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Phase 2a > ICS > Flashcards

ICS Flashcards

1
Q

Define inflammation

A

The body’s response to injury/infection

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2
Q

Name the two types of inflammation

A

Acute (neutrophil-mediated inflammation)
Chronic (macrophage/lymphocyte mediated inflammation)

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3
Q

Why are neutrophils polymorph?

A

They have polylobed nuclei

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4
Q

Where are neutrophil polymorphs made + what is their lifespan?

A

Made in bone marrow, 2-3 days

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5
Q

What do neutrophils do?

A

Phagocytosis + contain lysosomes to kill + digest bacteria

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6
Q

What are the first cells to arrive at the site of acute inflammation?

A

Neutrophils

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7
Q

What are the first cells to arrive at the site of chronic inflammation?

A

Macrophages + lymphocytes

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8
Q

What do fibroblasts do?

A

Produce collagenous connective tissue in scarring following some types of inflammation

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9
Q

What is the process of acute inflammation?

A

-Injury/infection
-Neutrophils arrive, phagocytose + release enzymes
-Resolution/progression to chronic inflammation

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10
Q

Examples of acute inflammation

A

Acute appendicitis, frostbite, Streptococcal sore throat

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11
Q

What is the process of chronic inflammation?

A

-Progression from acute/starts as chronic e.g. infectious mononucleosis
-Macrophages + lymphocytes, then fibroblasts arrive
-Resolves if no tissue damage, often repair + scar tissue formation

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12
Q

What is the lifespan of macrophages?

A

Months-years

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13
Q

What do macrophages do?

A

Phagocytosis + transport material to lymph nodes, also APC to induce secondary immune reactions

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14
Q

What is the name of macrophages in the liver?

A

Kupffer cells

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15
Q

What is the name of macrophages in bone?

A

Osteoclasts

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16
Q

What is the name of macrophages in the brain?

A

Microglial cells

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17
Q

What are granulomas?

A

Types of chronic inflammation with collections of macrophages/histiocytes surrounded by lymphocytes-can be due to myobacterial infection e.g. TB/leprosy

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18
Q

What do lymphocytes do?

A

Control inflammation + produce antibodies, from B cells-immunological memory-re-infection

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19
Q

What are corticosteroids?

A

Anti-inflammatories

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20
Q

What is laminar flow?

A

When cells travel in the centre of arterial vessels and don’t touch the sides

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21
Q

Give two reasons why clots are rare

A

-Laminar flow
-Endothelial cells that line vessels aren’t ‘sticky’ when healthy

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22
Q

What is thrombosis?

A

Formation of a solid mass from blood constituents in an intact vessel in a living person

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23
Q

What are the stages of thrombosis?

A

-Platelet aggregation
-Clotting cascade
-Fibrin mesh formation

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24
Q

What three factors can cause a thrombosis?

A

-Change in vessel wall
-Change in blood flow
-Change in blood constituents

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25
Q

How can smoking lead to a thrombosis?

A

-Smoking causes endothelial cell injury
-This causes a change in vessel wall + change in blood flow over the injured/absent cells

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26
Q

What is embolism?

A

The process of a solid mass (often a thrombus) in the blood being carried through the circulation to a place where it gets stuck + blocks the vessel

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27
Q

What can cause embolisms?

A

-Thrombus
-Air
-Tumour
-Amniotic fluid
-Fat
-Cholesterol crystals

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28
Q

What does aspirin do?

A

Inhibits platelet aggregation

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29
Q

What will happen to a venous embolism?

A

-Travels to vena cava
-Lodges somewhere in pulmonary arteries ( depends on size)
-Can’t reach arterial circulation as lung blood vessels split down to capillaries-too small

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30
Q

What will happen to an arterial embolus?

A

-Can travel anywhere downstream of entry point

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31
Q

What is ischemia?

A

Any reduction in blood flow

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32
Q

What is an infarction?

A

Reduction in blood flow to a tissue so severe that it can’t support cell maintenance-so cells die

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33
Q

Why is it bad that most organs have end arterial supply?

A

Only one artery supplying blood-very susceptible to infarction if supply interrupted

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34
Q

Which organs have dual arterial supply?

A

-Liver-HPV + hepatic artery
-Lungs-pulmonary venous + bronchial artery
-Brain-around circle of Willis

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35
Q

What is the difference between resolution + repair?

A

-Resolution=initiating factor removed + tissue undamaged/can regenerate
-Repair=factor still present + tissue damage-can’t regenerate

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36
Q

What are the two types of wound healing?

A

-Healing by 1st intention
-Healing by 2nd intention

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37
Q

What is healing by 1st intention?

A

When wound edges can be approximated/brought together e.g. after surgical incision

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38
Q

What is healing by 2nd intention?

A

When wound edges can’t be brought together so healing must occur from bottom of wound upwards

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39
Q

What are the 4 stages of wound healing?

A

-Haemostasis
-Inflammation
-Proliferation
-Remodelling

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40
Q

Name 6 cells that regenerate

A

-Hepatocytes
-Pneumocytes
-All blood cells
-Gut epithelium
-Skin epithelium
-Osteocytes

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41
Q

Which cells don’t regenerate?

A

-Myocardial cells
-Neurones

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42
Q

Define atherosclerosis

A

The accumulation of fibrolipid plaques in systemic (vs pulmonary) arteries

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43
Q

What does atherosclerosis do?

