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Phase 2 mine > ICS immunology and pathology > Flashcards

ICS immunology and pathology Flashcards

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

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2
Q

Who referrs to a coroner?

A

Doctors, relatives poleace registrar, anatomical pathology technicians

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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

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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?

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5
Q

What is involved in an autopsy?

A

pictures of outside potentially scans, microbioloy internal eternal removal of organs histology.

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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.

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7
Q

How can inflammation be a problem?

A

space occupying lesions, fibrosis from chronic inflammation can dirupt the structure and function of tissues

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8
Q

What is acute inflammation?

A

Initial and transiant erios of tissue reactions to injury

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9
Q

What is chronic inflammation?

A

The subsequent and prolonged tissue reactions following acute inflamation

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10
Q

What separates chronic and acute inflammation?

A

the types of cells involved in the inflammatory response

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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.

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12
Q

What are the end points of acute inflammation?

A

Resolution, suppuration(abscess) organisation or progression to chronic inflammation

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13
Q

What can cause acute inflammation?

A

Microbial infection, hypersensitivity reactions, pysiical agents like trauma or radiation, chemicals bacterial toxins or tissue necrosis

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14
Q

How is microbial infection inflammation mediated?

A

Viruses destroc cells, bacteria release exotoxins, additionally some orgnisms cause immunologically mediated inflamation from hypersenistibity

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15
Q

What is a hypersensitivity reaction?

A

when the reaction is not proportiantd to the dammage to cells

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16
Q

Why might tissue necrosis occur?

A

Death of tissues from lack of oxygen or nutrients often from inadequate blood flow,

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17
Q

What are the macroscopic appearaces of acute inflammation?

A

Rubor(redness) Calor(heat) Tumor(swelling) Dolor(pain)

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18
Q

What causes redness?

A

Dilatation of small blood vessels of the area

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19
Q

What causes heat in inflammation?

A

Increased peripheral bloodflow (hyperaemia) or a systemic fever

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20
Q

What is cellulitis?

A

Acute inflammation and redness (erythema) on the lateral side of the foot due to vasclar dilatation

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21
Q

What causes swelling in inflammation?

A

From oedema accumulation of fluid in the extravascular space as part of the fluid exudate

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22
Q

What causes pain in inflammation?

A

tissue deformation, some chamical mediators can induce pain, serotoin prostalandins and bradykinin

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23
Q

What happens in the early stages of acute inflammation?

A

Fibrin oedema fluid, neutrophil polymorphs accumlate

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24
Q

What happens in blood vessels during inflammation?

A

they dilate and become more permeable.

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25
Q

What increases vascular permeability?

A

histamine bradykinin, nitric oxide, C5a leucotriene B4 platelety activating factors

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26
Q

How do white blood cells leave the vessels?

A

Through the endothelial gaps through the basal lamina into the adventitia

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27
Q

What are the effects of histamine and thrombin on the endothelial surcace?

A

Increase expression of molecules that activate neutrophils to adhere to the endothelium

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28
Q

What chemical mediators are released by cells?

A

Histamine also lysosomal compounds ecosanoids serotonin(5hydroxytruptamine and chemokines

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29
Q

what are the four enzymatic cascade systems of plasma?

A

Complement, the kinins, coagulation factors and the fibrinolytic system

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30
Q

What feeds the complement system?

A

Kinin and fibrinolytic sustem

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31
Q

What is the kinin system?

A

Factor 12 produces kallikrein and kininogens that produce kinins lie bradykinin

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32
Q

What are the differences in the transient phase and prolonged phase of vascular permeability?

A

Histamine is transient then other mediators prolong it. NO, Leucotriene, Prostaglandins, Bradykinin

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33
Q

What does neutrophil polymorph do?

A

They engulf lysosomes and phagocytic vacuoles,

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34
Q

What are the negative effects of inflammation?

A

Digestion of normal tissues, Swelling inappropriate inflammation response.

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35
Q

What causes suppuration?

A

Excessive exudate and cn lead to rupture and discharge of pus.

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36
Q

What can happen after excessive necrosis?

A

Repair and organisation and fibrosis

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37
Q

What leads to chronic inflammation?

A

Persistent causal agents often leads to chronic inflammation

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38
Q

What are the systemic effects of inflammation?

