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Phase 2A > ICS: Pathology & Immunology > Flashcards

ICS: Pathology & Immunology Flashcards

1
Q

Define inflammation

A

local reaction to an injury or infection involving cells such as neutrophils & macrophages

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2
Q

Advantages of inflammation (2)

A
  • Good during infections & injuries
  • Prevents further spread - destroys microorganisms & walls off abscess
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3
Q

Disadvantages of inflammation (3)

A
  • during autoimmunity & overreaction to stimulus
  • disease may still persist & altered function
  • swelling, compression & destruction of normal tissue
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4
Q

Define exudate

A

Protein rich fluid that leaks out of vessel walls due to increased vascular permeability

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5
Q

Characteristic of acute inflammation (3)

A
  • sudden onset
  • short duration
  • usually resolves on its own
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6
Q

Example of acute inflammation

A

appendicitis

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7
Q

Main type of cells involved in acute inflammation

A

Neutrophil polymorphs (WBC)

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8
Q

Main diagnostic characteristic of acute inflammation

A

Presence of neutrophil polymorphs (NP migration)

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9
Q

Causes of acute inflammation (6)

A
  • microbial infection
  • hypersensitivity reaction
  • physical agent
  • corrosive chemicals
  • bacterial toxins
  • tissue necrosis
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10
Q

Possible resolutions of acute inflammation

A
  • resolution
  • suppuration (formation of pus)
  • organisation (healing by fibrosis - scar formation)
  • progression to chronic inflammation
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11
Q

Main response components of acute inflammation (2)

A

Vascular: dilation of vessels
Exudative - vascular leakage of protein rich fluid

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12
Q

Macroscopic appearance of acute inflammation (5)

A
  • redness (rubor)
  • heat (calor)
  • swelling (tumor)
  • pain (dolor)
  • loss of function
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13
Q

Systemic effects of acute inflammation (5)

A
  • pyrexia (fever)
  • weight loss
  • lymphadenopathy (swelling of ..)
  • increased WBC count
  • amyloidosis (deposition of protein in tissue)
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14
Q

Characteristic of chronic inflammation (3)

A
  • slow onset / after acute
  • long duration
  • may not resolve
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15
Q

Examples of chronic inflammation (3)

A

Tuberculosis, myocardial fibrosis post MI, leprosy

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16
Q

Main types of cells involved in chronic inflammation (3)

A

macrophages, plasma cells & lymphocytes

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17
Q

Causes of chronic inflammation

A
  • primary chronic inflammation
  • !! transplant rejection
  • progression from / recurrent episodes of acute inflammation (most common = from suppurative)
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18
Q

Macroscopic appearance of chronic inflammation

A
  • Chronic ulcer / abscess cavity
  • Thickening of the walls of a hollow organ
  • Granulomatous tissue (when walled off but unable to eliminate → forms granuloma)
  • Fibrosis (thickening or scarring of connective tissue)
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19
Q

Response process of chronic inflammation

A
  • Paracrine stimulation of connective tissue proliferation (formation of new blood vessels = angiogenesis & fibroblast proliferation = collagen synthesis, granulomatous inflammation)
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20
Q

Define granulomas

A
  • lump of macrophages surrounded by lymphocytes // epithelioid histiocytes with little phagocytic activity
  • formation of chronic inflammatory cells
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21
Q

Define granulation tissue

A

composed of small blood vessels in a connective tissue matrix with myofibroblasts. important in healing and repair.

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22
Q

Diagnostic characteristic of granulomas (histological)

A

Ziehl-Neelsen stain (comes up bright red)

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23
Q

Diagnostic characteristic of granulomatous disease (enzyme)

A

Angiotensin converting enzyme

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24
Q

Treatment of inflammation (5)

A
  • ice
  • histamine
  • steroid, coticosteroid
  • NSAIDs
  • antibiotics
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25
Q

Examples of granulomatous disease

A

TB, Sarcoidosis, Crohn’s disease

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26
Q

Briefly outline the Neutrophil Polymorph Migration as seen in acute inflammation

A
  1. margination of neutrophils: axial to plasmatic flow
  2. adhesion of neutrophils: pavementing
  3. neutrophil migrate through walls of venules & small veins
  4. diapedesis: mvt of neutrophils out of circulatory system to site of damage or infection
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27
Q

Normal cell flow in vessels

A

axial = central zone of blood stream OR laminar flow = cell travel in centre of vessels & do not touch sides

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28
Q

Damaged cell flow in vessels

A

plasmatic = flows towards endothelium

(mostly due to loss of intravascular fluid & increased plasma velocity)

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29
Q

Define pavementing

A

Neutrophil adherance to vascular endothelium

  • in early acute inflam.
  • increased adhesion from interact. bet. leukocyte & endo surface
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30
Q

Causes of pain associated with acute inflammation

A
  1. Stretching and distortion of tissues due to oedema and pus under high pressure in an abscess cavity.
  2. Chemical mediators e.g. bradykinin and prostaglandins, are also known to induce pain.
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31
Q

Difference between resolution and repair

A

Presence of initial factor (repair = present) & ability of tissue to regenerate (repair = unable)

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32
Q

Bringing edge of wound together, no infection, nice healing

A

Healing by 1st intention

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33
Q

Skin is lost, gaping wound (e.g. TA or trauma wounds, granulation tissue)

A

Healing by 2nd intention

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34
Q

‘Resolution’ for repair tissues

A
  • Damaged tissue replaced by fibrous tissue
  • Collagen produced by fibroblasts
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35
Q

Cells that regenerate

A
  • hepatocytes
  • pneumocytes
  • all blood cells
  • osteocytes
  • epithelium - gut & skin
  • peripheral nerves
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36
Q

Cells that don’t regenerate

A
  • myocardial cells
  • central neurons
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37
Q

Cell types that regenerate (bigger groups!)

