Introduction to clinical sciences Flashcards

(212 cards)

1
Q

What is inflammation?

A

A reaction to an injury or infection involving neutrophils or macrophages

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

When is inflammation good?

A

°Fighting infections

°Protection from injury

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

When is inflammation bad?

A

°Autoimmune conditions

°Over-reaction to stimulus

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

How is acute inflammation classified?

A

°Sudden onset
°Short duration
°Usually resolves itself

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

How is chronic inflammation classified?

A

°Slow onset
°Long duration
°May never resolve

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

What cells are involved in inflammation?

A
°Neutrophil polymorphs
°Macrophages
°Lymphocytes
°Endothelial cells
°Fibroblasts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Properties of neutrophil polymorphs?

A

°Short lived (~5 days)
°First on the scene of inflammation
°Have cytoplasmic granules full of enzymes to kill bacteria
°Die at the scene
°Release cytokines to attract other cells

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

Properties of macrophages?

A

°Long lived
°Phagocytic
°Ingest bacteria and debris
°Can present antigens

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

Properties of lymphocytes?

A

°Live for years
°Can produce cytokines
°Are capable of producing memory cells

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

Properties of endothelial cells?

A

°Line capillaries
°Can become sticky to allow inflammatory cells to appear
°Can become porous to allow cells to pass through to tissue
°Grow into areas of damage to form new capillary vessels

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

Example of acute inflammation?

A
Acute appendicitis-
    °Unknown factors for inflammation
    °Neutrophils are present
    °Blood vessels dilate
    °Inflammation of serosal surface
    °Pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Example of chronic inflammation?

A

Tuberculosis-
°No initial acute inflammation
°Mycobacteria ingested by macrophages
°Macrophages fail to kill bacteria
°Lymphocytes and additional macrophages appear
°Fibrosis occurs

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

Properties of fibroblasts?

A

°Long lived cells

°Form collagen in area of chronic inflammation and repair

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

How do granulomas occur?

A

When two or more macrophages attempt to engulf the same material at once, the cells end up joining together

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

Causes of acute inflammation?

A
°Microbial infections
°Hypersensitivity reactions
°Physical agents (trauma)
°Chemicals
°Bacterial toxins
°Tissue necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

3 processes of the inflammatory response?

A

°Changes in the vessel calibre and flow
°Increased vascular permeability and formation of fluid exudate
°Formation of cellular exudate - emigration of neutrophil polymorphs to extracellular space

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

Causes of increased vascular permeability?

A

°Immediate transient chemical mediators e.g -
°Histamine
°Bradykinin
°C5a
°NOx
°Leucotrine B4
°Platelet activating factor
°Immediate sustained severe vascular trauma
°Delayed prolonged endothelial injury e.g. x-ray

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

What can endogenous chemical mediators cause?

A
°Vasodilation
°Emigration of neutrophils
°Chemotaxins
°Increased vascular permeability
°Itching and pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the systemic effects of inflammation?

A
°Pyrexia (fever)
°Weight loss
°Reactive hyperaemia of the reticuloendothelial system
°Haematological changes
°Amyloidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Appearances of chronic inflammation?

A
Macroscopic - 
    °Ulcers
    °Abscess cavity
    °Thickening of hollow viscus wall
    °Granulomatous inflammation
    °Fibrosis
Microscopic - 
    °Lymphocytes and macrophages
    °A few eosinophils
    °Destruction of tissue and formation of fibrous tissue
    °Tissue necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Special multinucleate giant cells?

A

°Langhans cells (tuberculosis) horseshoe arrangement of peripheral nuclei
°Touton giant cells (xanthomas/dermatofibromas of the skin) have a central ring of nuclei peripheral to lipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the difference between repair and resolution?

A

Resolution -
°Initiating factor is removed
°Tissue is undamaged or can regenerate
Repair -
°Initiating factor is still present
°Tissue is damaged can cannot regenerate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the features of lobar pneumonia?