A

Pyrexia, constitutional symptoms, weight loss reactive hyperplasia of reticuloendothelial system, haematological changes amyloidosis.

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39
Q

What is resolution?

A

initiating factor removed. tissue undamaged or able to regenerate

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40
Q

What is repair?

A

Initiating factor still present, tissue damaged and unable to regenerate

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41
Q

What happens in the repair of skin?

A

Replacement of damaged tissue by fibrous tissue

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42
Q

Which cells are thought to not regeneragre/

A

The heart cells and neurones

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43
Q

Which cells are known to regenerate?

A

Hepatocytes, neumocytes all blood cells gut epithelium skin epithelium and osteocytes

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44
Q

What are required for a thrombus to form?

A

Change in the vessel wall, change in blood flow or a change in blood constituents

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45
Q

What is an embolus?

A

A mass of material in the vascualr system able to become lodged within a vessel and block it

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46
Q

What is ischemia?

A

Reduction in blood flow

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47
Q

What is an MCCD?

A

Medical certificate cause of death

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48
Q

which cells come first in inflamation?

A

neutrophil polymorphs

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49
Q

What do macrophages do?

A

They break up old tissue and ingest bateria and debris can be antigen presenting

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50
Q

How long can lymphocytes like?

A

Years

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51
Q

What do lymphocytes do?

A

They produce chemicals which attract other inflammatory cells and memory

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52
Q

What is the role of fibroblasts?

A

They produce fibrous tissue.(scar tissue)

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53
Q

What is a granuloma?

A

Specific pattern of lymphocytes and macrophages in inflamation in TB sarcoidosis, leprocy

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54
Q

What is granulation tissue/

A

Macroscopic tissue that looks bobbly

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55
Q

What is prostaglandin synthetase?

A

It is an enzyme that produces prostaglandins

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56
Q

How do steroids reduce inflamation?

A

They regulate DNA that give more inhibitors of inflammation.

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57
Q

What is antihistamine?

A

competitive inhibitor for histamine

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58
Q

What is resolution?

A

It goes back to normal it can repair fully or the tissue is undamaged

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59
Q

What can the liver regenerate from?

A

When you have one big insult to it it can go back to normal

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60
Q

What permanently damages the liver?

A

continuous damage, to the liver

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61
Q

What is fibrous vs cirrhosis?

A

cirrhoses is nodular when regrowth has begun.

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62
Q

What are the lungs like in repair/ regeneration?

A

Resolution can happen as long as architecture is not damage

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63
Q

What is the affect of COVID-19 on lungs?

A

Can cause small damage and fluid but can cause fibrosis

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64
Q

What happens in skin abrasion repair?

A

The cells at the bottom divide and repain the skin, can grow back from the hair follicle

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65
Q

What is first intention healing?

A

Heals after the incision and bring the edges together to allow strong collagen to join it.

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66
Q

What is second intention healing?

A

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

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67
Q

What is granulation tissue in skin healing?

A

Small loops of blood vessels causing granulations on damaged skin

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68
Q

Where does fibrous tissue usually form?

A

In tissue that can’t regenerate, spinal cord heart attack, brain, skin somethimes

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69
Q

What is gliosis?

A

Brain scarring fibrous tissue has thinner fibrous strands

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70
Q

What makes up a granuloma?

A

Macrophages and fused macrophages with lymphocytes around the outside

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71
Q

What type of inflammation is a granuloma?

A

Chronic inflammation

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72
Q

What can inflammation do even when treated?

A

can destroy tissue still

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73
Q

What do anti inflammatory drugs also affect?

A

They can affect immunity

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74
Q

what is rebound tenderness?

A

When remove pressure from abdomen it causes pain acute abdomen infection

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75
Q

What is diverticulitis?

A

When outpouching of large bowel ruptures and gets infected

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76
Q

What are the key element of acute inflamation?

A

Polymorph neutrophils formation of puss

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77
Q

What prevents clotting normally?

A

Laminar flow and the endothelial lining

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78
Q

How does COVID affect thrombosis?

A

Damages the blood vessels with microthrombi

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79
Q

What is an end artery?

A

only have one blood supply to get it

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80
Q

Which organs are not end artery supplied?

A

Lungs liver some ares of the brain

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81
Q

When does atherosclerosis usually happen?