A

labile, stable cell populations, stem cells

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38
Q

Cell types that doesn’t regenerate (bigger groups)

A

permanent cells

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39
Q

Define apoptosis

A

Programmed cell death of individual cells without producing harmful products

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40
Q

Define necrosis

A

Unprogrammed traumatic cell death, often in masses, which induces inflammation and repair

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41
Q

Triggers for apoptosis

A
  • DNA damage: detected by p53, regulates caspase
  • Virus
  • Withdrawal of growth factor
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42
Q

Protein that switches on apoptosis

A

P53 protein - detects DNA damage & initiate repair, if beyond repair then apoptose

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43
Q

Conductor of apoptosis

A

Caspase enzyme

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44
Q

Protein that promotes apoptosis (Bcl-2 family)

A

Bax protein

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45
Q

Protein that inhibits apoptotic factors (therefore apoptosis)

A

Bcl-2 protein

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46
Q

Activation of these extrinsic receptors can activate caspase & therfore apoptosis

A

Fas (fas ligand binds here) & Tumor Necrosis Factor Receptor (TNFR) 1

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47
Q

Intrinsic activation of apoptosis

A

Through P53 protein which also mediates the Bcl-2 family of proteins

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48
Q

Disease with too little apoptosis

A

Cancer, mutations in p53 = cell damage undetected

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49
Q

Disease with too much apoptosis

A

HIV

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50
Q

Examples leading to necrosis

A

Spider venom, frostbite, cerebral infarction

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51
Q

Differences between apoptosis & necrosis (3)

A
  • programmed vs unprogrammed
  • single vs en mass
  • DNA (genetics) vs external
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52
Q

Define thrombosis

A

solidification of blood contents formed within vascular system during life; esp when platelet aggregation is activated within an intact vessel

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53
Q

Define clot

A

blood coagulated outside of the vascular system after death

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54
Q

Three factors that can cause thrombosis, one or more can precipitate

A
  • change in vessel wall
  • change in blood flow
  • change in blood constituents

= Virchow’s triad

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55
Q

Why is thrombosis uncommon (2)

A
  1. Laminar flow.
  2. Non sticky endothelial cells.
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56
Q

Cause of arterial thrombosis

A

atheromatous plaque

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57
Q

Two drugs to treat thrombosis

A

Aspirin to prevent;
Warfarin for severe & patients with thrombus history

As: inhibit platelet agg // War: inhibit vitamin K - clotting factor

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58
Q

Define embolus

A

A mass of material (often a thrombus) in the vascular system that is able to become lodged in a vessel and block it.

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59
Q

Most common cause of embolism

A

thrombus (DVT), also air, amniotic fluid etc

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60
Q

Which type of embolism cannot travel to the other side of the body under normal conditions?

A

Pulmonary (venous) embolism

Normally in pulmonary arteries & cannot cross unless perforated lung

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61
Q

Define ischaemia

A

reduction in blood flow caused by constriction or blockage of the supplying blood vessel

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62
Q

Define gangrene

A

When whole regions of a limb or gut have their arterial supply cut off & large areas of mixed tissues die in bulk

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63
Q

Difference between wet & dry gangrene

A

Dry - tissue dies & healing occurs above it, eventually falls off & patient is fine
Wet - bacterial infection occurs & patient dies of sepsis

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64
Q

Define infarction

A

necrosis of part or the whole organ that occurs when the arterial supply becomes blocked

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65
Q

Why are tissues with an end arterial supply more susceptible to infarction?

A

They only have a single arterial supply and so if this vessel is interrupted infarction is likely.

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66
Q

Give 3 examples of organs with a dual arterial supply.

A
  1. Lungs (bronchial arteries and pulmonary veins).
  2. Liver (hepatic arteries and portal veins).
  3. Some areas of the brain around the circle of willis.
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67
Q

What can happen if ischaemia is rectified?

A

Re-perfusion injury can occur due to the release of waste products accumulated during lack of O2

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68
Q

Potential consequences of ischaemia

A

Infarction or gangrene

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69
Q

Consequences of arterial embolus?

A

An arterial embolus can go anywhere! The consequences could be stroke, MI, gangrene etc.

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70
Q

What are the consequences of a venous embolus?

A

An embolus in the venous system will go onto the vena cava and then through the pulmonary arteries and become lodged in the lungs causing a pulmonary embolism. This means there is decreased perfusion to the lungs.

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71
Q

Define atherosclerosis

A

disease characterised by the formation of atherosclerotic plaque in the intima of vessel walls

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72
Q

3 main components of atherosclerotic plaque

A
  • Fibrous tissue IN the artery
  • Lipid in the form of cholesterol
  • Lymphocytes
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73
Q

Is atherosclerosis more common in the systemic or pulmonary circulation?

A

It is more common in the systemic circulation because this is a higher pressure system.

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74
Q

Primary cause of atherosclerosis

A

Endothelial cell damage

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75
Q

Give 5 risk factors for atherosclerosis.

A
  1. Cigarette smoking.
  2. Hypertension.
  3. Hyperlipidaemia.
  4. Uncontrolled diabetes mellitus.
  5. Lower socioeconomic status.
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76
Q

Preventive measures for atherosclerosis?