A

Can cause serious illness by reducing blood flow

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44
Q

Describe the time course of atherosclerosis

A

-Birth-none
-Late teens/early 20s-fatty streaks in aorta, may not progress to atherosclerosis
-30s-50s-development of established atherosclerotic plaques
-40s-80s-complications of atherosclerotic plaques e.g. thrombosis, intraplaque haemorrhage

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45
Q

What are the risk factors for atherosclerosis?

A

-Hypertension
-Hyperlipidaemia
-Smoking
-Poorly controlled diabetes mellitus

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46
Q

What is the lipid insudation theory?

A

Disproved model that suggest atherosclerotic plaques develop from accumulation of lipids in vessel wall

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47
Q

What theory describes the pathogenesis of atherosclerosis?

A

Endothelial cell damage theory

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48
Q

How do atherosclerotic plaques form from smoking?

A

-Free radicals, nicotine, carbon monoxide etc damage delicate endothelial cells

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49
Q

How do atherosclerotic plaques form from high blood pressure?

A

-High blood pressure causes shearing forces on endothelial cells

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50
Q

How do atherosclerotic plaques form from high poorly controlled diabetes?

A

Glycosylation products + superoxide anions damage endothelial cells

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51
Q

How do established atherosclerotic plaques develop?

A

Cumulative damage leads to endothelial ulceration, microthrombi + eventually plaques

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52
Q

What are the complications of atherosclerosis?

A

-Plaque blocks artery=infarct + organ death
-Pieces of plaque can break off + embolise downstream-can cause small embolisms + infarct downstream

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53
Q

What is apoptosis?

A

Programmed cell death-orderly + takes place in single cells, important part of cell turnover

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54
Q

Which protein detects levels of DNA damage in cells?

A

p53

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55
Q

Why does a cell ‘decide’ to apoptose?

A

When DNA damage is detected

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56
Q

How does a cell apoptose?

A

Cell triggers cascade of activated enzymes that autodigest the cell

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57
Q

Name the enzymes involved in cell apoptosis

A

Caspases

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58
Q

When is apoptosis used in health?

A

-Development-removal of cells during development e.g. interdigital webs
-Cell turnover-removal of cells during normal turnover e.g. cells in intestinal villi at the tips, replaced by cells form below

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59
Q

How does cancer affect cell apoptosis?

A

-Tumour cells often don’t apoptose when they should-leads to larger tumours + accumulation of genetic mutations-often due to p53 mutations

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60
Q

How does HIV use apoptosis?

A

HIV virus can induce apoptosis in CD4 helper cells-can make you immunodeficient

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61
Q

What is necrosis?

A

Largescale destruction of many cells by an external factor-causes lots of tissue damage

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62
Q

Give 4 examples of necrosis

A

-Frostbite
-Toxic venom
-Pancreatitis
-Infarction due to loss of blood supply e.g. myocardial/cerebral infarction

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63
Q

How does the body react to necrosis?

A

Has to clear it up by macrophages phagocytosing dead cells + replacing necrotic tissue with fibrous scar tissue

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64
Q

What is hypertrophy?

A

-Increase in the size of an organ due to increase in size of its constituent cells
–Occurs in organs where cells cannot divide

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65
Q

Give 2 examples of hyperplasia

A

-Benign prostatic hyperplasia
-Endometrial hyperplasia

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66
Q

What is hyperplasia?

A

-Increase in size of an organ due to increase in number of its constituent cells
-Occurs in organs where cells can divide

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67
Q

Give an example of hypertrophy

A

Skeletal muscle in body builders

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68
Q

Give an example of mixed hypertrophy/hyperplasia

A

Smooth muscle cells of the uterus in pregnancy

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69
Q

What is atrophy?

A

Decrease in size of an organ due to decrease in size OR number of constituent cells or both

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70
Q

Give 2 examples of atrophy

A

-Alzheimer’s dementia
-Quadriceps muscle following knee injuries

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71
Q

What is metaplasia?

A

Change in cell differentiation, from one fully-differentiated cell type to another fully-differentiated type

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72
Q

What causes metaplasia?

A

A consistent change in the environment of an epithelial surface

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73
Q

Give 3 examples of metaplasia

A

-Barrett’s oesophagus (squamous->glandular)
-Bronchi after smoking (bronchial epithelium ciliated columnar-> squamous)
-Uterine cervix at puberty (columnar->squamous)

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74
Q

What is dysplasia?

A

Morphological changes in cells in the progression on to the development of cancer (neoplasia)

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75
Q

What staining can be used to view dysplasia?

A

H&E

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76
Q

Give an example of dysplasia

A

Bronchial epithelium in smoking (ciliated->squamous=metaplasia, then development of dysplasia in the squamous epithelium)

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77
Q

What is the Hayflick limit?

A

The limit to how many times a human cell can divide

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78
Q

How does telomere length change with age?

A

Telomere length shortens with age

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79
Q

Is telomere length maternally or paternally inherited?

A

Paternally

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80
Q

How does telomere length affect the Hayflick limit?

A

-At each cell division, telomere length shortens, this means fewer future divisions (shorter length=lower hayflick limit)

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81
Q

What is the only definitive method of slowing ageing + why?

A

Calorie restriction as it reduces metabolic processes

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82
Q

How does ageing affect the skin, why + how to reduce it?

A

-Causes wrinkling of skin (dermal elastosis)
-Caused by UV-B light causing protein cross-linking
-Reduced by wearing high protection sun cream

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83
Q

How does ageing affect the eyes, why + how to reduce it?

A

-Causes cataracts
-Caused by UV-B protein cross-linking
-Prevented by wearing UV sunglasses + can be treated by lens replacement

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84
Q

How does ageing affect bones, why + how to reduce it?