A

°Single lobe of the lung
°Caused by streptococcus pneumonia
°Anti-biotics to clear
°Pneumocytes in the lung can regenerate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Healing by 1st intention?

A

°Involves a wound where the skin can be pulled together
°Space is filled with fibrin
°Forms a weak join
°Filled with collagen by fibroblasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Healing by 2nd intention?
°Wound cannot be pulled together °Capillaries, fibroblasts and collagen all form to repair the wound °Grows in from the edges
26
How does repair happen in the brain?
Gliosis, collagen is produced by glial cells
27
Which cell types can regenerate?
``` °Hepatocytes °Pneumocytes °Blood cells (all) °Gut epithelium °Skin epithelium °Osteocytes ```
28
Why don't clots form all the time?
°Laminar flow in the centre of the artery | °Endothelial cells are not sticky when they are healthy
29
What can cause thrombosis?
°Change in the vessel wall °Change in the flow of blood °Change in the blood constituents
30
How does thrombosis occur?
°Platelet aggregation leads to the coagulation cascade °Platelets stick to collagen which is exposed under damaged endothelial cells °Disrupts laminar flow and red blood cells get trapped with platelets °Fibrin is deposited into the clot °Positive feedback loop
31
What is a thrombus?
A solid mass of blood constituents formed within an intact vascular system during life
32
How do you prevent thrombosis?
°Movement °Compression stockings °Aspirin
33
What is an embolus?
A mass of material in the vascular system able to become lodged within a vessel and block it
34
What is ischaemia?
Reduction in blood flow without any other complications
35
What is infarction?
Reduction in blood flow that is so reduced that it cannot support the maintenance in the cells of a tissue, so they begin to die
36
Why are tissues with an end arterial supply more susceptible to infarction?
They only have a single arterial supply and so if this vessel is interrupted infarction is likely.
37
What are 3 organs with a dual arterial supply?
°Lungs °Liver °Brain
38
What happens after ischaemia is fixed?
Re-perfusion injury meaning that the waste products that have accumulated during the reduced blood flow period are released
39
What are the consequences of an arterial embolus?
An arterial embolus can travel around the body with the consequences being stroke, MI, gangrene
40
What are the consequences of a venous embolus?
An embolus in the venous system will go onto the vena cava and then through the pulmonary arteries and become lodged in the lungs causing a pulmonary embolism
41
What is the definition of atherosclerosis?
Inflammatory process characterised by hardened plaques in the intima of a vessel wall.
42
What forms an atherosclerotic plaque?
°Fibrous tissue °Lipids (cholesterol) °Crystals (these dissolve) °Lymphocytes
43
Which system do you find atherosclerosis in?
Low pressure systems such as the pulmonary ateries
44
How does a plaque form?
°Endothelial dysfunction °Formation of lipid layer or fatty streak within the intima °Migration of leukocytes and smooth muscle cells into the vessel wall °Foam cell formation °Degradation of extracellular matrix.
45
What complications can arise from atherosclerosis?
``` °Cerebral infarction °Carotid atheroma °Myocardial infarction °Aortic °Gangrene ```
46
What are the risk factors for atherosclerosis?
``` °Cigarette smoking. °Hypertension. °Hyperlipidaemia. °Uncontrolled diabetes mellitus. °Lower socioeconomic status. ```
47
How does smoking impact atherosclerosis?
Free radicals, nicotine and CO damage the endothelial cells
48
How does hypertension impact atherosclerosis?
Sheering forces created by high blood pressure causes damage to the endothelial cells which is the first stage of plaque formation
49
What is the definition of apoptosis?
The programmed death of a single cell
50
How does a cell apoptose?