A
  1. lifestyle changes
  2. aspirin: for those within clinical evidence of the illness, inhibits platelet aggression
  3. statins: cholesterol reducing drug
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77
Q

Why can cigarette smoking lead to atherosclerosis?

A

Cigarette smoking releases free radicals, nicotine and CO into the body. These all damage endothelial cells

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78
Q

Why can hypertension lead to atherosclerosis?

A

A higher blood pressure means there is a greater force exerted onto the endothelial cells and this can lead to damage.

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79
Q

Define hypertrophy

A

increase in size of a tissue caused by an increase in size of the constituent cells (without the cells dividing)

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80
Q

Define hyperplasia

A

increased in the size of a tissue caused by an increase in number of constituent cells (with division through mitosis)

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81
Q

Define atrophy

A

decrease in size of a tissue caused by either a decrease in cell size or number

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82
Q

Give example of a disease that demonstrates atrophy

A

Dementia - loss of neurons

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83
Q

Define metaplasia

A

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

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84
Q

Give example of a disease that demonstrates metaplasia

A

Barrett’s oesophagus - the cells at the lower end of the oesophagus change from stratified squamous cells to columnar

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85
Q

Define dysplasia

A

morphological changes seen in cells in progression to becoming cancer

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86
Q

What is a telomere

A

Random repetitive DNA at the tip of each chromosome, not copied prior to mitosis & shortens with each replication

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87
Q

What happens when a telomere becomes too short

A

The cell cannot replicate anymore as DNA polymerase is unable to engage

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88
Q

When are telomeres replicated (exceptions)

A

In germ cells & embryos

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89
Q

Give an example of a dividing and a non-dividing tissue

A
  • Gut or skin tissue can divide.
  • Brain tissue is non dividing.
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90
Q

When should chemotherapy used over excision?

A

When the illness is systemic / circulates all over the body

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91
Q

Difference between carcinogenic & oncogenic

A

Carcino-x: cancer causing
Onco-x: tumour causing

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92
Q

Define neoplasms

A

Autonomous abnormal persistent growth; suffix -oma

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93
Q

What needs to be done usually for chemical carcinogens before it causes disease?

A

Metabolic conversion from pro-carcinogens to ultimate carcinogens

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94
Q

What 2 types of cancer can polycyclic aromatic hydrocarbons cause?

A

Lung & Skin cancer

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95
Q

What exposes people to polycyclic aromatic hydrocarbons?

A

Smoking cigarettes and mineral oils.

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96
Q

What types of cancer do aromatic amines cause?

A

Bladder cancer

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97
Q

Three reasons behind how alcohol can cause cancer

A
  • ethanol makes it easier for cells in oropharynx to absorb other carcinogens
  • ethanol increases oestrogen levels
  • alcohol’s metabolite, acetaldehyde, is a mutagen
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98
Q

What types of people are more susceptible to bladder cancer caused by aromatic amine exposure?

A

People working in the rubber / dye industry

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99
Q

Name 3 biological agents that can cause cancer

A
  1. hormones: oestrogen & anabolic steroids
  2. mycotoxins
  3. Parasites
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100
Q

What type of cancer do nitrosamines cause?

A

Gut cancer

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101
Q

What type of cancer do alkylating agents cause?

A

Leukaemia but risk is small in humans

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102
Q

Host factor which may increase a person’s risk of having cancer?

A
  • race
  • diet
  • constitutional factors - age, gender
  • premalignant lesions
  • transplacental exposure
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103
Q

Give an example of a situation when transplacental exposure lead to an increase in cancer risk.

A

The daughters of mothers who had taken diethylstiboestrol for morning sickness had an increased risk of vaginal cancer.

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104
Q

Composition of a stroma

A

Neoplastic cells & stroma (supporting network)

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105
Q

Describe neoplastic cells

A
  • derived from monoclonal cells
  • growth pattern & synthetic activity usually related to parent cell
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106
Q

Describe stroma

A
  • Supportive, connective tissue framework for neoplasms, provides nutrition.
  • May consist of fibroblasts, fibrous connective tissues & blood vessels
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107
Q

Two types of benign neoplasms of epithelial cells?

A

Papilloma & adenoma

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108
Q

Define papilloma

A

Benign tumour of non-glandular non-secretory epithelium

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109
Q

Define adenoma

A

benign tumour of glandular or secretory epithelium

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110
Q

Define carcinoma

A

malignant epithelial neoplasm

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111
Q

Define osteoma

A

benign tumour of the bone

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112
Q

Define chondroma

A

benign tumour of the cartilage

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113
Q

Define lipoma

A

benign tumour of the adipocytes

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114
Q

Define adenocarcinoma *

A

malignant tumour of glandular epithelium

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115
Q

Define angioma

A

Benign tumour of the vascular connective tissues

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116
Q

Define sarcoma

A

(general) malignant tumour of the connective tissues

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117
Q

How are tumours classified histologically?

A

Depending on their degree of differentiation
Grade 1 = well differentiated, resembles parent tissue more
Grade 2
Grade 3 = poorly differentiated

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118
Q

Define anaplastic

A

Poorly differentiated to the extent that there are no recognisable histological features

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119
Q

5 types of carcinoma that can spread to the bones ( & vice versa)

A
  1. Breast.
  2. Kidney.
  3. Lung.
  4. Prostate.
  5. Thyroid.
120
Q

carcinoma that can spread to the lymph nodes

A

breast carcinoma

121
Q

Adv’s & disadv’s of conventional chemotherapy

A
  • Advantage: works well for treatment against fast dividing tumours e.g. lymphomas.
  • Disadvantage: it is non selective for tumour cells, normal cells are hit too; this results in bad side effects such as diarrhoea and hair loss.
122
Q

Chemotherapy is most effective against what type of carcinomas?

