precede by viraemia
  • In some cases spread occurs by direct contact by the neurones at the primary site of infection
137
Q

Viral pathogenesis: (3)
- Definition
- Occurence
- Practicality?

A
  • the process by which a viral infection leads to disease, Often of no value to the virus.
  • Many viruses are subclinical
  • It is of no interest to the virus evolution to harm the host
138
Q

Factors in pathogenesis (5)

A
  • Cellular pathogenesis
  • Portal of entry and course of infection
  • Cell/tissue tropism
  • Cell tissue damage
  • Host immune response
139
Q

Viral pathogenesis terms:
- Virulent virus:
- Avirulent or attenuated strain:
- Host factors:

A
  • Causes significant disease
  • Causes no or reduced disease
  • Age, gender, immunity/immunosuppression, genetic susceptibility
140
Q

Types of outcome for viral infections: Acute infection

A
  • Recovery with no residual effects - typical
  • Recovery with residual effects
  • Death
  • Progression to chronic infection
141
Q

Types of outcome for viral infection: chronic infection (5)

A
  • Silent subclinical infection for life (CMV, EBV)
  • A long silent period before disease (HIV)
  • Reactivation to cause acute disease (herpes, shingles)
  • Chronic disease with relapse and exacerbations (HBV,HBC)
  • Cancers (EBV, HTLV-1, HPV etc.)
142
Q

Viral tropism:

A
  • After host entry, tropism influences disease type. It is the capacity of viruses to infect and multiply in discrete tissue and cells
143
Q

Types of viral tropisms:
- Lungs
- Liver
- Brain
- Skin
- Joint tissue

A
  • Lungs = pneumonia
  • Liver = jaundice
  • Brain = encephalitis
  • Skin = rashes
  • Joint tissue = arthritis
144
Q

Germ history: three main areas of study

A
  1. Observations of the contagious nature of disease
  2. Experimentation with vaccination
  3. Research into the nature of microorganisms
145
Q

Bacterial form diversity: three main shapes

A
  1. Coccus (pl. cocci, egg shaped, pink)
  2. Bacillus (pl. bacilli, cylindrical, yellow)
  3. Spirochete (spiral, orange)
146
Q

Prokaryotes VS Eukaryotes
- no. DNA strands
- Histones
- Imported DNA?
- T and T

A
  • One copy of double strand DNA, contained in a nucleoid
  • Histones not required for DNA conformation
  • Can contain up to 34% imported DNA (plasmids)
  • Transcriptiion and translation are coupled (proteins encoded as mRNA is synthesised)
147
Q

Bacterial structure - genome
- Genome
- Core genome
- Accessory genome

A
  • Genome: the entirety of genetic information contained within a cell
  • Core genome: Conserved genes for fundamental and essential cellular processes, shared between most members of a species
  • Accessory genome: Almost infinite pool of genes which may be recruited into the genome of the bacterial cell (PLASMIDS)
148
Q

Bacterial cytoplasmic features: structure

A
  • 30S and 50S subunits forming a 70S ribosome
149
Q

Bacterial cytoplasmic features: proteins produced (3)

A
  • Structural proteins
  • Enzymes
  • Regulators (inducible system)
150
Q

Bacterial cytoplasmic membrane: (4)
-Symporter
- Flagellum
- Antiporter
- Cytochrome

A
  • Symporter: Simultaneous transport of two ions across membrane in same direction
  • Flagellum: movement
  • Antiporter: simultaneous transport of two ions across membrane in different directions
  • Cytochrome: Redox activation protein, for ATP generation, 2H+ in, ADP + P = ATP
151
Q

Gram negative bacteria:

A
  • Surrounded by a thin peptidoglycan cell wall, which is surrounded by an outer membrane of lipopolysaccharide
152
Q

Gram positive bacteria structure:

A
  • Cell-wall is composed of thick layers of peptidoglycan, linked by inter-peptide bridges. Absence of outer membrane
153
Q

Transpeptidases and Carboxypeptidases:
- Role
- Targeted
- Effect

A
  • Enzymes responsible for cross linkages
  • Target sites for beta-lactam antibiotics (penicillin), works by inhibiting cross linking of peptidoglycan chains
  • The bacterial cells leak and lyse (die)
154
Q

Gram staining: (4)

A
  1. Crystal violet is added
  2. Iodide complexes added to the crystal violet
  3. Decolourizer releases loosely bound stain (gram negative)
  4. Counter stain utilised for cells not dyed, resulting in
    purple = gram + pink = gram -
155
Q

Bacterial structures: toxins
- exotoxin

A
  • Exotoxin: natural product of metabolism, actively secreted out of the cell, E.G. toxic shock syndrome toxin 1
156
Q