A

-Causes osteoporosis (loss of bone matrix, mainly after menopause)
-Can be prevented by HRT + calcium/vit D supplements

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85
Q

How does ageing affect the brain, why + how to reduce it?

A

-Can cause dementia
-Genetic + lifestyle causes + preventatives

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86
Q

How does ageing affect muscles, why + how to reduce it?

A

-Causes loss of muscle (sarcopenia)
May be caused by reduced levels of GH + testosterone in later life
Can be prevented by regular exercise

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87
Q

How does ageing affect the ears, why + how to reduce it?

A

-Causes deafness due to cells in cochlear not dividing so not replaced when damaged
-Prevented by avoiding high volume sounds

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88
Q

What is a granuloma?

A

An aggregate of epithelioid histiocytes

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89
Q

Describe the spread of basal cell carcinomas

A

They don’t spread to other parts of the body-only invade locally

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90
Q

How do you cure basal cell carcinomas?

A

Complete local excision

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91
Q

What is a carcinoma?

A

A malignant tumour of the epithelial cells

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92
Q

Name 5 common symptoms of leukemia

A

-Weight loss
-Fatigue
-Easy bleeding/bruising
-Muscle weakness
-Joint pain/tenderness

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93
Q

Describe the spread of general carcinomas

A

-Spread to lymph nodes that drain the site of the carcinoma
-Can also spread through the blood to bone

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94
Q

Name the 5 cancers that most commonly spread to bone

A

-Breast
-Prostate
-Lung
-Thyroid
-Kidney

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95
Q

What are the steps of treatment for breast cancer?

A

-Confirm breast cancer diagnosis (with biopsy)
-Check if spread to lymph nodes in axilla (then removed)
-Check if spread to rest of body with bone scan (chemo/surgery needed)

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96
Q

What is adjuvant therapy?

A

Extra treatment given after surgical excision

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97
Q

What is tamoxifen + what does it do?

A

-SERM (selective oestrogen receptor modulator)-treatment for breast cancer

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98
Q

What is carcinogenesis?

A

The transformation of normal cells to neoplastic cells through permanent genetic alterations/mutations

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99
Q

What is oncogenesis?

A

The creation of benign + malignant tumours

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100
Q

Define carcinogenic

A

Cancer causing

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101
Q

Define oncogenic

A

Tumour causing

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102
Q

Define mutagenic

A

Acts on DNA

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103
Q

What is the latent interval?

A

Gap between exposure to carcinogen + formation of neoplasm/development of cancer

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104
Q

What are the classes of carcinogens?

A

-Chemical
-Viral
-Ionising/non-ionising radiation
-Hormones, parasites + mycotoxins
Miscellaneous

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105
Q

What type of carcinogens require metabolic conversion from pro-carcinogens to ultimate carcinogens?

A

Chemical

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106
Q

Give 4 examples of common chemical carcinogens + where they come from

A

-Polycyclic aromatic hydrocarbons-smoking/mineral oils
-Aromatic amines-rubber/dye industry
-Nitrosamines-found in treated foods e.g. cured meats
-Alkylating agents-found in chemotherapy drugs

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107
Q

What % of cancers are caused by viral carcinogens?

A

10-15%

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108
Q

Give 7 examples of viruses that cause cancer + the cancer they cause

A

-Human herpes virus 8-Kaposi sarcoma
-Epstein Barr virus-Burkitt lymphoma/nasopharyngeal carcinoma
-Hepatitis B virus-hepatocellular carcinoma
-Human papillomavirus (HPV)-squamous cells carcinomas of the cervix, anus, penis, head + neck
-Merkle cell polyomavirus (MCV)-Merkle cell carcinoma
Human T-lymphotropic virus-adult T-cell leukaemia
-Hepatitis C virus (HCV)- hepatocellular carcinoma

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109
Q

How does UV light cause carcinoma?

A

-Exposure to UVA/UVB, increases risk of basal cell carcinoma/melanoma

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110
Q

What is xeroderma pigmentosum?

A

-Recessive condition that increases risk of developing cancer due to mutations in nucleotide excision repair

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111
Q

Give 3 examples of cancer caused by radiation

A

-Skin cancer in radiographers
-Lung cancer in uranium miners
-Thyroid cancer in Ukrainian children post-Chernobyl

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112
Q

Give 3 examples of biological agents that cause cancer

A

-Hormones e.g. oestrogen increase=mammary/endometrial cancer risk increase
-Mycotoxins e.g. aflatoxin B1=hepatocellular carcinoma
-Parasites e.g. shistosoma=bladder cancer

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113
Q

Give 2 examples of miscellaneous carcinogens

A

-Asbestos
-Metals

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114
Q

What host factors affect likelihood of developing cancer?

A

-Ethnicity
-Diet/lifestyle
-Age
-Gender
-Transplacental exposure

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115
Q

How does ethnicity affect your risk of developing cancer?

A

-Local customs e.g. reverse smoking in SE Asia=increase in oral cancer
-Less skin cancer in those with darker skin

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116
Q

How do age + gender affect your risk of developing cancer?

A

-Increase in age=increase in exposure to carcinogens
-Gender-breast cancer F:M=200

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117
Q

How does lifestyle affect your risk of developing cancer?

A

-Diet/exercise-XS alcohol=increase in mouth, oesophagus, liver, colon and breast cancer
Exercise reduces risk of colon + breast cancer
-Unprotected sex-increases risk of HPV

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118
Q

Give an example of how transplacental carcinogenesis affects your risk of developing cancer

A

-DES (diethylstilboestrol)-prescribed to pregnant women 1940-71 to prevent miscarriage=increase in risk of vaginal cancer

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119
Q

What is an invasive carcinoma?