A

In later years of life around 50 onwards

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82
Q

Which arteries are most likely to get atheroma and why?

A

The aorta and systemic arteries because they are at a higher pressure

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83
Q

What is atheroma?

A

Build up of tissue in the arteries

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84
Q

What forms an atherosclerotic lesion?

A

Lipids and cholesterol then fibrous tissue builds up as inflammation takes place

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85
Q

What layer starts an atherosclerotic plaque?

A

the endothelial lining can affect the internal elastic lamina

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86
Q

What are the risk factors of atheroma?

A

Smoking Diabetes high BP high lipids being a man

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87
Q

What is it about smoking that affects endothelial cells?

A

free radicals nicotine and CO

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88
Q

Why does diabetes cause endothelial damage?

A

Superoxide anions, glycosylation products.

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89
Q

What factors can lead to apoptosis?

A

detachment from the adhesion surface certain extracellular factors, DNA dammage

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90
Q

What can induces apoptosis?

A

DNA damage

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91
Q

What signals the cell to apoptose?

A

Fas ligands Bcl2 protein activating, caspases

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92
Q

How is apoptoses involved in disease?

A

HIV too much cancer too little

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93
Q

What can cause necrosis?

A

Venom, frost bite burns, ischemia infection with bacteria

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94
Q

What are the types of necrosis?

A

Coagulative, liquifactive and caseous necrosis

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95
Q

What is the first stage of atherosclerosis?

A

fatty streak can be undone

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96
Q

What makes up a plaque?

A

Fibrous tissue, lipids(cholesterol), lymphocytes(chronic inflammation),

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97
Q

Does diabetes always damage arteries?

A

Not unless it is uncontrolled

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98
Q

What is lipid insudation theory?

A

the theory that high lipids lead to lipids passing through endothelial lining. disproven now.

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99
Q

What is the main theory of the formation of plaque?

A

The endothelial dammage theory. they can be killed or damage by toxins from various sources, high blood pressure shearing forces on endothelia cells

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100
Q

what prevention can there be?

A

Baby aspirin to stop platelet aggregation

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101
Q

How does apoptosis happen?

A

Nucleus condenses pyknosis, the organelles go into blebs and phagocytes eat the blebs

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102
Q

What are caspases?

A

They are molecules that initiate apoptosis

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103
Q

What is fas ligand?

A

The ligand for fas receptor to signal apoptosis

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104
Q

What is the use of apoptosis in embryology?

A

Helps the formation of the shape of organs and tissues

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105
Q

What is coagulative necrosis?

A

semi solid death

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106
Q

What is liquefactive necrosis?

A

When the brain digests all of the material in that has died.

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107
Q

What is caseous necrosis?

A

Smooth cheese texture often in TB

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108
Q

Are all congenital diseases genetic?

A

No some can come from foetal nutrition or exposure to toxins

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109
Q

What does multifactorial mean?

A

That there are many causes both genetic and environmental that affect the incidence of disease

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110
Q

What shows strong evidence of genetic causes for disease?

A

Family studies and studies on twins

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111
Q

What are HLA types?

A

Human leucocyte antigens they are expressed on the surface of nucleated cells and on the cells that interact with t lymphocytes

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112
Q

What is a neoplasm?

A

They are tumours new growths

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113
Q

What chemical agents can cause disease?

A

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

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114
Q

How does carbon monoxide affect the arterial endothelial cells/

A

It causes hypoxia

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115
Q

What are the types of growth?

A

Hypertorphy and hyperplasia

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116
Q

What is hypertrophy?

A

The size of the cells themselves increases

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117
Q

What is hyperplasia?

A

When the cells repilcate and increase in number

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118
Q

Where does hyperplasia happen in normal function?

A

Breast tissue during lactation

119
Q

What can cause pathological atrophy?

A

Loss of blood supply, denervation, pressure lack of nutrients, lack of hormonal stimulation or from hormonal stimulation

120
Q

What is metaplasia?

A

Reversible transformation of one type of mature cell into another fully differentiated cell type.

121
Q

When does metaplasia happen?

A

As an adaptive response to injurios stimuli

122
Q

What is dysplasia?

A

A premalignant condition characterised by increased growth cellular atypua and decreased differentiation

123
Q

What is ageing?