A

Slower dividing tumours e.g. lung, colon and breast.

123
Q

What kind of drugs can be used in chemotherapy?

A

Monoclonal antibodies (MAB) and small molecular inhibitors (SMI).

124
Q

Define carcinoma in situ

A

a malignant epithelial neoplasm that has not yet invaded through the original basement membrane

125
Q

Define invasive carcinoma

A

a carcinoma that has invaded through the original basement membrane

126
Q

What is required for a carcinoma to become invasive?

A
  • enzymes (e.g. collagenase for invasion of blood stream)
  • cell motility
127
Q

Maximum size a tumour can grow to before needing its own blood vessels

A

~1mm

128
Q

Two promoters of angiogenesis

A
  1. Vascular endothelial growth factors.
  2. Fibroblast growth factors.
129
Q

Three inhibitors of angiogenesis

A
  1. Angiostatin.
  2. Endostatin.
  3. Vasculostatin.
  • statin ending!
130
Q

What is the process during which ‘a malignant carcinoma breaches through the basement membrane and spread to other parts of the tissue’ known as

A

Invasion

131
Q

What is the entire spread process ‘of the tumour where it spreads from its primary site to produce secondary tumours at distant sites’ known as

A

Metastasis

132
Q

What three mechanisms must a tumour have to achieve growth at secondary metastatic site?

A
  1. evasion of host immune defence
  2. arrest
  3. Extravasation
133
Q

What are three mechanisms a tumour may use to evade host immune defence

A
  • aggregation with platelets
  • shedding of surface antigens
  • adhesion to other tumour cells
134
Q

Example of tumour that can spread to the lung

A

Sarcoma (via venae cavae -> heart -> pulmonary arteries)

135
Q

Example of tumour that can spread trans-coelomically

A

colorectal, stomach & pancreas = all can spread to liver via portal venous system

136
Q

What are the two ways in which neoplasms can be classified?

A

Behavourial & histological

137
Q

How are neoplasms classified bahavourially

A

Neoplasms can be classified as benign, malignant or borderline. Borderline tumours (e.g. some ovarian lesions) defy precise classification.

138
Q

7 main features of benign neoplasms

A
  1. Localised.
  2. Non-invasive.
  3. Slow growth, low mitotic activity.
  4. Close resemblance to normal tissue.
  5. Normal nuclei.
  6. Necrosis and ulceration are rare due to slow growth.
  7. Exophytic growth.
139
Q

4 consequences of benign neoplasms

A
  1. Pressure on adjacent structures.
  2. Obstruction to flow.
  3. Transformation into malignant neoplasms.
  4. Anxiety.
140
Q

7 main features of malignant neoplasms

A
  1. INVASIVE!
  2. Metastases.
  3. Rapid growth, high mitotic activity.
  4. Resemblance to normal tissue.
  5. Poorly defined border due to invasive nature.
  6. Necrosis and ulceration are common.
  7. Endophytic growth.
141
Q

Consequences of malignant neoplasms

A

Destroy surrounding tissue, blood loss due to ulceration, pain, anxiety.

142
Q

Define teratoma

A

neoplasm of germ cell origin that forms cells representing all three germ cell layers of the embryo; ectoderm, mesoderm & endoderm

143
Q

Define carcinosarcoma

A

mixed malignant tumours showing characteristics of epithelium & connective tissue

144
Q

Define carcinogenesis

A

A multistep process in which normal cells become neoplastic cells due to mutations.

145
Q

What must the immune system do in order to be effective?

A

Differentiate self from non-self

146
Q

Define innate immunity

A

instinctive, non-specific, present from birth. NO lymphocytes YES lysosomes

147
Q

Define adaptive immunity

A

Specific ‘acquired / learned’ immunity. Quicker response. Memory. B / T lymphocytes & antibodies

148
Q

Examples of innate defence mechanisms?

A
  • Physical barriers - skin, gut, bronchi, pH
  • Phagocytic cells
  • blood proteins
149
Q

Examples of adaptive defence mechanisms?

A
  • Antigen presenting cells
  • T cells
  • Major Histocompatibility Complex (MHC)
  • Antigens - intrinsic & extrinsic
150
Q

Lock and key system in detecting microbes

A

Pathogen Associated Molecular Patters (PAMPs) & Pattern Recognition Receptors (PRRs)

151
Q

Define PAMPs

A

Pathogen Associated Molecular Patterns - describes general molecular features common to all pathogens, used by innate i.s. to recognise microbes

152
Q

Define PRRs

A

Pattern Recognition Receptors Family of proteins which recognise & bind to pathogen ligands, thereby increasing likelihood of successful T cell activation

e.g. Toll-like receptor on macrophages, dendritic cells & neutrophils

153
Q

What are the O2 dependent killing mechanisms of the innate immunity system?

A

Superoxides & nitric oxide

154
Q

What are the O2 independent killing mechanisms of the innate immunity system?

A

enzymes: defensins, lysozyme, pH, tumor necrosis factor

155
Q

Function of lysozyme

A

destroys bacteria cell walls

156
Q

3 examples of polymorphonuclear leukocytes

A
  1. Neutrophils.
  2. Basophils.
  3. Eosinophils.
157
Q

3 examples of mononuclear leukocytes

A
  1. Monocytes.
  2. B lymphocytes.
  3. T lymphocytes.
158
Q

In which primary lymphoid tissue do T cells mature?