A

One that has spread to the basement membrane + therefore can metastasise to the rest of the body

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120
Q

Name 3 types of carcinoma

A

-Carcinoma in situ
-Micro-invasive carcinoma
-Invasive carcinoma

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121
Q

How do tumour cells evade host immune defence?

A

-Aggregation with platelets
-Shedding of surface antigens
-Adhesion to other tumour cells

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122
Q

Name 2 angiogenesis promoters

A

-Vascular endothelial growth factor
-Basic fibroblast growth factor

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123
Q

Name 3 angiogenesis inhibitors

A

-Angiostatin
-Endostatin
-Vasculostatin

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124
Q

Which tumours most commonly metastasise to the lungs?

A

Sarcomas. any common cancers

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125
Q

Which tumours most commonly metastasise to the liver?

A

-Colon
-Stomach
Pancreas
-Carcinoid tumours of the intestine

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126
Q

Name an antimicrotubule agent

A

Vinblastine

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127
Q

How do antimicrotubule agents work?

A

They reduce tumour size by binding to micro tubules + stopping them from attaching to chromatin

128
Q

What are 2 drawbacks of conventional chemotherapy?

A

-Not selective for tumour cells-except they might be dividing faster
-Usually also affects normal dividing cells-cause of hair loss, myelosuppression (decrease in bone marrow activity), diarrhoea etc

129
Q

Name 5 fast dividing tumours

A

-Germ cell tumours of testis
-Acute leukaemia
-Lymphomas
-Embryonal paediatric tumours
-Choriocarcinomas

130
Q

What is a neoplasm?

A

A lesion resulting from the abnormal growth of cells after the initiating stimulus has been removed

131
Q

What are 5 characteristics of benign tumours?

A

-Non-invasive
-Localised
-Low mitotic activity
-Well-circumscribed
-Bland cell morphology

132
Q

What are 5 characteristics of malignant tumours?

A

-Invasive
-Local + distant spread (metastasis)
-Poorly circumscribed
-Abnormal cell morphology
-High mitotic activity

133
Q

What are benign tumours from secretory/glandular epithelium called?

A

Adenomas

134
Q

What are benign tumours from non-glandular, non-secretory epithelium called?

A

Papillomas

135
Q

What are benign tumours from connective tissues (smooth + striated muscle, vascular, adipocytes, bone, nerves) called?

A

-Leiomyomas-smooth muscle
-Rhabdomyoma-striated muscle
-Angiomas-vascular
-Lipomas-adipocytes
-Osteoma-bone
-Neuroma-nerves

136
Q

What are malignant epithelial tumours called?

A

Carcinomas

137
Q

What do you call malignant glandular epithelial tumours?

A

Adenocarcinomas

138
Q

What are malignant tumours from connective tissue called?

A

Sarcomas (same prefix before sarcoma as for benign)

139
Q

What are malignant tumours with hemopoietic origins called?

A

Lymphomas, leukaemia/myeloma

140
Q

What are other (not from epithelium, connective tissue or hemopoietic origins) malignant tumours called?

A

Melanomas/mesotheliomas

141
Q

What 4 ways can we acquire genetic changes?

A

-Chance-spontaneous mutations
-Hereditary-inherited mutations
-Environment-exposures/toxins
-Micro-organisms-oncogenic viruses/bacteria

142
Q

Give 2 examples of a hereditary inherited genetic mutation that could increase risk of cancer

A

-Lynch syndrome (aka hereditary non-polyposis colorectal cancer)
-Xeroderma pigmentosa

143
Q

Give 3 examples of micro-organisms that can increase your risk of developing cancer

A

-Epstein Barr virus
-HPV
-H pylori

144
Q

What are proto-oncogenes?

A

Genes which promote cell growth + survival-promoting carcinogenesis

145
Q

What are tumour suppressor genes?

A

Genes which inhibit cell growth + proliferation, can inhibit carcinogenesis

146
Q

What is tumour grading?

A

Comparing a tumour to its normal counterparts-how much does it resemble them e.g well/poorly differentiated

147
Q

What is tumour staging?

A

Assessing how much the tumour has spread-looks at lymph nodes + other organs/tissue

148
Q

What does TNM staging stand for?

A

T-tumour size/depth
N-nodes, has it spread to lymph nodes?
-M-metastases, has it spread to rest of body?

149
Q

Name the 4 modes of metastases

A

-Direct
-Lymphatic
-Blood vessel
-Transcoeleomic

150
Q

What is a tumour?

A

Any abnormal swelling (includes neoplasms)

151
Q

What are neoplasms made up of?

A

-Neoplastic cells
-Stroma

152
Q

Where do neoplastic cells derive form?

A

Nucleated nuclei

153
Q

What is the stroma in neoplasms?

A

Connective tissue framework that provides mechanical support + nutrition

154
Q

What are the 3 stages of tumour angiogenesis?

A

-Cell transforms-avascular tumour nodule
-Vascularised tumour
-Vascularised tumour with central necrosis

155
Q

What size (mm) would a neoplasm without a blood supply be?

A

<2mm

156
Q

Name 5 ways benign neoplasms cause morbidity + mortality

A

-Press on adjacent structures
-Obstruct flow
-Produce hormones
-Transform to malignant
-Anxiety

157
Q

Compare the nuclear morphometry of benign + malignant neoplasms

A

Benign=often normal
Malignant=hyperchromatic + pleomorphic (able to assume diff shapes) nuclei

158
Q

What does anaplastic mean?

