ICS immunology and pathology Flashcards
(294 cards)
1
Q
Why is a death reffered to a coroner?
A
Cause of death not known, not seen by doctor in last illness, peri/post operative deaths, anaesthetic deaths, accidents suicide unlawful killings
2
Q
Who referrs to a coroner?
A
Doctors, relatives poleace registrar, anatomical pathology technicians
3
Q
Who performs autopsies?
A
Histopathologists usually for natural deaths and hospital deaths or a forensic pathologist who does it for crimes or death due to a 3rd party
4
Q
What are the roles of a coroner/
A
Find out who they were, when they died, where the died, how did they come about their death?
5
Q
What is involved in an autopsy?
A
pictures of outside potentially scans, microbioloy internal eternal removal of organs histology.
6
Q
What is the purpose of inflammation to the body?
A
Destruction of invading microorganisms and the walling off of a cavity to prevent infection spreading.
7
Q
How can inflammation be a problem?
A
space occupying lesions, fibrosis from chronic inflammation can dirupt the structure and function of tissues
8
Q
What is acute inflammation?
A
Initial and transiant erios of tissue reactions to injury
9
Q
What is chronic inflammation?
A
The subsequent and prolonged tissue reactions following acute inflamation
10
Q
What separates chronic and acute inflammation?
A
the types of cells involved in the inflammatory response
11
Q
What are the steps involved in acute inflammation?
A
Injury to tissue, dilation of vessels, exudative vascular leakage of protein-rich fluid, neutrophil polymorph is the characteristic cell that is recruited.
12
Q
What are the end points of acute inflammation?
A
Resolution, suppuration(abscess) organisation or progression to chronic inflammation
13
Q
What can cause acute inflammation?
A
Microbial infection, hypersensitivity reactions, pysiical agents like trauma or radiation, chemicals bacterial toxins or tissue necrosis
14
Q
How is microbial infection inflammation mediated?
A
Viruses destroc cells, bacteria release exotoxins, additionally some orgnisms cause immunologically mediated inflamation from hypersenistibity
15
Q
What is a hypersensitivity reaction?
A
when the reaction is not proportiantd to the dammage to cells
16
Q
Why might tissue necrosis occur?
A
Death of tissues from lack of oxygen or nutrients often from inadequate blood flow,
17
Q
What are the macroscopic appearaces of acute inflammation?
A
Rubor(redness) Calor(heat) Tumor(swelling) Dolor(pain)
18
Q
What causes redness?
A
Dilatation of small blood vessels of the area
19
Q
What causes heat in inflammation?
A
Increased peripheral bloodflow (hyperaemia) or a systemic fever
20
Q
What is cellulitis?
A
Acute inflammation and redness (erythema) on the lateral side of the foot due to vasclar dilatation
21
Q
What causes swelling in inflammation?
A
From oedema accumulation of fluid in the extravascular space as part of the fluid exudate
22
Q
What causes pain in inflammation?
A
tissue deformation, some chamical mediators can induce pain, serotoin prostalandins and bradykinin
23
Q
What happens in the early stages of acute inflammation?
A
Fibrin oedema fluid, neutrophil polymorphs accumlate
24
Q
What happens in blood vessels during inflammation?
A
they dilate and become more permeable.
25
What increases vascular permeability?
histamine bradykinin, nitric oxide, C5a leucotriene B4 platelety activating factors
26
How do white blood cells leave the vessels?
Through the endothelial gaps through the basal lamina into the adventitia
27
What are the effects of histamine and thrombin on the endothelial surcace?
Increase expression of molecules that activate neutrophils to adhere to the endothelium
28
What chemical mediators are released by cells?
Histamine also lysosomal compounds ecosanoids serotonin(5hydroxytruptamine and chemokines
29
what are the four enzymatic cascade systems of plasma?
Complement, the kinins, coagulation factors and the fibrinolytic system
30
What feeds the complement system?
Kinin and fibrinolytic sustem
31
What is the kinin system?
Factor 12 produces kallikrein and kininogens that produce kinins lie bradykinin
32
What are the differences in the transient phase and prolonged phase of vascular permeability?