A

thymus

159
Q

In which primary lymphoid tissue do B cells mature?

A

Bone marrow

160
Q

What is the main source of histamine within the body?

A

Mast cells; histamine is stored in granules in their cytoplasm.

161
Q

How are antigens presented to T cells?

A

Through complex of Antigen Presenting Cell & Major Histocompatibility Complex

162
Q

Marker for activated T Cells?

A

CD25

163
Q

Three categories of T cells

A

Naive, effector or memory

164
Q

What type of antigens do T cells respond to

A

Only intracellular antigens presented via MHC’s

Does not respond to soluble antigens!

165
Q

Define T cell selection

A

Where T cells that recognises itself are killed in the foetal thymus as they mature

166
Q

Function of T helper 1 (CD4)

A

helps the immune response against intracellular pathogens. Secretes cytokines.

Also

  • activate macrophages triggering inflammation
  • regulate monocytes & macrophages
167
Q

Function of T helper 2 (CD4)

A

helps produce antibodies against extracellular pathogens through B cells. Secretes cytokines.

168
Q

Function of T reg

A

Regulate immune response

169
Q

Function of Cytotoxic T cells (CD8)

A

kill cells directly by binding to antigens; induce apoptosis

170
Q

What kind of cells respond to soluble antigens?

A

B cells

171
Q

What kind of cells respond to intracellular presented antigens via APC & MHC’s?

A

T cells

172
Q

What type of antigens do MHC 1 bind to?

A

Intracellular antigens

173
Q

Which type of cells express MHC 1’s

A

Virtually all cells of the body except erythrocytes

174
Q

Which type of cell binds to MHC 1’s

A

Cytotoxic T cells (CD8)

175
Q

Which MHC would an intracellular antigen (endogenous) lead to the expression of?

A

MHC 1’s

176
Q

Which MHC would an extracellular antigen (exogenous) lead to the expression of?

A

MHC 2’s

177
Q

Which type of cells express MHC 2’s

A

on surfaces of macrophages, B cells & dendritic cells (i.e. antigen presenting cells)

178
Q

Which type of cell binds to MHC 2’s

A

Helper T cells (CD4)

179
Q

What category of T cells do cytotoxic t cells (CD8) eventually evolve to?

A

Effector or memory cells

180
Q

What do B cells differentiate into?

A

Plasma cells. The plasma cells then produce antibodies.

181
Q

What does a T helper cell bind to?

A

A T cell receptor which is bound to an antigen epitope which is bound to MHC2 on an APC

182
Q

Function of B cells

A

Antibody factory
Plasma & memory cells
Express membrane bound immunoglobulin

183
Q

How many antibodies can each B cell make?

A

Each B cell can only make 1 antibody. This 1 antibody can only bind to 1 epitope.

184
Q

What happens to B cells that recognise ‘self’?

A

Killed in bone marrow

185
Q

How many antibodies can each B cell make?

A

1 antibody which can only bind to 1 epitope

186
Q

Process where B cells divide so all new cells will recognise the same antigen

A

Clonal expansion

187
Q

Briefly outline the activation process of B cells

A
  1. Phagocytosis of pathogen by B cell & present to T helper 2 via MHC !!
  2. Macrophage release IL-1: B cell activated
  3. T helper 2 binds to MHC II, which release interleukins that induce B cells to divide via clonal expansion
  4. B cells differentiates into plasma & memory cells which will produce antibodies. Increased recognition & faster response!
188
Q

Which interleukin activates B cells

A

IL-1

189
Q

3 functions of antibodies

A
  1. Neutralise toxins.
  2. Opsonisation.
  3. Activate classical complement system.
190
Q

Function of mast cells

A

Release histamine (stored in granules in their cytoplasm). Only found in tissues!

191
Q

Function of neutrophils

A

Innate - phagocytosis. Involved in acute inflammation! (Neutrophil Polymorph Migration!)

192
Q

Function of eosinophils

A

Neutralises histamine
Combats parasites

193
Q

Function of basophils

A

Allergic reaction: release histamine

194
Q

Function of natural killer cells

A

recognise & kill via apoptosis virus infected & tumour cells

195
Q

Function of dendritic cells

A
  • antigen presenting cells
  • both innate & adaptive
  • detect & chew then present pathogens on surface
  • only these cells can induce primary immune response in inactive / resting T lymphocytes
196
Q

Give 3 examples of APC’s

A

Macrophages, dendritic cells, B cells

197
Q

Examples of dendritic cells

A

Kupffer cells in liver, Langerhans in skin

198
Q

Define complement

A

20 serum factors secreted by the liver that when activated, will aim to remove or destroy antigen, either by direct lysis or opsonisation

199
Q

How are complement activated

A

achievable via 3 pathways = classical, alternatives & lectin. main goal is to cleave c3 → c3a & c3b: create membrane attack complex & enhance inflammation

200
Q

Define lysis

A

using membrane attack complex, create a hole in pathogen → influx of fluids → lysis → destruction

201
Q

Define opsonisation

A

antigen becomes coated with substances (= complement) making it easier to be engulfed by phagocytic cells as macrophages have special receptors for complement proteins

202
Q

Contrast antibodies & antigens

A 
Antibodies = specific protein produced in response to antigen 
Antigen = molecule on microbes
203
Q

What is the part of antigen that binds to antibody / receptor binding site called

A

Epitope

204
Q

Define affinity

A

Measure of binding strength between epitope & antibody binding site - the higher the affinity the better

205
Q

Briefly describe the structure of the antibody

A

Y shaped with four chains, ‘V’ area = Fab region: has antigen binding region
‘I’ area = Fc region, has Fc receptor which bind to complement, phagocytes, natural killer cells & B cells

206
Q

What does the Fab region on the antibody bind to

A

Specific antigens

207
Q

What does the Fc region on the antibody bind to

A

complement, phagocytes, natural killer cells & B cells

208
Q

Where are complement system plasma proteins secreted from?

A

Liver

209
Q

Which immunoglobulin is found in breast milk and other secretions?

A

IgA

210
Q

What are the 2 most common immunoglobulins (that are also first to respond)?

A

IgM & IgG

211
Q

Which immunoglobulin is most commonly involved in allergic responses?

A

IgE

212
Q

Which cells express high affinity IgE receptors?

A

Mast cells, basophils and eosinophils.

213
Q

What trigger the release of histamine?

A

Binding between IgE & cells with IgE specific receptor

214
Q

Name the 5 types of cytokines

A
  • Interferons
  • Interleukins
  • Colony stimulating factors
  • Tumour necrosis factors
  • Chemokines
215
Q

Function of cytokines

A

soluble proteins secreted by lymphocytes or macrophage / monocytes that act as stimulatory or inhibitory signals between cells

216
Q

Function of interferons

A

induce antiviral resistance in uninfected cells & limit spread of viral infections

217
Q

Function of interleukins

A

cause cell division and differentiation

218
Q

Function of colony stimulating factors

A

directs division & differentiation of bone marrow stem cells (precursor of leukocytes)

219
Q

Function of TNF’s

A

mediate inflammation and cytotoxic reactions

220
Q

Function of chemokines

A

Attract & direct leukocytes to sites of infection

221
Q

Contrast the two types of PRR’s

A

Secreted & circulating PRR - soluble & everywhere activates complement, improve phagocytosis

Cell associated PRR - present on cell membrane or cytosol of cells

222
Q

4 receptors that make up the PRR family

A
  1. toll - like receptor (TLR)
  2. C-type lectin receptors
  3. nod-like receptors (NLR)
  4. Rig-like receptors (RLR)
223
Q

Main functions of TLR

A

Separates bacteria from virus
Monitors endosome
TLR4 also identify damage & signal for initiation of tissue repair; can be used as a vaccine adjuvant

224
Q

Key characteristic that allows TLR to identify damage

A

hydrophobicity

225
Q

Main function of C-type lectin receptors

A

may participate in pathogen recognition (specifically fungi) & phagocytosis

226
Q

Main functions of NLR

A

in cytoplasm - detect intracellular microbial pathogens. release cytokines and can cause apoptosis if the cell is infected

227
Q

Disease where NLR’s are nonfunctioning & hyperfunctioning

A

non: crohn’s
hyper: blau syndrome

228
Q

Main function of RLRs

A

in cytoplasm - detect intracellular double-stranded viral RNA, activation of interferon production, enabling an antiviral response

229
Q

Type of TLR’s used in vaccine adjuvants

A

TLR4 agonists

230
Q

2 examples of intracellular PRR’s

A

NLR’s & RLR’s

231
Q

example of extracellular PRR

A

TLR’s

232
Q

What happens when a PAMP is recognised by a PRR?

A

The innate immune response and inflammatory response is triggered.

233
Q

Additional roles of TLR4

A

used as vaccine adjuvant
recognition of host molecules in autoimmune disease, failure to do so increases inflammatory responses

234
Q

Aim of a perfect vaccine (5)

A
  • safe
  • introduce suitable immune response - no booster needed
  • t & b cell memory
  • stable and easy to transport
  • affordable and accessible
235
Q

types of immunisations

A

passive & active immunisation

236
Q

define inoculation

A

introduction of viable microorganisms into the subject

237
Q

define passive immunisation

A

transfer of pre-formed antibodies

238
Q

adv’s & disadv’s of passive immunisation

A
  • does not activate immunological memory so no long term protection!
  • antisera used to neutralise toxins after immune system eliminated the primary infection → possibility of reaction to it!
239
Q

Three major types of passive immunisations

A
  • anti-toxins
  • prophylactic use to reduce chance of establishing infection after exposure
  • antivenin (venom)
240
Q

Examples of passive immunisations (say if active or passive)

A
  • DTa, rubella, mumps, polio: natural (cross-placenta & milk)
  • anti-toxins & anti-venins: artificial
  • pathogen with a short incubation time & disease with complications: artificial
241
Q

define active immunisation

A

manipulating the immune system to generate a persistent protective response against pathogens by safely mimicking natural infection (without risk of actual infection!)