A

Cell type of origin for a tumour cannot be determined

159
Q

Define carcinoma

A

A malignant epithelial neoplasm

160
Q

What are the top 4 biggest killers in the UK?

A

-Cancer (42%)
-CVD (22%)
-Respiratory disease (9%)
-Liver disease (6%)

161
Q

What is the purpose of tumour immunology?

A

To induce clinically effective anti-tumour immune responses that can discriminate between tumour cells + normal cells in cancer patients

162
Q

What are TSAs?

A

Tumour specific antigens, found only on tumours, from viral antigens, occur as a result of point mutations/gene rearrangements

163
Q

What are TAAs?

A

Tumour associated antigens

164
Q

Where are TAAs found?

A

Found on normal + tumour cells-overexpressed in cancer cells

165
Q

What is tumour escape?

A

When the immune response changes tumours so it can no longer be seen by the immune system

166
Q

What is tumour evasion?

A

When tumours change the immune response by promoting immune suppressor cells

167
Q

Give an example of active immunotherapy

A

Vaccination

168
Q

Give 2 examples of passive immunotherapy

A

-Adoptive cellular therapy (T cells)
-Anti-tumour antibodies

169
Q

Where are dendritic cells found?

A

Throughout the body:
-Interstitial cells (liver. heart, liver)
-Langerhans cells of epidermis

170
Q

What do dendritic cells do?

A

APCs-break up pathogens + present piece on surface

171
Q

Name 3 cells that can be used in tumour immunotherapy

A

-Dendritic cells
-T killer cells
-Macrophages

172
Q

What is passive immunisation?

A

Administration of pre-formed immunity from one person/animal to another

173
Q

What are the limitations of passive immunisation?

A

-Only antibody mediated (doesn’t work if cell mediated)
-Short-lives
-Possible transfer of pathogens
-‘Serum sickness’ on transfer of animal sera

174
Q

What are the advantages of passive immunisation?

A

-Gives immediate protection
-Effective in immunocompromised patients

175
Q

Give 4 examples of passive immunisation

A

-Human tetanus Ig
-Human rabies specific Ig
-Human hepatitis B Ig
-Varicella zoster Ig

176
Q

What is HNIG?

A

Human normal immunoglobulin-from pools of 100+ donors, contains antibodies against measles, mumps, varicella, hep A etc

177
Q

What are the 3 approaches to making a vaccine (parts used)?

A

-Using whole virus/bacterium
-Using parts that trigger immune system
-Using just genetic material

178
Q

What are the 3 types of vaccine given in whole microbe approaches?

A

-Inactivated vaccine
-Live-attenuated vaccine
-Viral vector vaccine

179
Q

Name 4 limitations of whole killed vaccines

A

-Organisms grown to high titre in vitro-expensive
-Can cause more adverse reactions
-Immune response not always close to normal response to infection
-Normally need 2+ doses

180
Q

Give 4 examples of bacterial whole killed vaccines

A

-Diphtheria
-Tetanus
-Pertussis
-Cholera

181
Q

Give 5 examples of viral whole killed vaccines

A

-Polio
-Influenza
-Hep A
-Rabies
-SARS-Co-V2

182
Q

What are the benefits of live attenuated vaccines?

A

-Immune response better mimics real infection-better protection
-Better immune response so lower doses needed
-Route of administration may be better (oral)
-Fewer doses required

183
Q

What is attenuation?

A

Where an organism is cultured in such a way that it does not cause disease when inoculated into humans

184
Q

Limitations of live attenuated vaccines

A

-Hard to balance attenuation + it still working
-Can reverse to virulence
-Transmissibility
-Live vaccines may not work as well in immunocompromised hosts

185
Q

Give 2 examples of bacterial live attenuated vaccines

A

-BCG (some protection against TB)
-Salmonella typhi

186
Q

Give 3 examples of viral live attenuated vaccines

A

-Poliomyelitis
-Vaccinia virus (smallpox)
-MMR

187
Q

Give 3 reasons why it is hard to produce vaccines

A

-Pathogen hard to grow
-Killed pathogen doesn’t work as vaccine )shape changes)
-Some condition have too many strains causing disease

188
Q

What are recombinant protein vaccines?

A

Genetically engineered vaccines made from bacteria, yeast, insect/mammalian cells

189
Q

Give 3 examples of recombinant protein vaccines on the market

A

-Hep B surface antigen
-HPV Cervarix + Gardasil
-SARS-Co-V2-Novavax

190
Q

What are live attenuated vector vaccines? Give an example

A

Safe living attenuated viruses that have inserted genes encoding foreign antigens e.g. SARS-Co-V2

191
Q

What is innate immunity?

A

Instinctive, non-specific, no reliance on lymphocytes, present from birth

192
Q

What is adaptive immunity?

A

Specific, acquired/learned immunity, requires lymphocytes, antibodies

193
Q

What 3 layers does contrifuged blood form?

A

-Plasma-water, electrolytes, proteins, lipids, sugars etc
-Buffy coat/middle layer-leukocytes
-Haematocrit (45%)-erythrocytes, platelets

194
Q

What is serum?

A

Plasma minus fibrinogen/other clotting factors

195
Q

Name the process by which blood cells are formed

A

Haematopoiesis

196
Q

What is the progenitor of all blood cells?

A

Pluripotent haematopoietic stem cells

197
Q

Name 3 polymorphonuclear leukocytes

A

-Neutrophils
-Eosinophils
-Basophils

198
Q

Name 3 mononuclear leukocytes

A

-Monocytes
-T-cells
-B-cells

199
Q

What cells produce macrophages?

A

Monocytes

200
Q

What cells produce plasma cells?

A

B-cells

201
Q

Name 3 types of T cell

A

-T-regs
-T-helper cells (CD4)
-Cytotoxic T cells (CD8)

202
Q

What do mast cells do?

A

Contain histamine-important in allergic reactions

203
Q

What are natural killer cells?

A

Type of T cell-functions like neutrophil-important in anti-tumour response

204
Q

What are dendritic cells?

A

Surveillance cells-live in epithelium

205
Q

What is complement?

A

Series of around 20 proteins made by liver that circulate in an inactive form around the body

206
Q

What are the 3 modes of action of complement?

A

-Direct lysis
-Attract more leukocytes to site of infection
-Coat invading organisms

207
Q

What are the 5 subclasses of immunoglobulin?

A

-IgG
-IGA
-IgM
-IgD
-IgE

208
Q

Describe the basic structure of an antibody

A

–Antigen binding site
-Fab region (recognises non-self)
-Fc region
-Light + heavy chains
-All connected by disulphide bonds

209
Q

What is the most common Ig in human serum?

A

IgG

210
Q

Where is IgM found + how common is it in serum?

A

Found in blood-too big to cross endothelium, 10% of serum

211
Q

Which Ig is the main primary immune response?

A

IgM

212
Q

What is IgA found in?

A

Mucous secretions e.g. saliva, colostrum, milk, bronchiolar + genitourinary secretions

213
Q

Is IgA a monomer or dimer in humans?

A

Monomer (dimer in most animals)

214
Q

What is the least common Ig?

A

IgE

215
Q

Where is IgD found?

A

Found on mature B cells

216
Q

What cells have receptors complementary to IgE?

A

Basophils + mast cells

217
Q

What does IgE release?

A

Histamines in hypersensitivity response + defence against parasitic infections

218
Q

What are cytokines?

A

Proteins secreted by immune + non-immune cells

219
Q

Give 4 examples of cytokines?

A

-Interferons (IFN)
-Interleukins (IL)
-Colony stimulating factors (CSF)
-Tumour necrosis factors (TNF)

220
Q

What are chemokines?

A

Chemotactic cytokines-
Around 40 proteins that direct movement of leukocytes from bloodstream into tissue/lymph by binding to specific receptors

221
Q

Give 3 examples of chemokines

A

-CXCL
-CCL

222
Q

What do interferons do?

A

Induce antiviral resistance in uninfected cells-limit spread of viral infection

223
Q

What do interleukins do?

A

Can cause cells to divide/differentiate/secrete factors. Can be pro-inflammatory or anti-inflammatory

224
Q

What do colony stimulating factors do?

A

Direct division + differentiation on bone marrow stem cells

225
Q

What do tumour necrosis factors do?

A

Mediate inflammation + cytotoxic reactions

226
Q

Name 5 physical barriers that contribute to innate immunity

A

-Lysozyme in tears
-Physical skin barrier + fatty acids
-Low pH of vagina
-Mucus + cilia in bronchi
-Acid + rapid pH change in gut

227
Q

Describe the 7 steps in an inflammatory response

A

-Stop bleeding (coagulation)
-Acute inflammation
-Kill pathogens, neutralise toxins, limit pathogen spread
-Clear pathogens/dead cells
-Proliferation of cells to repair damage
-Remove blood clot-remodel extracellular matrix
-Re-establish normal structure/function of tissue

228
Q

Name 3 hallmarks of inflammation

A

-Increased blood supply
-Increased vascular permeability
-Increased leukocyte migration

229
Q

Name the cells that sense microbes in blood

A

Monocytes + neutrophils

230
Q

Name the cells that detect microbes in tissues

A

Macrophages + dendritic cells

231
Q

What are PRR?

A

Pattern recognition receptors-on cells

232
Q

What are PAMP?

A

Pathogen-associated molecular patterns-on microbe

233
Q

What expresses C-type lectin receptors + what do they do?

A

-Expressed by macrophages + dendritic cells
-Bind to carbohydrates in a Ca dependent manner

234
Q

What are scavenger receptors?

A

Group of membrane-bound receptors that mainly recognise lipids

235
Q

What do scavenger receptors do to LDL

A

Bind + internalise them-if process is dysregulated, it can lead to atherosclerosis

236
Q

What are the 3 activation pathways of complement factors?

A

-Classical-Ab bound to microbe
-Alternative-C’ binds to microbe
-Lectin-activated by mannose

237
Q

What are the 2 killing pathways present in neutrophils + macrophages?

A

-O2 dependent
-O2 independent

238
Q

How does O2 dependent microbe killing work?

A

-Reactive oxygen intermediates are used e.g. superoxides->H2O2->OH free radical
-Nitric oxide also causes vasodilation, increases extravasation + anti-microbial

239
Q

How does O2 independent microbe killing work?

A

Enzymes e.g. lysozyme + proteins e.g. defensins + pH are used to kill microbes

240
Q

What is the purpose of extravasation?

A

To get neutrophils from the blood, through the epithelium, into tissue

241
Q

What are the steps of extravasation?

A

-Rolling
-Tethering
-Firm adhesion
-Locomotion

242
Q

Where are T + B cells + APC’s matured?

A

-T cells matured in thymus
-B cells matured in bone marrow
-APC’s in bone marrow

243
Q

What is the secondary lymphoid (where they circulate) for T, B + APC cells?

A

Spleen, lymph nodes + mucosa and associated lymphoid tissue (MALT)

244
Q

What antigens do T cells respond to?

A

Intracellular presented antigens

245
Q

What is T cell selection?

A

When T cells that recognise self are killed in the foetal thymus as they mature-so adult T cells only recognise foreign bodies

246
Q

What do T cell receptors bind to?

A

MHC-major histocompatibility complex bound to peptide on foreign antigen

247
Q

What does MHC do?

A

Display peptides from self or non-self proteins e.g. degraded microbial proteins on surface-invasion alert

248
Q

What are the 2 types of MHC + where are they present?

A

MHC I-present on all nucleated cells
MHC II-present only on APC

249
Q

What is an example of clonal expansion?

A

T cell division

250
Q

What do Th2 cells do?

A

Antibody production

251
Q

What do Th1 cells do?

A

Secrete interferon gamma-helps kill intracellular pathogens

252
Q

Which Igs can B cells bind to?

A

IgM/IgD

253
Q

What is B cell selection?

A

When B cells that recognise self are killed in foetus in the bone marrow

254
Q

Describe the interaction between APC, T cells + B cells

A

-APC eats + presents antibody to naïve T cell via MHC II
-Th2 cell becomes primed
-TH2 binds to B cell that are presenting the antibody
-Th2 secretes cytokines
-Cytokines cause B cell division + clonal expansion + differentiate into:
-Plasma cells + memory B cells

255
Q

What are the primary lymphoid tissues?

A

-Thymus
-Bone marrow

256
Q

What are the secondary lymphoid organs + tissues?

A

-Waldeyer’s ring (tonsils + adenoids)
-Spleen
-Peyer’s patch
-Urogenital lymphoid tissue
-Lymph nodes
-Bone marrow
-Bronchus associated lymphoid tissue

257
Q

What do antibodies do?

A

-Neutralise toxins by binding to them
-Increase opsonisation-phagocytosis
-Activate complement

258
Q

What are DAMPs?

A

Damage associated molecular patterns-endogenous molecules created to alert the host to tissue injury + initiate repair

259
Q

Give 3 examples of the main PRRs

A

-Pentraxins
-Lectins
-Collectins

260
Q

What do pentraxins do?

A

Activate complement + promote phagocytosis

261
Q

What do lectins + collectins do?

A

Bind to carbohydrates + lipids in microbe walls-activate complement + improve phagocytosis
e.g. surfactant proteins A+D

262
Q

Name 3 other membrane bound PRRs + where they are found

A

-Mannose receptors-on macrophages (fungi)
-Dectin-1-on phagocytes
-Scavenger receptors-on macrophages

263
Q

What are RIG-I-like receptors (RLRs), give 3 examples?

A

Receptors that detect viral RNA in the cytoplasm
-RIG-I
-MAD-5
-LGP2

264
Q

What do NLRs do?

A

NOD-like receptors sense cytoplasmic bacterial pathogens + DAMPs + regulate inflammatory + cell death responses

265
Q

What is the damage chain reaction?

A

-Tissue damage leads to inflammation
-This causes the release of DAMPs + then TLRs
-TLRs then trigger pro-inflammatory mediators + increase inflammation, which causes more tissue damage
-Cycle repeats

266
Q

What is the cytokine storm?

A

-Big increase in cytokines, chemokines + interferons
-Causes severe inflammation + tissue damage
-Induced due to genetics of host + persistence of pathogen (evasion mechanisms)

267
Q

What do PRRs do?

A

Detect infection, initiate immunity, eliminate pathogens + hold in check until adaptive immunity develops

268
Q

What are the two strategies of immunomodulation?

A

Agonists (enhance TLR signalling)
Antagonists (inhibit TLR signalling)

269
Q

How do agonists enhance TLR signalling?

A

Adjuvant effect (used with primary Tx e.g. vaccines), stimulate + modify immune response

270
Q

How do antagonists inhibit TLR signalling?

A

Block binding of ligands _ interfere with common signalling pathways

271
Q

Antibodies are also known as…

A

Immunoglobulins

272
Q

What antibody mediates type 1 hypersensitivity reactions?

A

IgE

273
Q

What are the hallmarks of ageing on a cellular level?

A

-Cellular senescence
-Stem cell exhaustion
-Altered intercellular communication

274
Q

What are the hallmarks of ageing on a systemic level?

A

Nutritional dysregulation
Reduced nutrient sensing

275
Q

What are the hallmarks of ageing on a molecular level?

A

-Telomere shortening
-Genomic instability
-Epigenetic alteration
-Mitochondrial dysfunction

276
Q

What is immunosensescence?

A

Dysregulated immune function that contributes to the increased susceptibility of the elderly to infection + possibly to autoimmune disease + cancer

277
Q

What happens to the innate immune response with age?

A

-Less interferons produced
-More inflammatory cytokines produced
-XS inflammation

278
Q

What happens to the adaptive immune response with age?

A

-Less naïve B + T cells
-XS inflammation

279
Q

What immune cells are reduced with age?

A

-Macrophages
-Naive B + T cells
-Dendritic cells

280
Q

What immune cells increase with age?

A

-Memory B + T cells
-MDSCs

281
Q

What happens to these immune tissues with age?
-Thymus
-Bone marrow
-Spleen
-Lymph nodes
-Lungs

A

All decrease output + cell production except lungs-increase infiltration of pro-inflammatory cells + lung damage

282
Q

What lifestyle modifications can you make to reduce immunosenescence inflammaging?

A

-Increase physical activity
-Restrict calories
-Maintain optimal nutrition
-Weight loss
-Modulate gut microbiota e.g. probiotics

283
Q

What pharmacological interventions can you perform to reduce immunosenescence inflammaging?

A

-Reversal of thymic atrophy-IL7 therapy
-Statins
-P13kinase inhibitors
-Antioxidants
-Anti-inflammatories

284
Q

What is meningitis?

A

Inflammation of the meninges-membrane which cover the brain + spinal cord

285
Q

What are the infective causes of meningitis?

A

-Viruses e.g. herpes, influenza, HIV
-Bacteria e.g. meningococcus, pneumococcus
-Other e.g. fungi, protazoa + parasites

286
Q

What are the non-infective causes of meningitis?

A

-Medications e.g. antibiotics, NSAIDs
-Cancers e.g. melanoma, leukemia
-Autoimmune disease e.g. SLE, Behcets

287
Q

Name 6 differential diagnoses of meningitis

A

-Viral/fungal/TB/drug-induced meningitis
-HIV infection
-Brain tumour
-Sepsis
-Encephalitis
-Brain abscess

288
Q

What is invasive meningococcal disease?

A

Infection with Neisseria meningitidis-carried by 10-24% population-humans=reservoirs

289
Q

What are the manifestations of meningococcal disease?

A

-Meningitis
-Septicaemia

290
Q

Which serogroups cause most cases of meningococcal disease?

A

A, B, C, W, X, Y

291
Q

Which serogroups of N.meningitidis are most common in Europe?

A

B, C, Y

292
Q

How is meningitis transmitted + when do cases rise?

A

-Aerosol droplets/direct contact with upper resp secretion-need prolonged close contact
-Most prevalent in winter

293
Q

Who is most commonly affected by meningitis?

A

Extremes of age, <2 + >60, also spike in adolescence and early adulthood (due to close contact/ social mixing?)

294
Q

Name 8 risk factors of meningitis

A

-Extremes of age
-Immunocompromised
-Smokers
-Cochlear implants
-Cancer
-Sickle cell disease
-Living in overcrowded households
-Cranial anatomical defects

295
Q

Name 6 symptoms of meningitis for adults

A

-Fever
-Stiff neck
-Headache
-Confusion
-Increased sensitivity to light
-Nausea + vomiting

296
Q

Name 6 symptoms of meningitis for babies

A

-Slow/inactive
-Irritable
-Vomiting
-Feeding poorly
-Bulging fontanelle

297
Q

What is Brudzinski’s sign?

A

When child’s head is pulled up, knees come up automatically to relieve pressure on meninges

298
Q

What are the symptoms of Meningococcal septicaemia?

A

-Fever + chills
-Fatigue
-Vomiting
-Cold hands + feet
-Rapid breathing
-Petechiae (non-blanching rash)
Later stages = purpura (dark, purple rash)

299
Q

Describe the course of meningitis

A

-Acute onset
-Fulminating infection - occurs suddenly, escalates quickly + can be rapidly fatal
-Prolonged + persistent coccaemia (bloodstream infection)
-Long-term complications

300
Q

What are some of the complications of meningitis?

A

-Deafness/hearing loss
-Seizures
-Motor deficits
-Cognitive impairment
-Blindness
-Amputations

301
Q

Is meningitis a notifiable disease?

A

Yes! Meningitis of any cause + meningococcal septicaemia are notifiable

302
Q

What tests would you run on a potential meningitis patient?

A

-Blood test for blood culture + PCR
-CSF for microscopy
-Throat swab

302
Q

When do you notify UKHSA health protection team about meningitis?

A

When a case is suspected-don’t wait for lab confirmation

303
Q

What Tx is given for meningitis?

A

Antibiotics-to stop throat carriage (to stop passing on-doesn’t kill infection) e.g. ciprofloxacin, rifampicin

304
Q

What is prophylaxis?

A

Tx given/action taken to prevent disease

305
Q

Who is included for contact tracing of a case of meningitis?

A

-Living in same household
-Anyone who slept overnight in household within 7 days
-Intimate kissing contacts (including CPR) within 7 days

306
Q

What public health action would be taken after a case of meningitis?

A

-Chemoprophylaxis of close contacts
-Notify school/uni/nursery
-Standard warning letter
-Offer leaflets
-Media handling

307
Q

Give 2 examples of locations for large meningitis outbreaks

A

-Outbreaks associated with pilgrimage to Hajj
-Epidemics in meningitis belt of Sub Saharan Africa

308
Q

Name 5 causes of epidemic meningitis

A

-Dry season Dec-June-dust laden winds
-Upper resp tract infections due to cold nights
-Decrease in local immunity in pharynx
-Overcrowded housing
-Large population displacement due to pilgrimages + traditional markets

309
Q

What is the new meningitis vaccine?

A

MenAfriVac-new conjugate Men A vaccine developed by WHO/PATH partnership
-Launche din Burkina Faso, Mali + Niger
-Affordable

310
Q

What is primary vaccine failure?

A

When a person doesn’t develop immunity from a vaccine

311
Q

What is secondary vaccine failure?

A

When there is an initial response but protection waned over time

312
Q

What acts mean doctors have a legal responsibility to notify about certain diseases?

A

-Health (Control of Disease) Act 1984
-Health Protection Regulations 2010

313
Q

What is the role of disease surveillance?

A

-Outbreak detection
-Early warning
-Forecasting

314
Q
A

Phase 2a (8 decks)

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