Histamine is transient then other mediators prolong it. NO, Leucotriene, Prostaglandins, Bradykinin
33
What does neutrophil polymorph do?
They engulf lysosomes and phagocytic vacuoles,
34
What are the negative effects of inflammation?
Digestion of normal tissues, Swelling inappropriate inflammation response.
35
What causes suppuration?
Excessive exudate and cn lead to rupture and discharge of pus.
36
What can happen after excessive necrosis?
Repair and organisation and fibrosis
37
What leads to chronic inflammation?
Persistent causal agents often leads to chronic inflammation
38
What are the systemic effects of inflammation?
Pyrexia, constitutional symptoms, weight loss reactive hyperplasia of reticuloendothelial system, haematological changes amyloidosis.
39
What is resolution?
initiating factor removed. tissue undamaged or able to regenerate
40
What is repair?
Initiating factor still present, tissue damaged and unable to regenerate
41
What happens in the repair of skin?
Replacement of damaged tissue by fibrous tissue
42
Which cells are thought to not regeneragre/
The heart cells and neurones
43
Which cells are known to regenerate?
Hepatocytes, neumocytes all blood cells gut epithelium skin epithelium and osteocytes
44
What are required for a thrombus to form?
Change in the vessel wall, change in blood flow or a change in blood constituents
45
What is an embolus?
A mass of material in the vascualr system able to become lodged within a vessel and block it
46
What is ischemia?
Reduction in blood flow
47
What is an MCCD?
Medical certificate cause of death
48
which cells come first in inflamation?
neutrophil polymorphs
49
What do macrophages do?
They break up old tissue and ingest bateria and debris can be antigen presenting
50
How long can lymphocytes like?
Years
51
What do lymphocytes do?
They produce chemicals which attract other inflammatory cells and memory
52
What is the role of fibroblasts?
They produce fibrous tissue.(scar tissue)
53
What is a granuloma?
Specific pattern of lymphocytes and macrophages in inflamation in TB sarcoidosis, leprocy
54
What is granulation tissue/
Macroscopic tissue that looks bobbly
55
What is prostaglandin synthetase?
It is an enzyme that produces prostaglandins
56
How do steroids reduce inflamation?
They regulate DNA that give more inhibitors of inflammation.
57
What is antihistamine?
competitive inhibitor for histamine
58
What is resolution?
It goes back to normal it can repair fully or the tissue is undamaged
59
What can the liver regenerate from?
When you have one big insult to it it can go back to normal
60
What permanently damages the liver?
continuous damage, to the liver
61
What is fibrous vs cirrhosis?
cirrhoses is nodular when regrowth has begun.
62
What are the lungs like in repair/ regeneration?
Resolution can happen as long as architecture is not damage
63
What is the affect of COVID-19 on lungs?
Can cause small damage and fluid but can cause fibrosis
64
What happens in skin abrasion repair?
The cells at the bottom divide and repain the skin, can grow back from the hair follicle
65
What is first intention healing?
Heals after the incision and bring the edges together to allow strong collagen to join it.
66
What is second intention healing?
When there is a hole in the skin and it cant be brought back together and healing takes longer to get together as cells grow in from the edges
67
What is granulation tissue in skin healing?
Small loops of blood vessels causing granulations on damaged skin
68
Where does fibrous tissue usually form?
In tissue that can't regenerate, spinal cord heart attack, brain, skin somethimes
69
What is gliosis?
Brain scarring fibrous tissue has thinner fibrous strands
70
What makes up a granuloma?
Macrophages and fused macrophages with lymphocytes around the outside
71
What type of inflammation is a granuloma?
Chronic inflammation
72
What can inflammation do even when treated?
can destroy tissue still
73
What do anti inflammatory drugs also affect?
They can affect immunity
74
what is rebound tenderness?
When remove pressure from abdomen it causes pain acute abdomen infection
75
What is diverticulitis?
When outpouching of large bowel ruptures and gets infected
76
What are the key element of acute inflamation?
Polymorph neutrophils formation of puss
77
What prevents clotting normally?