Bacterial structures: toxins
- Endotoxin

A
  • Integral to the cell wall, not actively secreted, released upon cell death
157
Q

Bacterial structures: Capsule (2)

A
  • Capsules are rigid, slime layers
  • Highly variable, resulting in multi-faceted functions
158
Q

Bacterial capsule functions (3)

A
  1. Protects from dehydration and environmental extremes
  2. Protects from phagocytosis
  3. Mimics host carbohydrates
159
Q

Bacterial structures: flagellum

A
  • Utilised for motility via rotation, not possessed by all bacteria
160
Q

Flagellum organisation:
- Polar
- Lophotrichous
- Amphitrichous
- Peritrichous

A
  • Polar: singular, one end
  • Lophotrichous: multiple, one end
  • Amphitrichous: Singular at each end
  • Peritrichous: Multiple all over
161
Q

Bacterial structure: pili/fimbriae
- Role
- Organisation
- Target

A
  • Proteinaceous fibres used for adhesion
  • Organised peritrichously (all over) the bacterial cell surface, may number 1000s
  • Generally have a specific target on host surface
162
Q

Bacterial structure: sex pili
- Conjugation

A
  • Transfers plasmids between bacterium
  • Conjugation: the direct transfer of plasmids between bacterium, plasmids become facilitators of horizontal gene transfer
163
Q

Colonisation:

A
  • The presence of a microorganism on/in a host, with growth and multiplication of the organism, but with no host-organism interaction
164
Q

Contamination:

A
  • Non-intended/accidental introduction of infectious material or their toxins/by-products
165
Q

Invasions:

A
  • The infection and multiplication of microorganisms (bacteria, viruses, parasites) that are not normally present within the body
166
Q

Ecto-parasites:

A
  • Parasitic organisms that may live on, but not within, a host
  • E.g. Headlice
167
Q

Endo-parasites:

A
  • Parasitic organisms that live, or complete most of their life cycle, within a host
168
Q

Incubation period:

A
  • the time interval between initial contact with infectious agent and the first appearance of symptoms
169
Q

Period of communicability:

A
  • the time during which an infectious agent may be transferred directly or indirectly from an infected organism
170
Q

Neisseria menigitis:
- transmission

A
  • Aerosol transmitted bacterium
171
Q

Neisseria meningitidis: dissemination (2)

A
  • Enters the nasopharynx and forms a colony on the epithelium using a receptor that binds to a ligand (CEACAM1).
  • The bacteria then either enters the epithelium (invades) or detaches and goes elsewhere
172
Q

Neisseria meningiditis: effects

A
  • Causes inflammation of the meninges in the brain. Once the infection reaches the dura mater, onset is very fast, inflammation is induced and infection spreads quickly
173
Q

Mechanisms of mucosal penetration: Transcellular

A
  • Pathogen binds to ligand receptors on the cell surface membrane, either activating a pathway or activating toxins to break through
174
Q

Mechanisms of mucosal penetration: Trojan-horse mechanism

A
  • Pathogen is phagocytosed and carried into the cell, it exits the macrophage and disseminates through the body
175
Q

Mechanisms of mucosal penetration: Paracellular

A
  • Pathogen passes through tight junctions by breaking them down, it then reseals the junctions, preventing them from being pushed out
176
Q

Bacteraemia:

A
  • the presence of bacteria within the bloodstream
177
Q

Sepsis:

A
  • a life-threatening reaction to an infection. The immune system begins to damage the body’s own tissues and organs
178
Q

Hypersensitivity
- definition

A
  • General term used to describe adverse reaction to an antigen
179
Q

Hypersensitivity: Type 1

A
  • IgE mediated
180
Q

Hypersensitivity: type 2

A
  • IgG mediated
181
Q

Hypersensitivity: type 3

A
  • Immune complex mediated
182
Q

Hypersensitivity: type 4

A
  • t cell mediated
183
Q

Adaptive immune response: virally infected cell (2)

A
  • Cell presents viral peptide via class 1 MHC
  • Activates cytotoxic T cell, killing the infected cell and releasing interferons to increase viral resistance
184
Q

Adaptive immune response: APCs for viruses

A
  • Class 2 MHC on a macrophage presents viral peptide
  • Activates TH1 cell, producing cytokines (IL-2). These kill the presented virus and activate cytotoxic T cells
185
Q

Adaptive immune response: APC for bacteria

A
  • Bacterial peptide presented to TH2 cell
  • Cytokines IL-4, 5, and 6 are produced, which activate B cells to produce antibodies
186
Q

Factors favouring protective immunity (Th1): (4)

A
  • Presence of older siblings
  • Early exposure to day care
  • Tb, measles or Hep A infection
  • Rural environment
187
Q