242
Q

steps of active immunisation

A
  1. Engage innate immune system
  2. Elicit danger signals that activate immune system
    - triggers e.g. molecular fingerprint of infection - Pathogen-associated molecular patterns and engage TLR receptors
  3. Activate specialist antigen presenting cells
    - e.g. Langerhans cells
  4. Engage the adaptive immune system
    - generate memory T and B cells
    - activate T cell help
243
Q

Cells involved in primary response to active immunisation

A

innate immune system
- memory T and B cells generated and circulated for years

244
Q

Cells involved in secondary response to active immunisation

A
  • rapid and large scale
  • high affinity IgG
  • T cell help
245
Q

4 main vaccine designs

A
  1. attenuated (live)
  2. dead or inactivated
  3. dna vaccines
  4. recombinant
246
Q

adv’s & disadv’s of attenuated / live vaccines

A
  • transient infection so full natural immune response
  • memory response in t & b cells
  • often only single immunisation required
  • imcompromised: may become infected as a result
  • complications to death
  • occasionally the attenuated organism can revert to virulent form → may lead to potential outbreak!
247
Q

examples of attenuated / live vaccines

A

e.g. Tuberculosis - Bacillus Calmette-Guerin, polio sabin, typhoid, mumps

248
Q

subtypes of dead / inactivated vaccines & examples

A
  • inactivated: anthrax, cholera, hepB
  • subunit: diptheria & tetanus
  • carbohydrate
  • conjugated
  • synthetic peptides
249
Q

adv’s of inactivated vaccines

A

e. g. anthrax, cholera, hepB
- no risk of infection
- less critical storage
- wider range of different antigenic components are presented so good immune response

250
Q

adv’s of subunit vaccines

A

e. g. diphtheria, tetanus
- purified molecular components as immunogenic agents
- safe, only part of the pathogen used
- no risk of infection
- easier to store & preserve

251
Q

define conjugated vaccines

A

polysaccharide (weak antigen) linked to a carrier protein to increase its immunogenicity when used as a vaccine

benefit: long term protective response even in infants

252
Q

define vaccines of synthetic peptides (new)

A

novel technique aiming to produce a peptide that includes immunodominant B cell epitopes and stimulate memory T cell development

253
Q

what are DNA vaccines

A
  • aims to transiently express genes from pathogens in host cells
  • generate immune response similar to natural infections, leading to T and B cell memory responses
254
Q

mechanism of DNA vaccines

A

DNA plasmid vector vaccines carry the genetic info encoding an antigen which is taken up into cells and transcribed into nucleus → allowing the antigen to be produced inside of a host cell → leading to a cell mediated immune response via the MHC I pathway

255
Q

example of dna vaccines

A

covid vaccine
- AZ is viral vector: once inside the body, spike protein is produced and initiates immune response

256
Q

adv’s & disadv’s of dna vaccines

A
  • safe: especially in immunocompromised patients
  • may require booster
  • no transient infection
  • easy store and transport
  • drug delivery is simple and adaptable to widespread vaccination programs
257
Q

define recombinant vaccines

A

Aim is to imitate the effect of transient infection with pathogen but using a non-pathogenic microorganism
- viral or bacterial

258
Q

adv’s & disadv’s of recombinant vaccines

A
  • Produce immunological memory
  • Safe - relative to live attenuated pathogen
  • requires refrigeration for transport
  • Immune response to virus in subject can negate effectiveness
259
Q

define adjuvants

A

Any substance that is added to a vaccine to stimulate the immune system to ensure a powerful immune response

260
Q

examples of adjuvants

A
  • whole killed organisms
  • toxoids
  • proteins
  • chemicals: Aluminium salts (extend the half life of immunogen in the site of the injection, resulting in a depot effect the slow release of vaccine) & Paraffin oil
261
Q

define allergy

A

abnormal response to harmless foreign material (allergens)

262
Q

define atopy

A

inherited tendency to develop allergies / overproduction of IgE antibodies to common environmental antigens

263
Q

Examples of low affinity lgE receptor expressing cells

A

B cells, T cells, monocytes, platelets & neutrophils

264
Q

Functions of low affinity lgE receptor expressing cells

A
  • regulate lgE synthesis
  • trigger cytokine release by monocytes
  • antigen presentation by cells
265
Q

examples of high affinity lgE expressing cells

A

eosinophils, mast cells & basophils

266
Q

Functions of high affinity lgE expressing cells

A
  • involved in host defence against parasites
  • eosinophils: express a different range of granule content to mast cells & baso // mast cells only exist in tissues whereas the other two circulate in blood!
267
Q

Mast cells

  • what are they?
  • what is their function?
A
  • main effector for IgE mediated immunity - cause of reaction during anaphylaxis and inflammatory symptoms
  • have a primary role in both innate and adaptive immunity
268
Q

How are mast cells activated?

A

Through Indirect activation

  • allergens via IgE - prior sensitisation required, generally through mucus surface
  • bacterial / viral antigens via IgE

Through phagocytosis

Through direct activation

  • cold / mechanical deformation i.e. asthma
  • aspirin, tartrazin, preservatives, nitric oxide
  • complement products, c3a and c5a
269
Q

What happens if mast cells are activated? (4)

A
  • they release the mediators stored inside them = degranulation

They will cause anaphylactic symptoms, e.g.

  • skin: swelling, itching, reddening
  • airways: excessive mucus production, bronchoconstriction
  • GI: abdominal bloating, vomiting, diarrhoea
  • Anaphylaxis: airway, breathing, circulation
270
Q

What products are released if mast cells are activated and what are their effects?

A
  • histamine (increase vascular permeability, smooth musc contract)
  • cytokines
    • IL4, IL13 - promotes Th2 differentiation, IgE production
    • TNF - alpha - promotes tissue inflammation
  • lipid mediators - leukotrines and prostaglandins - + vasc perm, smooth musc contr, mucus secretion, chemoattractants for T, eosino, mast and baso
271
Q

name the mechanisms of activating mast cells

A
  • indirect activation via lgE
  • phagocytosis
  • direct activation (3)
  • cold / mechanical deformation (i.e. asthma)
  • aspirin, tartrazine, preservatives, nitric oxide
  • complement products - c3a & c5a
272
Q

summary of the types of cells involved in allergy (5)

A
  1. Mast cells
  2. Lymphocytes (typically Th2)
  3. Dendritic cells
  4. Neurons
  5. Non-immune cells
273
Q

What makes an allergen?

A
  • particulate delivery of antigens
  • presence of **WEAK pathogen associated molecular patterns (PAMPs)** resulting in a weak innate immunity activation but **NOT adaptive** as it goes into memory and thus wont be an allergen
  • nasal / skin delivery
  • low doses
274
Q

define anaphylaxis

A

severe and life threatening reaction to an allergen with systemic symptoms, e.g. severe hypotension, vasodilation and bronchoconstriction

involves mast cell or basophil activation through IgE or direct

275
Q

6 features of anaphylaxis?

A
  1. rapid onset
  2. blotchy rash
  3. swelling of face and lips
    4 wheeze
  4. hypotension
  5. cardiac arrest if severe
276
Q

4 broad indications of anaphylaxis?

A
  • skin: swelling, itching, reddening
  • airways: excessive mucus production, bronchoconstriction
  • GI: abdominal bloating, vomiting, diarrhoea
  • Anaphylaxis: airway, breathing, circulation
277
Q

principles of treatment of anaphylaxis

A

Airway, Breathing, Circulation, Disability, Exposure (ABCDE)

  • ABC = basic life support
  • stop infusion of drug
  • give adrenaline and anti-histamines!
278
Q

examples of allergy diseases

A

asthma, eczema, allergic rhinitis

279
Q

6 principal ways of treating allergy

A
  • desensitisation
  • prevent lgE production
  • anti-lgE therapy
  • anti-cytokine antibodies
  • prevent mast cell activation
  • inhibit mast cell products
280
Q

principle of desensitisation as an allergy treatment

A
  • giving increasing doses of antigen as immunotherapy, can be admitted sub-lingual or sub-cutaneous (SCIT)
  • limited use: no benefits for atopic eczema and asthma
  • usually for severe allergies only
281
Q

principle of desensitisation as an allergy treatment **

A
  • giving increasing doses of antigen as immunotherapy, can be admitted sub-lingual or sub-cutaneous (SCIT)
  • limited use: no benefits for atopic eczema and asthma
  • usually for severe allergies only
282
Q

principle of anti-lgE therapy as an allergy treatment

A
  • xolair (omalizumab) = recombinant humanised IgG1K monoclonal antibody that selectively binds to IgE
  • inhibit binding of IgE to high-affinity IgE receptor
  • effective for allergic asthma but highly contested
283
Q

principle of anti-cytokine antibodies as an allergy treatment

A
  • targeting IL-5 antibody, IL-5 receptor antibody, anti-IL4 / IL-13 receptor antibody
  • example: mepolizumab - for adults with severe asthma
284
Q

mechanisms through which preventing mast cell activation can act as an allergy treatment **

A
  • mast cell stabiliser: sodium cromoglycate: reduce mediator release
  • beta 2 agonist: salmeterol
  • increase cAMP
  • Glucocorticoids
  • inhibit gene transcription
  • long term side effects
  • calcium channel blockers
  • signalling inhibitors
285
Q

principle of inhibiting mast cell products as an allergy treatment **

A

through

  • histamine receptor (H1) antagonists (numerous target cells)
  • leokotrine antagonists through inhibiting activation of Th2
  • tryptase inhibitors: preventing airway smooth muscle activation
  • protease - activated receptor (PAR)
286
Q

How are lgE related to allergies

A
  • lgEs are made to things we are allergic to
  • mast cells are the main effector cells for lgE mediated immunity - have a primary role in both innate and adaptive immunity
287
Q

Define hypersensitivity?

A

Diseases in which immune responses to environmental antigens cause inflammation and damage to the body itself

288
Q

give 4 risk factors for hypersensitivity?

A
  1. protein based macromolecules
  2. female > male
  3. immunosuppression
  4. genetic factors
289
Q

define type 1 hypersensitivity reactions according to gell & coombs classification

A
  • lgE primary, also G & A
  • allergic & acute reaction
  • acute anaphylaxis, hay fever

IMMEDIATE

290
Q

define type 2 hypersensitivity reactions according to gell & coombs classification

A
  • primarily IgG mediated cytotoxicity
  • e.g. transfusion reactions, autoimmune disease, some drug allergies, e.g. penicillin
291
Q

What can cause a type 2 hypersensitivity reaction?

A
  • transplant rejection (!)
  • transfusion reactions, drug-induced allergies (peniciliin e.g.)
292
Q

define type 3 hypersensitivity reactions according to gell & coombs classification

A
  • IgG / IgM dependent immune complex formation - which are not adequately cleared by innate immune cells, give rise to inflammatory response
  • e.g. serum sickness, contact dermatitis
293
Q

what can cause a type 3 hypersensitivity reaction?

A

SLE, Post strep glomerulonephritis

294
Q

define type 4 hypersensitivity reactions according to gell & coombs classification

A

delayed type hypersensitivity, DTH (= several days)

  • cell dependent Th1 / cytotoxic T / macrophage)
  • e.g. TB, contact dermatitis
295
Q

what can cause a type 4 hypersensitivity reaction?

A

TB & contact dermatitis

296
Q

role of **T lymphocyte** in complex allergic conditions such as asthma etc

A

especially Th-2

  • releases cytokines IL4 & 13 which stimulate lgE production
  • activates lgE
  • recruits lgE antibody-producing B cells, mast cells & eosinophils

Phase 2A (12 decks)

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