``` °Enzymes are released to shrink the cell °The nucleus condenses °The nucleus and DNA fragments °An apoptic body forms from the contents of the cell °The body is then phagocytosed ```
51
DNA damage can lead to a cell being apoptosed. What can happen to DNA to cause this?
°A single strand breaks °Both strands break °One of the bases becomes altered °There is cross linkage of the strands
52
Which protein detects DNA damage?
P53
53
Which family of proteins can turn on apoptosis?
Caspases
54
Which receptor turns the proteins which regulate apoptosis on?
FAS receptor
55
What is the purpose of apoptosis in development?
Can separate the digits of the foetus
56
What disease has a lack of apoptosis?
Cancer, with even less in breast and colorectal cancer
57
What disease has increased apoptosis?
HIV, the CD4 cells are apoptosed at an increased rate
58
What is the definition of necrosis?
The large scale, unplanned death of cells
59
What are some clinical examples of necrosis?
``` °Spider venom °Frostbite °Cerebral infarction °Avascular necrosis (head of femur, scaphoid) °Pancreatitis ```
60
What is coagulative necrosis?
A type of necrosis caused by ischaemia or infarction. The tissues are preserved for a few days . It can also be induced by a high temperature
61
What is liquefactive necrosis?
A type of necrosis which results in the tissues becoming liquidised. It is usually caused by a bacterial or fungal infection but can also be caused by an internal chemical burn
62
What is unique about caseous necrosis?
The presence of multinucleate giant cells
63
Define hypertrophy
An increase in the size of tissues caused by an increase in the size of the constituent cells
64
What are two ways that the size of cells can increase?
°Increase in the number of myofibrils present | °Increase in the volume of sarcoplasm
65
Define hyperplasia
An increase in the size of tissues caused by an increase in the number of constituent cells
66
What can cause endometrial hyperplasia?
Having more oestrogen than progesterone present
67
Define atrophy
A decrease in the size of a tissue caused by either a decrease in the number of constituent cells or a decrease in the size of the cells
68
Define metaplasia
A change in differentiation of a cell from one which is fully differentiated to a different fully differentiated cell
69
Give an example of metaplasia
Ciliated columnar epithelium in the trachea changing to because squamous epithelium due to smoking
70
Define dysplasia
Morphological changes seen in cells in the progression to becoming cancerous
71
What happens when telomeres get too short?
They can no longer replicate or divide
72
Give two examples of tissues that can divide
°Gut epithelium | °Skin epithelium
73
What is an example of a non-dividing tissue?
Brain
74
What can cause a reduction in dividing tissue?
°Free radicals °Cross-linking of DNA proteins °DNA damage °Mitochondrial DNA damage
75
What are the symptoms of ageing?
``` °Balding °Dementia °Deafness °Cataracts °Osteoporosis °Dermal elastosis ```
76
What causes dermal elastosis?
UV-B causes cross-linking of collagen proteins which makes them less elastic
77
What causes cataracts?
UV-B causes cross-linking of collagen proteins which makes the lens cloudy
78
What causes osteoporosis?
A lack of oestrogen causes an increase in bone resorption and a decrease in bone formation
79
What can cause dementia?
°Atrophy of brain tissue °Plaques (Lewy bodies) °Neurofibrillary tangles
80
What causes sarcopenia (and what is it)?
°Muscle loss °Decreased growth hormone °Decreased testosterone °Increased catabolic cytokines
81
What is unique about basal cell carcinoma?
It only invades the dermis of the skin and does not metastasise to other areas of the body = excision of the tumour will cure it
82
What is the definition of carcinogenesis?
The transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations
83
What is oncogenesis?
The same as carcinogenesis but only applies to malignant cells
84
What percentage of cancer risk is environmental?
85% environmental, 15% genetic
85
Where is hepatocellular carcinoma more common?
Rare in the UK/US but has a high incidence in areas with increased incidence of Hep B/C
86
What is the definition of a carcinoma?
Malignant tumour of epithelial tissue
87
Give examples of carcinomas that commonly metastasise to the bone?
``` °Prostate °Breast °Thyroid °Kidney °Lung ```
88
Why are adjuvant therapies used in cancer treatments?
Micro-metastases are possible even if a tumour is excised and so adjuvant therapy is given to suppress secondary tumour formation
89
What are the host factors that affect cancer risk?
``` °Race °Diet °Constitutional factors (gender, age) °Premalignant conditions °Transplacental exposure ```
90
What is one advantage of conventional chemotherapy and one disadvantage?
°Advantage: works well for treatment against fast dividing tumours e.g. lymphomas. °Disadvantage: it is non selective for tumour cells, normal cells are hit too; this results in bad side effects such as diarrhoea and hair loss.
91
What are the categories of carcinogens?
``` °Viral °Chemical °Radiation °Hormones, mycotoxins, parasites °Miscellaneous ```
92
What type of cancer do polycyclic aromatic hydrocarbons cause?
Skin and lung cancer via smoking and inhalation of mineral oils
93
What cancer do aromatic amines cause?
Bladder cancer (common in the rubber industry)
94
What type of cancer do nitrosamines cause?
Gut cancer
95
What cancer do alkylating agents cause?
Leukaemia
96
How is skin cancer caused?
UV-B rays
97
What cancer does the inhalation of radioactive uranium in mines cause?
Lung cancer
98
What cancer does radioactive iodine cause?
Thyroid
99
What cancer can increased oestrogen cause?
Mammary/endometrial cancer
100
What cancer does anabolic steroids cause?
Hepatocellular carcinoma
101
What cancer does Aflatoxin B1 cause?
Hepatocellular carcinoma
102
What cancer does chlorochis sinensis cause?
Cholangiocarcinoma
103
What cancer does shistosoma cause?
Bladder cancer
104
Which cancers can be caused by asbestos?
Mesothelioma, asbestosis, lung cancer
105
What is the definition of a neoplasm?
A lesion resulting from the 𝗮𝘂𝘁𝗼𝗻𝗼𝗺𝗼𝘂𝘀 or relatively autonomous 𝗮𝗯𝗻𝗼𝗿𝗺𝗮𝗹 growth of cells which 𝗽𝗲𝗿𝘀𝗶𝘀𝘁𝘀 after the initiating stimulus has been removed
106
What is the structure of neoplasms?
Made from neoplastic cells and a stroma
107
What are the characteristics of neoplastic cells?
°Derived from nucleated cells °Usually monoclonal °Growth pattern and synthetic activity are related to the parent cell
108
What are the characteristics of neoplasm stroma?
Connective tissue composed of fibroblasts and collagen; it is very dense. There is a lot of mechanical support and blood vessels provide nutrition for the neoplastic cells.
109
What needs to occur for a neoplasm to grow?
Angiogenesis
110
What does the neoplasm release in order to become vasculated?
Vascular endothelial growth factor
111
Why does necrosis occur in the centre of a neoplasm?
The neoplasm outgrows its vasculation so the centre does not receive blood flow and so necroses
112
Why do we classify neoplasms?
It helps to determine the appropriate treatment and prognosis
113
What are the two classifications of neoplasms?
°Behavioural | °Histological
114
What are the features of benign neoplasms?
``` °Localised and non-invasive °Slow growth rate °Low mitotic activity °Close resemblance to normal tissue °Circumscribed or encapsulated °Nuclear morphology is often normal °Necrosis and ulceration is rare °Growth on mucosal surfaces is often exocytotic (grows up and out) ```
115
What are the features of malignant neoplasms?
``` °Invasive °Metastases °Rapid growth rate °Variable resistance to normal tissue °Poorly defined/ irregular border °Hyperchromatic nuclei and pleomorphic nuclei °Increased mitotic activity °Necrosis and ulceration are common °Growth on mucosal surfaces is often endocytotic (grows down and in) ```
116
Why worry about benign neoplasms?
``` °Pressure is put on adjacent systems °Can obstruct blood flow °Can produce hormones °Sometimes can transform into malignant neoplasms °Anxiety ```
117
Why worry about malignant neoplasms?
``` °Destruction of adjacent tissue °Metastases °Blood loss from ulcers °Obstruction of blood flow °Hormone production °Paraneoplastic effects °Anxiety and pain ```
118
What is the meaning of histogenesis?
The specific cell of origin of a tumour
119
What is a papilloma?
Benign tumour of non-glandular, non-secretory epithelium
120
What is an adenoma?
Benign tissue of the glandular/secretory epithelium
121
What is a carcinoma?
Malignant tumour of epithelial cells
122
What would a benign neoplasm found in lipid tissue be called?
Lipoma
123
What would a benign neoplasm found in cartilage be called?
Chondroma
124
What would a benign neoplasm found in bone be called?
Osteoma
125
What would a benign neoplasm found in the vascular system be called?
Angioma
126
What would a benign neoplasm of neuronal cells be called?
Neuroma
127
What is a rhabdomyoma?
Benign neoplasm of striated muscle
128
What is a leiomyoma?
Benign neoplasm of smooth muscle
129
Which cancers do not follow sarcoma/carcinoma naming rules?
°Melanoma °Lymphoma °Mesothelioma
130
What is a cancer called when it is contained within a cell?
Carcinoma in situ
131
What is one advantage and one disadvantage of non-targeted chemotherapy?
``` °Advantage = works well for treatment against fast dividing tumours °Disadvantage = it is non selective for tumour cells, normal cells are hit too; this results in bad side effects such as diarrhoea and hair loss ```
132
What is required for a tumour to invade through a basement membrane?
°Proteases | °Cell motility
133
What is required for a tumour to enter the blood stream (intravasation)?
°Collagenases | °Cell motility
134
What is required for a tumour to exit the blood stream (extravasation)?
°Adhesion receptors °Collagenases °Cell motility
135
What is needed for a tumour to grow at a metastatic site?
Growth factors
136
What are the promoters of angiogenesis?
°Vascular endothelial growth factor | °Basic fibroblast growth factor
137
What are the inhibitors of angiogenesis?
°Angiostatin °Endostatin °Vasculostatin
138
What are the defence mechanisms of tumours to evade the host defence system?
°Platelet aggregation. °Adhesion to other tumour cells. °They shed surface antigens so as to 'distract' lymphocytes
139
Where do tumours which enter the right atrium typically metastasise to?
The lung, specifically in small capillaries
140
Where do tumours which enter the left atrium metastasise to?
Brain, bone, the entire body
141
Cancer metastasis in the liver could come from where?
Colon, stomach, pancreas, carcinoid tumours of the intestine
142
What is innate immunity?
Instinctive, non-specific, does not depend on lymphocytes, present from birth
143
What is adaptive immunity?
Specific ‘Acquired/ learned’ immunity, requires lymphocytes, antibodies
144
Which white blood cells are polymorphonuclear leukocytes?
Neutrophil, eosinophil, basophil
145
Which white blood cells are mononuclear leukocytes?
Monocytes, T-cells, B-cells
146
What can T-cells differentiate into?
°T-regulators °T-helper cells (CD4, Th1, Th2) °Cytotoxic (CD8)
147
What is complement?
Group of ~20 serum proteins secreted by the liver that | need to be activated to be functional.
148
What are the three ways in which complement works?
°Direct lysis °Attract more Leukocytes to site of infection °Coat invading organisms
149
What are the 5 Ig proteins that need to be memorised?
MAGED (see textbook/slides on 15/11/19 for images)
150
What are cytokines?
Proteins secreted by immune and non-immune cells
151
What are interferons and what do the different types do?
Induce a state of antiviral resistance in uninfected cells & limit the spread of viral infection °IFNα & β - produced by virus infected cells °IFNγ - released by activated Th1 cells
152
What is the function of interleukins?
°Can be pro-inflammatory (IL1) or anti-inflammatory (IL-10) °Can cause cells to divide, to differentiate and to secrete factors
153
What do colony stimulating factors do?
°Involved in directing the division and differentiation on bone marrow stem cells
154
What are chemokines?
Proteins that direct movement of leukocytes from the bloodstream into the tissues or lymph organs by binding to specific receptors on cells
155
What does the CXCL chemokine control?
Neutrophils
156
What does the CCL chemokine control?
Monocytes, lymphocytes, eosinophils, basophils
157
What does the CX3CL chemokine control?
T-lymphocytes and natural killer (NK) cells
158
What does the XCL chemokine control?
T-lymphocytes
159
What are the characteristics of innate immunity?
``` °Primitive (spread across species) °‘Un-learned/instinctive’ response °Does not depend on immune recognition by lymphocytes °Does not have long lasting memory °Integrates with Adaptive response ```
160
What are the characteristics of adaptive immunity?
°Response specific to antigen °Learnt behaviour °Memory to specific antigen °Quicker response
161
What 3 things compromise the innate immune system?
°Physical and chemical barriers °Phagocytic cells (neutrophils and macrophages) °Blood proteins (complement, acute phase)
162
What are the stages of immunisation?
``` °Exposure °Antigen presents to T-cells °Production of IgM °Establishment of IgG °Large amounts of IgG produced ```
163
What can be recognised by PRRs?
°Gram +ve/-ve °dsRNA °CpG motifs
164
What do secreted and circulating PRRs do?
°They are antimicrobial peptides secreted in lining fluids from epithelia and phagocytes °They disrupt pathogen motility and kill them °They also assist in phagocytosis
165
What are lectins and collectins?
°Peptides PRRs that also contain carbohydrates °They bind carbohydrates and lipids °Can also activate complements which improves phagocytosis
166
What are pentaxins?
°They are PRRs which have some antimicrobial actions °React with the C-polysaccharide of pneumococci °Active complements which improves phagocytosis
167
What can different TLRs detect?
``` °Gram +ve/-ve °Flagellin °CpG motifs °dsRNA °ssRNA °LTAs ```
168
What does TLR 1/2 detect?
Gram +ve lipopeptide
169
What does TLR 3 detect?
dsRNA (exogenous) and mRNA (endogenous)
170
What does TLR 4 detect?
Exogenous: °LPS, pneumolysin, viral proteins Endogenous: °Heat shock proteins, HMGB1, hyaluronan, fibrinogen
171
What does TLR 5 detect?
Flagellin
172
What does TLR 2/6 detect?
Gram +ve lipopeptide
173
What does TLR 7 detect?
ssRNA
174
What does TLR 8 detect?
ssRNA
175
What does TLR 9 detect?
CpG (exogenous) and DNA/mitochondrial DNA (endogenous)
176
What are the other membrane bound PRRs?
°Mannose receptors on macrophages (react to fungi) °Dectin-1 which is widespread on phagocytes and recognise beta-glucans in fungus °Scavenger receptors on macrophages
177
What are NLRs?
°Nod-like receptors | °Detection of peptidoglycan muranyl 1 dipeptide
178
What is NOD2?
°Recognises muranyl 1 dipeptide which comes from them breakdown of peptidoglycans °Activates the inflammatory signalling pathway °Non-function of NOD2 leads to Crohn's °Hyper function of NOD2 leads to Blau syndrome
179
What are RLRs?
°Rig-like receptors °RIG-1 and MDA5 detect dsRNA and DNA °Activate interferon production
180
What is the link between PRRs and homeostasis?
°Blood neutrophil numbers may depend on TLR 4 signalling, which is independent of LPS °Induction of endotoxin tolerance in the newborn gut °PRRs mature the newborn gut °Maintains the balance with commensal organisms
181
How do PRRs recognise damage?
°TLRs adapt to recognise endogenous damage molecules - they share hydrophobicity °Appearance of host molecules in unfamiliar contexts activate TLRs °TLR signalling activates immunity and initiates tissue repair
182
What are the extracellular damage molecules?
°Fibrinogen °Hyaluronic acid °Tenascin C
183
What are the intracellular damage molecules?
``` °HMGB1 °mRNA °Heat shock proteins °Uric acid °Stathmin ```
184
How do PRRs work in adaptive immunity?
°Activation of PRRs and TLRs drive cytokine production and increase the likelihood of T-cell activation °TLR 4 agonists are used in vaccine adjuvants °TLR 7/8/9 adjuvants are used in development
185
What conditions are PRRs linked to?
°Atherosclerosis °Arthritis °COPD °IBD
186
Which major diseases have been contained since vaccines have been introduced?
``` °Diptheria °Mumps °Tetanus °Pertussis (whooping cough) °Poliomyelitis °Smallpox ```
187
What diseases are anti-toxins (passive immunisation) used for?
°Botulism °Tetanus °Diptheria
188
What diseases are prophylaxis (passive immunisation) used for?
°Hepatitis °Measels °Rubella
189
What diseases are anti-veins (passive immunisation) used for?
°Snake bite °Insect bites °Jellyfish stings
190
What are the stages of active immunisation?
°Engage the innate immune system °Elicits 'danger' signals that activate the immune system and triggers the PAMPs etc °PAMPs activate TLRs °TLRs activate specialist APCs e.g. Langerhans cells °Engage the active immune system
191
What is the initial response to antigen exposure?
°IgM predominantly °Low affinity for Ab °Germline repertoire •Memory cells are made
192
What is the secondary response/what happens when a disease is re-introduced following vaccination?
°Rapid and large response °High levels and affinity of IgG °Uses somatic cell line °Hypermutation can occur
193
What are the advantages of using a whole organism vaccine?
°Allows transient infection °Activates full immune response °Prolonged contact with the immune system °1 dose required
194
What are the disadvantages of using a whole organism vaccine?
°Immunocompromised patients may become infected °Complications can occur °In areas of poor sanitation it can lead to an outbreak of disease
195
What are the advantages of using a whole inactivated organism vaccine?
°No risk of infection °Storage is less critical °Wide range of antigenic components present
196
What are the disadvantages of using a whole inactivated organism vaccine?
°Does not activate T-cells °Response can be weak °Boosters needed °Compliance issue
197
What are the advantages of using a subunit vaccine?
°Safe °No infection risk °Easy to store
198
What are the disadvantages of using a subunit vaccine?
°Response can be weak °Boosters needed °Consider gene heterogeneity of population by choice of antigen
199
What are the 3 types of subunit vaccine?
°Inactivated exotoxins °Capsular polysaccharide °Recombinant microbial agents
200
What effect does diphtheria toxin have on the body?
Inactivated mammalian elongation factor EF2
201
What effect does tetanus toxin have?
Muscle contraction
202
What is the aim of synthetic peptide vaccines?
To produce peptides including immunodominant B cell epitopes and stimulate memory T-cells
203
What are the difficulties of synthetic peptide vaccines?
HLA knowledge is needed
204
What is the aim of DNA vaccines?
Express genes from pathogen in host leading to T and B cell memory response
205
What are the advantages of DNA vaccines?
°Safe °No requirement for storage and transport °Delivery is simple and adaptable (use a DNA gun)
206
What are the disadvantages of DNA vaccines?
°Produces a mild response °Need boosters °Limited to proteins °Could induce tolerance
207
What is the aim of recombinant vector vaccines?
Imitate effects of transient infection with non-pathogenic organism
208
What is a pathogen?
An organism that causes or is capable of causing disease
209
What is a commensal organism?
An organism that colonises the host but causes no disease under normal circumstances
210
What is an opportunist pathogen?
A microbe that only causes disease if the host defence is immunocompromised
211
What is virulence/pathogenicity?
The degree to which a given organism is pathogenic
212
What is asymptomatic carriage?
When a pathogen is carried harmlessly at a tissue site where it causes no disease