Factors favouring allergic disease (Th2): (3)

A
  • Widespread use of antibiotics
  • Western lifestyle
  • Urban environment
188
Q

Type 1 hypersensitivity: Initiating event (3)
- Initiation
- Binding
- Re-exposure

A
  • A soluble antigen (allergen) triggers an IgE response from activated plasma cells
  • IgE binds to FcRs
  • Subsequent antigen exposure leads to interaction with IgE on mast cells / basophils causing degranulation and the release of mediators, causing acute allergic reaction
189
Q

Route and dose of allergen in type 1 hypersensitivity
1. IV high dose
2. SC low dose
3. Inhalation
4. Ingestion

A
  1. Systemic anaphylaxis
  2. Local wheal and flare
  3. Rhinitis / bronchospasm
  4. Urticaria, diarrhoea, vomiting
190
Q

Mediators of type 1 hypersensitivity: Cytokines
- Th2 response
- Eosinophil synthesis / release

A
  • IL-4 and IL-13 involved in Th2 response
  • IL-3, IL-5, GM-CSF involved in eosinophil synthesis / release
191
Q

Mediators of type 1 hypersensitivity: Lipid mediators
- What (2)
- What do they mediate?

A
  • Leukotrienes C4 and D4
  • Smooth muscle contraction, increased vascular permeability, mucus production
192
Q

Mast cell tryptase:
- Role
- Lifespan

A
  • Very specific marker of mast cell degranulation
  • Raised between 1 and 6 hours with short t 1/2 (~2 hours)
193
Q

Type 1 hypersensitivity: examples and causes (2)

A
  • Acute symptoms of allergic rhinitis: Allergens HDM, pollens, animal dander etc.
  • Anaphylaxis: Drugs, latex, insect venom
194
Q

Iatrogenic Anaphylaxis:
- Definition
- Symptoms in case

A
  • Life threatening allergic reaction caused by medical treatment
  • Tachycardia, cardiac arrest requiring CPR
195
Q

Type 2A hypersensitivity route of action:
- Character
- Antibody interaction
- Binding
- Mediation?

A
  • Cytotoxic
  • IgG antibody interacting with cell surface antigens
  • Binding of IgG to antigen cell (e.g. macrophage) causes lysis of target cell
  • Complement mediated
196
Q

Type 2A hypersensitivity examples: (3)

A
  • Certain allergic drug reactions (e.g. penicillin)
  • Incompatible blood transfusion
  • Auto-immune haemolytic anaemia
197
Q

Type 2B hypersensitivity:
- Affects?
- Antibody interactions

A
  • Cell stimulating reactions involving altered cell function
  • IgG interacts with cell surface receptors involved in signalling. IgG may be an agonist or antagonist
198
Q

Type 2B hypersensitivity examples:

A
  • Graves disease: agonist TSI
  • Myasthenia Gravis: antagonist anti-AChR antibody
199
Q

Type 3 hypersensitivity:
- Character
- Effects
- Example

A
  • an abnormal immune response is mediated by the formation of antigen-antibody aggregates called “immune complexes
  • Deposits in micro-vasculature, Activates the complement pathway, causes tissue inflammation
  • Immune complex glomerulonephritis (lupus nephritis)
200
Q

Type 4 TH1 Hypersensitivity:
- Character
- Cytokines involved (3)
- Effects

A
  • Antigen presentation to sensitised CD4 Th1 T cells
  • This triggers Th1 cytokine production + release (IL-1, 12 and IFNy)
  • Recruits inflammation cells to area, causing a macrophage rich inflammatory response
201
Q

Type 4 Th2 hypersensitivity:

A
  • Cell-mediated eosinophillic hypersensitivity (chronic allergic inflammation caused by sensitised CD4 Th2 T cells
  • Triggers Th2 cytokine production + release (IL-4, 5, 13)
  • Eosinophil rich inflammatory response
202
Q

Type 4 Th1 hypersensitivity examples: (2)

A
  • Tuberculin reaction
  • Contact dermatitis
203
Q

Type 4 Th2 hypersensitivity examples: (3)

A
  • Chronic asthma
  • Chronic allergic rhinitis
  • Atopic eczema
204
Q

Type 4 cytotoxic hypersensitivity:
- Definition
- How does it happen?