Laminar flow and the endothelial lining
78
How does COVID affect thrombosis?
Damages the blood vessels with microthrombi
79
What is an end artery?
only have one blood supply to get it
80
Which organs are not end artery supplied?
Lungs liver some ares of the brain
81
When does atherosclerosis usually happen?
In later years of life around 50 onwards
82
Which arteries are most likely to get atheroma and why?
The aorta and systemic arteries because they are at a higher pressure
83
What is atheroma?
Build up of tissue in the arteries
84
What forms an atherosclerotic lesion?
Lipids and cholesterol then fibrous tissue builds up as inflammation takes place
85
What layer starts an atherosclerotic plaque?
the endothelial lining can affect the internal elastic lamina
86
What are the risk factors of atheroma?
Smoking Diabetes high BP high lipids being a man
87
What is it about smoking that affects endothelial cells?
free radicals nicotine and CO
88
Why does diabetes cause endothelial damage?
Superoxide anions, glycosylation products.
89
What factors can lead to apoptosis?
detachment from the adhesion surface certain extracellular factors, DNA dammage
90
What can induces apoptosis?
DNA damage
91
What signals the cell to apoptose?
Fas ligands Bcl2 protein activating, caspases
92
How is apoptoses involved in disease?
HIV too much cancer too little
93
What can cause necrosis?
Venom, frost bite burns, ischemia infection with bacteria
94
What are the types of necrosis?
Coagulative, liquifactive and caseous necrosis
95
What is the first stage of atherosclerosis?
fatty streak can be undone
96
What makes up a plaque?
Fibrous tissue, lipids(cholesterol), lymphocytes(chronic inflammation),
97
Does diabetes always damage arteries?
Not unless it is uncontrolled
98
What is lipid insudation theory?
the theory that high lipids lead to lipids passing through endothelial lining. disproven now.
99
What is the main theory of the formation of plaque?
The endothelial dammage theory. they can be killed or damage by toxins from various sources, high blood pressure shearing forces on endothelia cells
100
what prevention can there be?
Baby aspirin to stop platelet aggregation
101
How does apoptosis happen?
Nucleus condenses pyknosis, the organelles go into blebs and phagocytes eat the blebs
102
What are caspases?
They are molecules that initiate apoptosis
103
What is fas ligand?
The ligand for fas receptor to signal apoptosis
104
What is the use of apoptosis in embryology?
Helps the formation of the shape of organs and tissues
105
What is coagulative necrosis?
semi solid death
106
What is liquefactive necrosis?
When the brain digests all of the material in that has died.
107
What is caseous necrosis?
Smooth cheese texture often in TB
108
Are all congenital diseases genetic?
No some can come from foetal nutrition or exposure to toxins
109
What does multifactorial mean?
That there are many causes both genetic and environmental that affect the incidence of disease
110
What shows strong evidence of genetic causes for disease?
Family studies and studies on twins
111
What are HLA types?
Human leucocyte antigens they are expressed on the surface of nucleated cells and on the cells that interact with t lymphocytes
112
What is a neoplasm?
They are tumours new growths
113
What chemical agents can cause disease?
Strong acids from body or environment, metabolic effects like alcohol impare processes, membranes can be dammaged, certain chemicals can affect embrysos and allergic reactions to chemicals
114
How does carbon monoxide affect the arterial endothelial cells/
It causes hypoxia
115
What are the types of growth?
Hypertorphy and hyperplasia
116
What is hypertrophy?
The size of the cells themselves increases
117
What is hyperplasia?
When the cells repilcate and increase in number
118
Where does hyperplasia happen in normal function?
Breast tissue during lactation
119
What can cause pathological atrophy?
Loss of blood supply, denervation, pressure lack of nutrients, lack of hormonal stimulation or from hormonal stimulation
120
What is metaplasia?
Reversible transformation of one type of mature cell into another fully differentiated cell type.
121
When does metaplasia happen?
As an adaptive response to injurios stimuli
122
What is dysplasia?
A premalignant condition characterised by increased growth cellular atypua and decreased differentiation
123
What is ageing?
Progressive degeneration or loss of function
124
What are common areas to lose function in with age?
The brain ear, joints,
125
What could lead to cells dying and therefore aging?
Free radicals defective repair fragility syndrome, telomeric shortening
126
What does aging to to skin?
Wrinkling due to loss of elastin and collaen, fragle and bruises easily.
127
What is sarcpenia?
Loss of muscle mass
128
What changes happen to bones with ageing?
Osteoarticular ageing where the bones lose mass and stretch and the articular surfaces wear.
129
What happens to the immune system in ageing?
Impaired immunity thymus atrophy leads to fewer immune cells,
130
What happens to the cardiovascular system in ageing?
Atherosclerosis, loss of elacticity in the aorta, distension of certain arteries, calcification of blood vessels,
131
What type of growth can nerve cells do?
Hyperplasia
132
What is optic atrophy?
The whitening of the optic disk
133
Which tissues are dividing?
Skin , gut epithelium
134
What is likely to cause sarcopenia?
Decreased growth hormone and testosterone
135
How does basal cell carcinoma spread?
Only spreads locally and never spreads to other parts of the body
136
How to cure basal cell carcinoma?
Remove the damaged tissue
137
Where does cancer spread first?
To the lymph nodes that drain that area of the body
138
Which are the most common cancers to spread to bone?
Breast, prostate, Lung thyroid and kidney
139
How do they go about breast cancer treatment?
Confirm diagnosis see if it has spread to the lymph nodes, if it has they need removing otherwise chemo or radiotherapy
140
Why does complete removal of a tumour not always work?
There can be micrometastases present in the body
141
What is adjuvant therapy?
Extra treatment given after surgery such as anti oestrogen after breast cancer
142
What often leads to systemic infection with cancer?
Cancers of the blood or circulatory cells
143
Are all tumours benign or malignant?
They are between the extremes of highly spreadable and not at all
144
What is carcinogenesis?
Transformation of normal cells to neoplastic cells through genetic alterations or mutations
145
What is oncogenesis?
Benign or malignant tumours
146
What is the first step of cancer formation?
Causative agent like a toxin or radiation or sporadic mutation
147
What is a carcinogenic subastance?
One that causes cancer
148
What is an oncogenic substance?
Causes a tumour to be formed
149
Where are most cancer risks coming from/
85% from the environment
150
What are occupational or behavioural risks of cancer?
Smoking or industrial work
151
How can cancers be investigated ?
animal testing but can be different in human models
152
What are the classes of carcinogen?
Chemical viral ionising and non-ionising radiation, hormones parasites and mycotoxins also others
153
What are chemical carcinogens?
No general structure, some directly act others are metabolised which leads to one that affects you
154
What kind of cancers can radiation cause?
Thyroid, lung skin cancer
155
Which biological gents lead to cancers?
Oestrogen to mamanry and endometriu, mycotocis to liver cancer, parasites to cholangiocarcinoma
156
List some premalignant conditions?
Undescended testis, ulcerative clitis, cervical dysplasia colonoc polyps
157
What is neoplasm vs tumour?
A tumour is any swelling that could be neoplasm inflammation hypertrophy hyperplasia
158
What are the characteristics of neoplasia?
Autonomous, abnormal, persistent, new growth
159
What are the characteristics of neoplastic cells?
Derive from nucleated cells, grow in sme pattern as parent and do the same function as parent cell
160
What is stroma neoplasm?
Connective tissue growth around the neoplastic cells
161
What step is essential to tumour growth greater than 2mm?
Angiogenesis
162
What are the uses of classifying a neoplasm?
To get right treatment, provide prognosis,
163
How can neoplasms be defined?
Behavioural: benign or malignant
Histogenetic: by cell of origin
164
What are benign neoplasms like?
Localised non-invasive, Slow growth rate low mitotic activity, close resemblance to normal tissue circumscribed or encapsulated. nucleus normal rare necrocis or ulceeration
165
Why can benign neoplasms cause problems?
Production of hormones, obstruc flow or put pressure on other structures, transformation to malignant neoplasm
166
what do malignant neoplasms look like?
Invasive, Metastases, rapid growth variable resemblance to normal tissue poorly defined or irregular border, hyperchromatic nucleu pleomorphic nucles more mitosis necrosis and ulceration are common
167
What are the problems with malignant neoplasms?
Destroys tissue, metastases, blood loss, obstruction of flow hormone production paraneoplastic effects, pain
168
What does suffix oma mean?
Neoplasm
169
What does the prefix of the cancer mean?
The behaviour and cell type
170
What is papilloma?
Benign tumour of non-glandular non secretory epithelium can prefix with squamous
171
What is adenoma?
Benign tumour of glandular or secretory epithelium
172
What is carcinoma?
Malignant tumour of epithelial cells
173
What is a carcinoma of glandular epithelium called?
Adenocarcinoma
174
What is lipoma?
adipocytes
175
What is chondroma?
cartilage
176
What is osteoma?
Bone
177
What is angioma?
Vascular
178
What is rhabdomyoma?
Striated muscle
179
What is leiomyoma?
Smooth muscle
180
What is neuroma?
Nerves
181
What is a malignant connective tissue name?
Sarcoma sar meaning fleshy
182
What does anaplastic mean?
Cant tell where it is from
183
What are nomenclature exceptions for cancerous growths?
Melanomer is malignant mesothelioma is malignant and lymphoma is malignant some omas are not neoplasms granuloma mycetoma tuberculoma
184
What does endophytic growth mean?
They grow into the underlying tissue
185
What is in-situ neoplasia?
epithelial neoplasms where the neoplasia has the basement membrane intact.
186
What is invasion?
When a malignant neoplasm spreads from the initial site to directly adjacent tissues.
187
What is metastasis?
When a malignant tumour spreads from its primary site to produce a tumour at a secondary site it can occur by blood vessels lymhatics or body cavities
188
What is haematogenous spread?
Spread by blood vessels
189
What is trans-coelomic?
Spread by body cavities
190
What is involved in the metastatic cascade?
Detachment invasion intravasation evasion of host defences arrest extravasation and vascularisation
191
What are the characteristics of chemotherapy?
non selective for tumour cells other than tumour will be more affected as its dividing more, hits normal cells like white blood cells hair causes diarrhoea
192
What is the appropriate treatment for in situ carcinoma?
Excision!
193
What is micro-invasive carcinoma?
one which has only just breached the basement membrane
194
What helps with invasion of cancer?
collagenase cathesin D urokinase-type plasminogen activator
195
How do the cancer cells avoid being recognised tumour cells ?
Aggregation with platelets, shedding surface antigens, adhesion to other tumour cells.
196
What is extravasation?
They have adhesin receptors, collagenases, cell motility to come out of the vessel into the tissue
197
Where is a common site for metastasises?
In the lungs
198
Where doses colon usually metastasise to?
The liver
199
What do lots of cancer drugs do?
They bind to apparatus to stop DNA replication
200
When do conventional cancer treatments not work?
They don't work in cancers where there is a lack of apoptosis rather than over replication
201
What types of genetic mutatios are cancerous?
Growth promoting proto-oncogenes, Growth inhibiting cancer suppressor genes, Genes that regulat apoptosis, genes that regulate repair of damaged DNA
202
What does the immune system do?
Recognise pathogens and destry organisms
203
What is the innate immunity?
Instinctive, non-specific does not depend on lymphocytes
204
What is the adaptive immune system?
Specific aquiredd and learned ummunity requires lymphocytes, antibodies.
205
What is serum?
Plasma without fibrinogen and other clotting factors
206
What is the mediator for phagocytes?
Complement and cytikines
207
What is the mediator for t cells?
Cytokines
208
What is not generated by the common myeloid progenitor?
The lymphocytes
209
Which lymphocytes are polymrphnuclear?
Neutrophil, eosinophil and basophil
210
What are the soluble mediators of the Immune system?
Complement antibodies and cytokines and chemokines
211
What are complement molecules?
They are secreted by the liver but need to be activated to be functional and they are activated as part of the immune response
212
What are the modes of action of complement?
Direct lysis, attract mroe leukocytes to the site of infection and coat invading organisms
213
What are antibodies?
Molecules that bind to antigens
214
What are the types of immunoglobulin?
IgG(1-4) IgA(1,2), IgM, IgD, IgE
215
What shape is IgG?
It is Y shaped
216
What shape is IgM?
Pentagon
217
Which is the most common antibody in the blood?
IgG 70-75%
218
Where are IgM antibodies found?
In the blood as too big to cross the endothelium
219
What are IgM antibodies involved with?
primary immune response initial contact with antigen
220
What shape is IgA?
Double ended one
221
Where is IgA found?
In mucous secretions
222
Where is IgD found?
Transmembrane monomeric present on mature B cells
223
Which is the least common antibody?
IgE
224
Which cells have a lot of IgE on the outside of them?
Basophils and mast cells
225
What do antibodies do?
Help things bind to antigens on a pathogen
226
What is an interferon?
Induce a state of antiviral resistance in uninfected cells and limit the spread of viral infection
227
What are interleukins?
They are produced by many cells and can be pro-inflammatory and cause cells to divide or secrete different factors
228
What are chemokines?
Chemotactic cytokines they direct movement of leukocytes and other celsl into the tissue
229
Is innate or adaptive immunity faster?
adaptive is faster
230
Which type of immunity is involved with lymphocytes/
Adaptive
231
What are the components of the innate immunity?
Physical and chemical barriers, phagocytic cells neutrophils and macrophages, blood proteins
232
What are the physical barriers of the body?
The skin, tears, saliva, bronchi, ph of intestines and stomach
233
What is extravasation?
Movement of leukocytes ut of the blood vessels
234
Where can microbes be sensed?
In the blood by monocytes and neutrophils and in tissues by macrophages and dendritic cells
235
What are PAMPs?
Pathogen associated molecular patterns
236
PRR
patter recognition receptors on cells
237
What are Toll like receptors?
They sense microbes with receptros
238
What are the two types of complement?
Classical bound antibodies bind to microbe and C' binds to microbe Lectin activated by mannose binding lectin bound to microbe
239
What does complement do?
Lyse microbes directly, chemotaxs opsonisation
240
What are the mechanisms of microbial killing?
Reactive oxygen intermediates, Superoxides, Nitric oxide (NO), also enzymes proteins and pH
241
Why is adaptive immunity needed?
Microbes are evolving and learn to Hide from our immune system
242
What attacks intracellular microbes?
Cell mediated T cells
243
What are primary lymphoid tissues?
thymus bone marrow
244
What are secondary lymphoid tissues?
Spleen, lymph nodes, MALT
245
Which cells react to antigen presenting cells?
T lymphocytes
246
What is major histocompatability complex?
It keeps the antigen presenting cells from being attacked by the immune system
247
What is the process of removal of self recognising T cells called?
T cell selection in thymus
248
what codes for major histocompatibility complex?
Human leukocyte antigen genes
249
Which MHC is on antigen resenting cells?
Class 2
250
Which T cell kills intracellular pathogen?
CD8
251
what are antibodies made of?
Soluble glycoprteins
252
How do antibodies protect against infection?
Neutralise toxins, immobilise microbes, prevent binding to host cells, form complexes, it can inhance innate mechanisms like complement and bind Fc receptors
253
What is the function of T helper cells(CD4+ve)?
Help B cells make antibodies help develop cytotoxic T cells and activate macrophages and natural killer cells
254
What is the function of cytotoxic cells?
Recognise and kill infected host cells (CD8+ve)
255
What do T regulatory cells do?
They supress the immune system
256
Which cells express MHC I?
All nucleated cells display antigens to T killer cells
257
Which cells express MHC 2?
Expressed by macrophaes, dendritic cells and B cells, display antigen to CD4+ve t helper cells
258
What are IL-2 gamma interferon and TNFbeta involved in?
Classic cell-mediated immunity and important in intracellular infections
259
What are TH2 cells that produce IL-4 5 6 10 and 13 involved in?
Activating eosinophils and mast cells involved in helminth infections and allergy
260
How does the body deal with viruses?
Kill the cell to stop replication
261
What are the groups of patterns that can be recognised by the body?
Gram positive or negative dsRNA CpG motifs in the cell walls and DNA
262
What are TLR molecules?
They recognise many different molecules on pathogens and then they can activate signalling inside the cell to react to an effect can also be for damage to tissues
263
What is passive immunisation?
Through the placenta or breast milk by transfer of maternal antibodies to the baby or from treatment with antibodies injected into an adult
264
What is the problem with passive immunity?
It doesn't providel long term immunity and doesnt contribute to immuniological memory
265
What is active immunisation?
vaccination where the immune system is sort of trained to be better and mobilise the right thing
266
What is the difference between innoculation and immunisation?
Inoculation is only introducing a pathogen into something immunisation is to stiulate a response and immunity
267
What are the stages of active immunisation?
Engage the innate immune system, elicit danger signals using PAMPs and TLR receptors that activate antigen presenting cells then engages adaptive immunity to generae memory T and B cells
268
What is usually happening with the secondary response?
IgG is more predominant much faster response and higher peak
269
What is the importance of onset time of diseases to be vaccinated against?
If its fast need to have enough immunity to ramp up antibody production quickly enough flu is fast acting polio can take 3 days
270
What are the classes of vaccine?
Whole organism, subunit. peptides, DNA vaccines, Engineered virus
271
What are the types of whole organism vaccine?
Live modified live attenuated pathogen, or killed inactivated
272
What are the benefits of a whole organism vaccine attenuated?
transient infection get a full natural immune response, prolongued contact witht eh immune system, T and B cell memory response, prolongued comprehensive protection, only often need single vaccianation
273
What are the negatives of whole organism vaccination attenuated?
immunocompromised patients can become infected and ill, complicatins like encephalitis, can revert to virulent form leading to outbreak
274
What are the benefits of inactivated pathogen?
No risk of infection easier storage, wide rance of antigneic components so good immune response
275
What are the risks of inactivated pathogen?
Tend to just activate humoral responses, can be weak immune response as no replication, repeat booser vaccine often needed which brings problems of compliance
276
What are sub unit vaccines?
Ones where part of a toxin is injectes or polysaccharides found on it or recombinant microbial antigens
277
What are the advantages of subunit vaccines?
Safe as only bits of the pathogen are used, easy to store and no risk of infection
278
What are the disadvantages of subunit vaccines?
Immune response less powerful repeated vaccinations and adjuvants and have to considered
279
Which vaccines use live attenuated pathogen?
TB polio
280
Which vaccines use inactivated pathogen?
Hep A
281
What are bacterial exotoxins?
The toxin that a pathogen can produce is given to sensitise the body to it a toxoid is an inactivated toxin
282
What are synthetic peptides as vaccines?
Can produce peptides that are good to select for Bcells and HLA is quite hard
283
What are DNA vaccines?
They are aiming to transiently epress genes from pathogens in host cels and generate an immune response similar to a natural infection leading to T and B cell memory responses.
284
What are the benefits of a DNA vaccine?
Safe even in immunocompromised patients. No requirement for complex storage and transportation, drug delivery can be simple and adaptable to widespread vaccination programs
285
What are hte disadvantage of DNA vaccines?
No transient infection and only induce a mild response so often need boosting
286
What are recombiant vector vaccines?
Aim to imitate the effects of transient infection with pathogen but using a non-pathogenic organism the genes for major pathogen antigens are introduced into a non-pathogening or attenuated organism and given to the host.
287
What are adjuvants in a vaccine?
Substances added to stimulate the immune system
288
What are Interferons?
They induce a state of antiviral resistance in uninfected cells
289
What are interleukins?
Produced by many cells can be pro-inflammatory or anti-inflammatory
290
What are colony stimulating factors?
Involved in directing the division and differentiation of bone marrow stem cells and precursors of leukocytes
291
How are microbes sensed in the blood?
Monocytes and neutrophils
292
How are microbes detected in tissues?
Macrophages and dendritic cells
293
What stimulates TH2 formation?
IL-12
294
What stimulates TH1 formation?
IL-4/5