A

Progressive degeneration or loss of function

124
Q

What are common areas to lose function in with age?

A

The brain ear, joints,

125
Q

What could lead to cells dying and therefore aging?

A

Free radicals defective repair fragility syndrome, telomeric shortening

126
Q

What does aging to to skin?

A

Wrinkling due to loss of elastin and collaen, fragle and bruises easily.

127
Q

What is sarcpenia?

A

Loss of muscle mass

128
Q

What changes happen to bones with ageing?

A

Osteoarticular ageing where the bones lose mass and stretch and the articular surfaces wear.

129
Q

What happens to the immune system in ageing?

A

Impaired immunity thymus atrophy leads to fewer immune cells,

130
Q

What happens to the cardiovascular system in ageing?

A

Atherosclerosis, loss of elacticity in the aorta, distension of certain arteries, calcification of blood vessels,

131
Q

What type of growth can nerve cells do?

A

Hyperplasia

132
Q

What is optic atrophy?

A

The whitening of the optic disk

133
Q

Which tissues are dividing?

A

Skin , gut epithelium

134
Q

What is likely to cause sarcopenia?

A

Decreased growth hormone and testosterone

135
Q

How does basal cell carcinoma spread?

A

Only spreads locally and never spreads to other parts of the body

136
Q

How to cure basal cell carcinoma?

A

Remove the damaged tissue

137
Q

Where does cancer spread first?

A

To the lymph nodes that drain that area of the body

138
Q

Which are the most common cancers to spread to bone?

A

Breast, prostate, Lung thyroid and kidney

139
Q

How do they go about breast cancer treatment?

A

Confirm diagnosis see if it has spread to the lymph nodes, if it has they need removing otherwise chemo or radiotherapy

140
Q

Why does complete removal of a tumour not always work?

A

There can be micrometastases present in the body

141
Q

What is adjuvant therapy?

A

Extra treatment given after surgery such as anti oestrogen after breast cancer

142
Q

What often leads to systemic infection with cancer?

A

Cancers of the blood or circulatory cells

143
Q

Are all tumours benign or malignant?

A

They are between the extremes of highly spreadable and not at all

144
Q

What is carcinogenesis?

A

Transformation of normal cells to neoplastic cells through genetic alterations or mutations

145
Q

What is oncogenesis?

A

Benign or malignant tumours

146
Q

What is the first step of cancer formation?

A

Causative agent like a toxin or radiation or sporadic mutation

147
Q

What is a carcinogenic subastance?

A

One that causes cancer

148
Q

What is an oncogenic substance?

A

Causes a tumour to be formed

149
Q

Where are most cancer risks coming from/

A

85% from the environment

150
Q

What are occupational or behavioural risks of cancer?

A

Smoking or industrial work

151
Q

How can cancers be investigated ?

A

animal testing but can be different in human models

152
Q

What are the classes of carcinogen?

A

Chemical viral ionising and non-ionising radiation, hormones parasites and mycotoxins also others

153
Q

What are chemical carcinogens?

A

No general structure, some directly act others are metabolised which leads to one that affects you

154
Q

What kind of cancers can radiation cause?

A

Thyroid, lung skin cancer

155
Q

Which biological gents lead to cancers?

A

Oestrogen to mamanry and endometriu, mycotocis to liver cancer, parasites to cholangiocarcinoma

156
Q

List some premalignant conditions?

A

Undescended testis, ulcerative clitis, cervical dysplasia colonoc polyps

157
Q

What is neoplasm vs tumour?

A

A tumour is any swelling that could be neoplasm inflammation hypertrophy hyperplasia

158
Q

What are the characteristics of neoplasia?

A

Autonomous, abnormal, persistent, new growth

159
Q

What are the characteristics of neoplastic cells?

A

Derive from nucleated cells, grow in sme pattern as parent and do the same function as parent cell

160
Q

What is stroma neoplasm?

A

Connective tissue growth around the neoplastic cells

161
Q

What step is essential to tumour growth greater than 2mm?

A

Angiogenesis

162
Q

What are the uses of classifying a neoplasm?

A

To get right treatment, provide prognosis,

163
Q

How can neoplasms be defined?

A

Behavioural: benign or malignant
Histogenetic: by cell of origin

164
Q

What are benign neoplasms like?

A

Localised non-invasive, Slow growth rate low mitotic activity, close resemblance to normal tissue circumscribed or encapsulated. nucleus normal rare necrocis or ulceeration

165
Q

Why can benign neoplasms cause problems?

A

Production of hormones, obstruc flow or put pressure on other structures, transformation to malignant neoplasm

166
Q

what do malignant neoplasms look like?

A

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
Q

What are the problems with malignant neoplasms?

A

Destroys tissue, metastases, blood loss, obstruction of flow hormone production paraneoplastic effects, pain

168
Q

What does suffix oma mean?

A

Neoplasm

169
Q

What does the prefix of the cancer mean?

A

The behaviour and cell type

170
Q

What is papilloma?

A

Benign tumour of non-glandular non secretory epithelium can prefix with squamous

171
Q

What is adenoma?

A

Benign tumour of glandular or secretory epithelium

172
Q

What is carcinoma?

A

Malignant tumour of epithelial cells

173
Q

What is a carcinoma of glandular epithelium called?

A

Adenocarcinoma

174
Q

What is lipoma?

A

adipocytes

175
Q

What is chondroma?

A

cartilage

176
Q

What is osteoma?

A

Bone

177
Q

What is angioma?

A

Vascular

178
Q

What is rhabdomyoma?

A

Striated muscle

179
Q

What is leiomyoma?

A

Smooth muscle

180
Q

What is neuroma?

A

Nerves

181
Q

What is a malignant connective tissue name?

A

Sarcoma sar meaning fleshy

182
Q

What does anaplastic mean?

A

Cant tell where it is from

183
Q

What are nomenclature exceptions for cancerous growths?

A

Melanomer is malignant mesothelioma is malignant and lymphoma is malignant some omas are not neoplasms granuloma mycetoma tuberculoma

184
Q

What does endophytic growth mean?

A

They grow into the underlying tissue

185
Q

What is in-situ neoplasia?

A

epithelial neoplasms where the neoplasia has the basement membrane intact.

186
Q

What is invasion?

A

When a malignant neoplasm spreads from the initial site to directly adjacent tissues.

187
Q

What is metastasis?

A

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
Q

What is haematogenous spread?

A

Spread by blood vessels

189
Q

What is trans-coelomic?

A

Spread by body cavities

190
Q

What is involved in the metastatic cascade?

A

Detachment invasion intravasation evasion of host defences arrest extravasation and vascularisation

191
Q

What are the characteristics of chemotherapy?

A

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
Q

What is the appropriate treatment for in situ carcinoma?

A

Excision!

193
Q

What is micro-invasive carcinoma?

A

one which has only just breached the basement membrane

194
Q

What helps with invasion of cancer?

A

collagenase cathesin D urokinase-type plasminogen activator

195
Q

How do the cancer cells avoid being recognised tumour cells ?

A

Aggregation with platelets, shedding surface antigens, adhesion to other tumour cells.

196
Q

What is extravasation?

A

They have adhesin receptors, collagenases, cell motility to come out of the vessel into the tissue

197
Q

Where is a common site for metastasises?

A

In the lungs

198
Q

Where doses colon usually metastasise to?

A

The liver

199
Q

What do lots of cancer drugs do?

A

They bind to apparatus to stop DNA replication

200
Q

When do conventional cancer treatments not work?

A

They don’t work in cancers where there is a lack of apoptosis rather than over replication

201
Q

What types of genetic mutatios are cancerous?

A

Growth promoting proto-oncogenes, Growth inhibiting cancer suppressor genes, Genes that regulat apoptosis, genes that regulate repair of damaged DNA

202
Q

What does the immune system do?

A

Recognise pathogens and destry organisms

203
Q

What is the innate immunity?

A

Instinctive, non-specific does not depend on lymphocytes

204
Q

What is the adaptive immune system?

A

Specific aquiredd and learned ummunity requires lymphocytes, antibodies.

205
Q

What is serum?

A

Plasma without fibrinogen and other clotting factors

206
Q

What is the mediator for phagocytes?

A

Complement and cytikines

207
Q

What is the mediator for t cells?

A

Cytokines

208
Q

What is not generated by the common myeloid progenitor?

A

The lymphocytes

209
Q

Which lymphocytes are polymrphnuclear?

A

Neutrophil, eosinophil and basophil

210
Q

What are the soluble mediators of the Immune system?

A

Complement antibodies and cytokines and chemokines

211
Q

What are complement molecules?

A

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
Q

What are the modes of action of complement?

A

Direct lysis, attract mroe leukocytes to the site of infection and coat invading organisms

213
Q

What are antibodies?

A

Molecules that bind to antigens

214
Q

What are the types of immunoglobulin?

A

IgG(1-4) IgA(1,2), IgM, IgD, IgE

215
Q

What shape is IgG?

A

It is Y shaped

216
Q

What shape is IgM?

A

Pentagon

217
Q

Which is the most common antibody in the blood?

A

IgG 70-75%

218
Q

Where are IgM antibodies found?

A

In the blood as too big to cross the endothelium

219
Q

What are IgM antibodies involved with?

A

primary immune response initial contact with antigen

220
Q

What shape is IgA?

A

Double ended one

221
Q

Where is IgA found?

A

In mucous secretions

222
Q

Where is IgD found?

A

Transmembrane monomeric present on mature B cells

223
Q

Which is the least common antibody?

A

IgE

224
Q

Which cells have a lot of IgE on the outside of them?

A

Basophils and mast cells

225
Q

What do antibodies do?

A

Help things bind to antigens on a pathogen

226
Q

What is an interferon?

A

Induce a state of antiviral resistance in uninfected cells and limit the spread of viral infection

227
Q

What are interleukins?

A

They are produced by many cells and can be pro-inflammatory and cause cells to divide or secrete different factors

228
Q

What are chemokines?

A

Chemotactic cytokines they direct movement of leukocytes and other celsl into the tissue

229
Q

Is innate or adaptive immunity faster?

A

adaptive is faster

230
Q

Which type of immunity is involved with lymphocytes/

A

Adaptive

231
Q

What are the components of the innate immunity?

A

Physical and chemical barriers, phagocytic cells neutrophils and macrophages, blood proteins

232
Q

What are the physical barriers of the body?

A

The skin, tears, saliva, bronchi, ph of intestines and stomach

233
Q

What is extravasation?

A

Movement of leukocytes ut of the blood vessels

234
Q

Where can microbes be sensed?

A

In the blood by monocytes and neutrophils and in tissues by macrophages and dendritic cells

235
Q

What are PAMPs?

A

Pathogen associated molecular patterns

236
Q

PRR

A

patter recognition receptors on cells

237
Q

What are Toll like receptors?

A

They sense microbes with receptros

238
Q

What are the two types of complement?

A

Classical bound antibodies bind to microbe and C’ binds to microbe Lectin activated by mannose binding lectin bound to microbe

239
Q

What does complement do?

A

Lyse microbes directly, chemotaxs opsonisation

240
Q

What are the mechanisms of microbial killing?

A

Reactive oxygen intermediates, Superoxides, Nitric oxide (NO), also enzymes proteins and pH

241
Q

Why is adaptive immunity needed?

A

Microbes are evolving and learn to Hide from our immune system

242
Q

What attacks intracellular microbes?

A

Cell mediated T cells

243
Q

What are primary lymphoid tissues?

A

thymus bone marrow

244
Q

What are secondary lymphoid tissues?

A

Spleen, lymph nodes, MALT

245
Q

Which cells react to antigen presenting cells?

A

T lymphocytes

246
Q

What is major histocompatability complex?

A

It keeps the antigen presenting cells from being attacked by the immune system

247
Q

What is the process of removal of self recognising T cells called?

A

T cell selection in thymus

248
Q

what codes for major histocompatibility complex?

A

Human leukocyte antigen genes

249
Q

Which MHC is on antigen resenting cells?

A

Class 2

250
Q

Which T cell kills intracellular pathogen?

A

CD8

251
Q

what are antibodies made of?

A

Soluble glycoprteins

252
Q

How do antibodies protect against infection?

A

Neutralise toxins, immobilise microbes, prevent binding to host cells, form complexes, it can inhance innate mechanisms like complement and bind Fc receptors

253
Q

What is the function of T helper cells(CD4+ve)?

A

Help B cells make antibodies help develop cytotoxic T cells and activate macrophages and natural killer cells

254
Q

What is the function of cytotoxic cells?

A

Recognise and kill infected host cells (CD8+ve)

255
Q

What do T regulatory cells do?

A

They supress the immune system

256
Q

Which cells express MHC I?

A

All nucleated cells display antigens to T killer cells

257
Q

Which cells express MHC 2?

A

Expressed by macrophaes, dendritic cells and B cells, display antigen to CD4+ve t helper cells

258
Q

What are IL-2 gamma interferon and TNFbeta involved in?

A

Classic cell-mediated immunity and important in intracellular infections

259
Q

What are TH2 cells that produce IL-4 5 6 10 and 13 involved in?

A

Activating eosinophils and mast cells involved in helminth infections and allergy

260
Q

How does the body deal with viruses?

A

Kill the cell to stop replication

261
Q

What are the groups of patterns that can be recognised by the body?

A

Gram positive or negative dsRNA CpG motifs in the cell walls and DNA

262
Q

What are TLR molecules?

A

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
Q

What is passive immunisation?

A

Through the placenta or breast milk by transfer of maternal antibodies to the baby or from treatment with antibodies injected into an adult

264
Q

What is the problem with passive immunity?

A

It doesn’t providel long term immunity and doesnt contribute to immuniological memory

265
Q

What is active immunisation?

A

vaccination where the immune system is sort of trained to be better and mobilise the right thing

266
Q

What is the difference between innoculation and immunisation?

A

Inoculation is only introducing a pathogen into something immunisation is to stiulate a response and immunity

267
Q

What are the stages of active immunisation?

A

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
Q

What is usually happening with the secondary response?

A

IgG is more predominant much faster response and higher peak

269
Q

What is the importance of onset time of diseases to be vaccinated against?

A

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
Q

What are the classes of vaccine?

A

Whole organism, subunit. peptides, DNA vaccines, Engineered virus

271
Q

What are the types of whole organism vaccine?

A

Live modified live attenuated pathogen, or killed inactivated

272
Q

What are the benefits of a whole organism vaccine attenuated?

A

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
Q

What are the negatives of whole organism vaccination attenuated?

A

immunocompromised patients can become infected and ill, complicatins like encephalitis, can revert to virulent form leading to outbreak

274
Q

What are the benefits of inactivated pathogen?

A

No risk of infection easier storage, wide rance of antigneic components so good immune response

275
Q

What are the risks of inactivated pathogen?

A

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
Q

What are sub unit vaccines?

A

Ones where part of a toxin is injectes or polysaccharides found on it or recombinant microbial antigens

277
Q

What are the advantages of subunit vaccines?

A

Safe as only bits of the pathogen are used, easy to store and no risk of infection

278
Q

What are the disadvantages of subunit vaccines?

A

Immune response less powerful repeated vaccinations and adjuvants and have to considered

279
Q

Which vaccines use live attenuated pathogen?

A

TB polio

280
Q

Which vaccines use inactivated pathogen?

A

Hep A

281
Q

What are bacterial exotoxins?

A

The toxin that a pathogen can produce is given to sensitise the body to it a toxoid is an inactivated toxin

282
Q

What are synthetic peptides as vaccines?

A

Can produce peptides that are good to select for Bcells and HLA is quite hard

283
Q

What are DNA vaccines?

A

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
Q

What are the benefits of a DNA vaccine?

A

Safe even in immunocompromised patients. No requirement for complex storage and transportation, drug delivery can be simple and adaptable to widespread vaccination programs

285
Q

What are hte disadvantage of DNA vaccines?

A

No transient infection and only induce a mild response so often need boosting

286
Q

What are recombiant vector vaccines?

A

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
Q

What are adjuvants in a vaccine?

A

Substances added to stimulate the immune system

288
Q

What are Interferons?

A

They induce a state of antiviral resistance in uninfected cells

289
Q

What are interleukins?

A

Produced by many cells can be pro-inflammatory or anti-inflammatory

290
Q

What are colony stimulating factors?

A

Involved in directing the division and differentiation of bone marrow stem cells and precursors of leukocytes

291
Q

How are microbes sensed in the blood?

A

Monocytes and neutrophils

292
Q

How are microbes detected in tissues?

A

Macrophages and dendritic cells

293
Q

What stimulates TH2 formation?

A

IL-12

294
Q

What stimulates TH1 formation?

A

IL-4/5

Phase 2 mine (13 decks)

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