A
  • Tissue injury by cytotoxic T cells
  • Antigen presented to sensitised CD8 T cells, antigen cell association causes cytotoxicity
205
Q

Autoimmunity vs auto-inflammation: similarities

A
  • Can share clinical features (joint pain, fever, rash, fatigue)
206
Q

Autoimmune vs auto-inflammatory: differences

A
  • Impacts on treatment options
  • Long-term health risks
  • Possible complications
207
Q

Autoimmune disease definition:

A
  • Adaptive immune system recognises self antigen as harmful and mounts an immune attack - via hypersensitivity mechanisms 2-4
208
Q

Auto-inflammatory disease:
- Cause
- Effects

A
  • Results from over-activity of the innate system. May be activated by triggers or genetic mutations
  • Inflammasome activity and recurrent fever syndromes
209
Q

Auto-inflammatory disease characteristics:
- Antibody involvement?
- Symptoms
- Signals
- Absence of …

A
  • Seronegative: no disease associated antibodies
  • Recurrent fever / symptom pattern
  • Raised inflammatory markers
  • Absence of infection
210
Q

Autoimmunity characteristics:
- Spectrum
- Causes

A
  • Wide disease spectrum (tissue specific vs systemic)
  • Genetic susceptibility combined with environmental influences
211
Q

Immune deficiency:
- Characterisation
- Causes
- Primary and secondary

A
  • Characterised by recurrent, persistent, severe or unusual infections
  • Occur when one or more components of the immune system are defective
  • Primary: inherited
  • Secondary: caused by an underlying condition
212
Q

Primary immunodeficiencies:

A
  • Commoner in males (often X-linked)
  • Selective asymptomatic deficiencies may occur in 1/400 people
  • Overall incidence of symptomatic primary immunodeficiency ~ 1/10,000
213
Q

Management of antibody deficiency:
- Timing
- Treatment
- Dosage

A
  • Early diagnosis essential to prevent further infections/complications
  • Treatment by immunoglobulin replacement therapy prepared from pooled blood blank plasma
  • Mostly IgG, 50mg/Kg body weight daily for 5 days, then 25 mg/Kg per week thereafter
214
Q

Management of defects in cell-mediated immunity: General measures (4)

A
  • Genetic counselling
  • Prenatal diagnosis
  • Avoid live vaccines and blood transfusions
  • Appropriate antimicrobial therapy
215
Q

Management of defects in cell-mediated immunity: therapeutic measures (2)

A
  • Bone marrow transplant
  • Gene therapy
216
Q

Acquired immunodeficiency: drugs (3)

A
  • can be caused by: Immunosuppressive, immunomodulatory, idiosyncratic
217
Q

Acquired immunodeficiency: underlying disease

A
  • HIV infection, causes progressive loss of T cells
  • Causes opportunistic infections and tumours
218
Q

Acquired immunodeficiency: marrow suppression

A
  • Malignancy, malnutrition, metabolic disease (renal and liver failure)
  • Protein loss (nephrotic syndrome, protein-losing enteropathy, severe burns)
  • Causes opportunistic infections
219
Q

Types of autoimmunity: (3)

A
  1. Organ-specific: T cell mediated
  2. Organ-specific: stimulating or blocking antibody related
  3. Systemic
220
Q

Organ specific autoimmune disease (DTH) examples

A
  • Type 1 diabetes
  • Multiple sclerosis
221
Q

Organ specific autoimmune disease (Ab) examples:

A
  • Graves’ thyroid disease
  • Myasthenia gravis
222
Q

Systemic autoimmune disease example:

A
  • SLE (systemic lupus erythematosus)
223
Q

T cell mediated autoimmune disease:
- Characterisation
- Mediation

A
  • Delayed type hypersensitivity damages target organ
  • Mediated by CD4 T cells, usually Th1 (IFNy) and Th17 (IL-17)
224
Q

T cell mediated autoimmune disease:
- Characterisation
- Mediation

A
  • Delayed type hypersensitivity damages target organ
  • Mediated by CD4 T cells, usually Th1 (IFNy) and Th17 (IL-17)
225
Q

Autoantibody mediated autoimmune disease:

A
  • Autoantibodies can occur in the absence of disease, or can precede disease
  • T helper cell dependant antibody isotopes
  • tumours can be an associated with some
226
Q

Sporadic autoimmunity:
- Description
- Interplay

A
  • Susceptibilty to common autoimmune diseases modified by polymorphisms in many genes
  • Strong interplay between “resistance” and “susceptibility” genes, strong evidence for environmental influences
227
Q

MHC genes regulate: 920

A
  • Autoantigen presentation
  • T cell repertoire selection
228
Q

Autoimmunity mechanisms: molecular mimicry

A
  • A peptide epitope from an infection looks the same as a self-protein
229
Q

Autoimmunity mechanics: bystander activation

A
  • Damage signals (often infectious) trigger adaptive responses to self-protein
230
Q

Autoimmunity mechanics: abnormal immune regulation

A
  • Post-infectious regulation of self-responsive T cells fails

Med Yr2 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions