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med 2a > pathology and immunology > Flashcards

pathology and immunology Flashcards

1
Q

Acute inflammation:

neutrophil polymorph action?

A
  • Short lived cells
  • First on the scene of acute inflammation
  • Cytoplasmic granules full of enzymes that kill bacteria
  • Usually die at the scene of inflammation
  • Release chemicals that attract other inflammatory cells such as macrophages
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2
Q

Acute inflammation:

acute vs chronic?

A

Acute:

  • sudden onset
  • short lived
  • usually resolves

Chronic:

  • slow onset or sequel to acute
  • long duration
  • may never resolve
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3
Q

Exudate vs transudate?

A

Exudate

  • fluid buildup outside vessels
  • the protein-rich fluid that leaks out from blood vessels
  • due to e.g. inflammation or local cellular damage
  • accumulation of neutrophil polymorphs outside the vessel in the extracellular space (they squeeze through gaps in endothelial cell layer)

Transudate

  • fluid buildup outside
  • due to changes in blood pressure in blood vessels
  • causing fluid to leave vascular system
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4
Q

Acute inflammation:

causes?

A
  • microbial infections, e.g. pyogenic bacteria, viruses
  • hypersensitivity reactions, e.g. parasites, tubercle bacilli
  • physical agents, e.g. trauma, ionising radiation, heat, cold
  • chemicals, e.g. corrosives, acids, alkalis, reducing agents,
  • bacterial toxins
  • tissue necrosis, e.g. ischaemic infarction
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5
Q

Acute inflammation:

essential macroscopic appearances of inflammation?

A
  • calor (Heat) - increased blood flow (hyperaemia) through the region, resulting in vascular dilatation and the delivery of warm blood to the area
  • rubor (redness) - vasodilation of small blood vessels in damaged area
  • tumor (swelling) - exudate but also to a lesser extent migration of neutrophil polymorphs to area
  • dolor (pain) - stretching and distortion of tissues due to inflammatory oedema but also bc of pus under pressure in an abscess
  • loss of function - movement of an inflamed area will consciously and reflexively be inhibited and severe swelling will also immobilise the tissues
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6
Q

Acute inflammation: describe macrophages?

A
  • Long lived cells (weeks to months) • Phagocytic properties
  • Ingest bacteria and debris
  • May carry debris away
  • May present antigen to lymphocytes
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7
Q

Acute inflammation: lymphocytes?

A
  • Long lived cells (years)
  • Produce chemicals which attract in other inflammatory cells
  • Immunological memory for past infections and antigens
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8
Q

Acute inflammation: endothelial cells?

A
  • Line capillary blood vessels in areas of inflammation
  • Become sticky in areas of inflammation so inflammatory cells adhere to them
  • Become porous to allow inflammatory cells to pass into tissues
  • Grow into areas of damage to form new capillary vessels
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9
Q

Acute inflammation:

4 outcomes of inflammation?

A
  1. Resolution
  2. Suppuration e.g. abscess formation/discharge of pus
  3. Organisation
  4. Progression to chronic inflammation
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10
Q

Acute inflammation:

5 signs of inflammation?

A
  1. Redness (rubor).
  2. Swelling (tumor).
  3. Pain (dolor).
  4. Heat (calor).
  5. Loss of function.
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11
Q

Chronic inflammation:

Causes of chronic inflammation?

A
  1. Primary chronic inflammation.
  2. Transplant rejection.
  3. Recurrent acute inflammation.
  4. Progression from acute inflammation.
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12
Q

chronic inflammation:

essential macroscopic features?

A
  1. Chronic ulcer.
  2. Chronic abscess cavity.
  3. Granulomatous inflammation.
  4. Fibrosis.
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13
Q

The activity of what enzyme in the blood can act as a marker for granulomatous disease?

A

Angiotensin converting enzyme.

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14
Q

Name 2 types of cells that are incapable of regeneration.

A
  1. Myocardial cells.

2. Neuronal cells.

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15
Q

Healing by first intention?

A

incision → no tissue loss → fibrinogen release → edges joined by fibrin [which forms a clot] → replaced by collagen [little scar tissue] → structure & function restored

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16
Q

Healing by 2nd intention?

A

loss of tissue → gap filled w/ granulomatous tissue → adhesion of edges → organisation & fibrosis formation [areas of fibrous tissue leads to a big scar]

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17
Q

Resolution vs repair?

A

Resolution:
when tissue is undamaged and able to regenerate (liver)

Repair:
Replacement of damaged tissue by fibrous tissue (tissue damage so can’t regenerate)

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18
Q

Thrombosis:
Definition?

Caused by?

A

solid mass of blood constituents formed within intact vascular system during life

Caused by:

  • change in vessel wall [endothelial injury by smoking]
  • change in blood flow [stasis]
  • change in blood constituents [which causes platelet aggregation, thrombus formation & fibrin deposition]
  • change in 2/3 of the Virchow’s triad;
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19
Q

Virchow’s triad?

A

Change in blood flow (stasis)
— endothelial injury (change in vessel wall)
— Change in blood constituents (hypercoaguability)

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20
Q

Atrophy?

A

decrease in size of a tissue caused by a decrease in number of the constituent cells or a decrease in their size

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21
Q

Hypertrophy?

A

Increase in size of a tissue caused by an increase in size of the constituent cells

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22
Q

Hyperplasia?

Can only do this in which tissues?

A

increase in size of a tissue caused by an increase in number of the constituent cells

  • Can only do this in tissues capable of regeneration
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23
Q

Metaplasia?

A

change in differentiation of a cell from one fully-differentiated type to a different fully-differentiated type

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24
Q

Dysplasia?

A

imprecise term for the morphological changes seen in cells in the progression to becoming cancer

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25
Q

Define embolus.

A

solid mass in the blood being carried through the circulation to a place where it gets stuck and blocks the vessel.

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26
Q

Define ischaemia.

A

Decreased blood flow.

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27
Q

Define infarction.

A

Decreased blood flow with subsequent cell death.

  • Tissues with an end arterial supply are more susceptible to infarction
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28
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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29
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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30
Q

Define atherosclerosis.

A

Inflammatory process characterised by hardened plaques in the intima of a vessel wall.

A hardened plaque in the intima of an artery. It is an inflammatory process.

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31
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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32
Q

3 main constituents of an atheromatous plaque?

A
  1. Lipids.
  2. Fibrous tissue.
  3. Lymphocytes.
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33
Q

primary cause of atherosclerosis?

A

Endothelial cell damage.

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34
Q

define apoptosis

A

programmed cell death wo the release of products harmful to surroudings

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35
Q

p53 protein role?

A

DNA damage via base alteration or cross linkage occurs and is sensed by p53 protein
protein assesses the damage and causes apoptosis

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36
Q

Define atrophy.

A

Decrease in the size of a tissue due to a decrease in the size of the constituent cells OR due to a decrease in the number of constituent cells.

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37
Q

describe telomeres and aging

A
  • help unravel dna, help w mitosis and dividing
  • telomeres get shorter with age
  • thus decreasing the ability of cells to divide → therefore only dividing cells are affected by ageing
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38
Q

Name of cells that produce collagen in fibrous scarring?

A

fibroblasts

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39
Q

which of the following is an example of acute inflammation?

a. glandular fever
b. leprosy
c. appendicitis
d. TB

A

c. appendicitis

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40
Q

in which of the following does granulomatous inflammation occur?

a. crohn’s
b. acute appendicitis
c. infectious mononucleosis
d. lobar pneumonia

A

c. infectious mononucleosis

aka glandular fever

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41
Q

in which of the following does granulomatous inflammation occur?

a. crohn’s
b. acute appendicitis
c. infectious mononucleosis
d. lobar pneumonia

A

a. crohn’s disease

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42
Q

what is the specific name of calcification in diseased (as opposed to normal) tissues?

A

dystrophic calcification

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43
Q

which one of the following is a chronic inflammatory process from the start?

a. appendicitis
b. cholecystitis
c. infectious mononucleosis
d. lobar pneumonia

A

c. infectious mononucleosis

aka glandular fever

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44
Q

arterial vs venous thrombus?

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.

arterial embolism can go anwhere downstream of its entry point - eg MI, gangrene, cardiac failiure

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45
Q

Malignant tumour of striated muscle?

A

Rhabdomyo sarcoma

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46
Q 
Which of the following tumours does not commonly metastasise to bone?		
A. Breast cancer
B. Lung cancer
C. Prostate cancer
D. Liposarcoma
A

D. Liposarcoma

47
Q

What is the name of benign tumour of glandular epithelium?

A

Adenoma

48
Q

Name of a tumour that doesn’t invade basement membrane?

A

Carcinoma in situ

49
Q

Name of benign tumour of adipocytes?

A

Lipoma

50
Q

Name of a malignant tumour of glandular epithelium?

A

Adenocarcinoma

51
Q 
Which of the following is not a feature of malignant tumours?
A. Vascular invasion
B. Metastasis
C. Increased cell division
D. Growth related to overall body growth
A

D.

52
Q

Transitional cell carcinoma is a malignant?

True/False?

A

True

53
Q

Leiomyoma is a benign tumour of smooth muscle?

True/False

A

True

54
Q

Radon gas is a cause of lung cancer?

True/False

A

True bc its ionising radiation

55
Q

Asbestos is a human carcinogen?

True/False

A

True

56
Q

Ovarian cancer commonly spreads in peritoneum?

True/False

A

True

57
Q
  1. Benign epithelial non glandular/non secretory epithelium?
  2. Benign epithelial Glandular or secretory epithelium?
  3. Malignant tumour of epithelial cells?
  4. Malignant tumour of glandular epithelium?
  5. Benign connective tissue of adipocytes?
  6. Benign connective tissue of cartilage?
  7. Benign connective tissue of bone?
  8. Benign connective vascular tissue?
  9. Benign connective tissue of striated muscle?
  10. Benign connective tissue of smooth muscle?
  11. Malignant connective tissue adipocytes?
  12. Malignant connective tissue of cartilage?
  13. Malignant connective tissue of bone?
  14. Malignant connective vascular tissue?
  15. Malignant connective tissue of striated muscle?
  16. Malignant connective tissue of smooth muscle?
  17. collection of epithelioid histiocytes?
  18. bacterial/fungal infection?
  19. non neoplastic mass caused by TB infection?
  20. malignant neoplasm of melanocytes (skin)?
  21. malignant neoplasm of mesothelial cells of the chest (pleura), abdomen (peritoneum) or heart (pericardium)?
  22. malignant neoplasm of lymphoid cells (lymphocytes– including Hodgkin’s]?
  23. neoplasm of plasma cells?
  24. malignant neoplasm of blood cells?
A
  1. Papilloma
  2. Adenoma
  3. Carcinoma
  4. Adenocarcinoma
  5. Lipoma
  6. Chondroma
  7. Osteoma
  8. Angioma
  9. Rhabdomyoma
  10. Leiomyoma
  11. Liposarcoma
  12. Chondrosarcoma
  13. Osteosarcoma
  14. Angiosarcoma
  15. Rhabdomyosarcoma
  16. Leiomyosarcoma
  17. Granuloma
  18. Mycetoma
  19. Tuberculoma
  20. Melanoma
  21. Mesothelioma
  22. Lymphoma
  23. Myeloma
  24. Leukaemia
58
Q

Apoptosis vs necrosis?

A
  1. Apoptosis is programmed cell death whereas necrosis is unprogrammed.
  2. Apoptosis tends to affect only a single cell whereas necrosis affects a large number of cells.
  3. Apoptosis is often in response to DNA damage. Necrosis is triggered by an adverse event e.g. frost bite.
59
Q

adaptive vs innate immunity?

A 
Must discriminateselffromnon-self
innate = 
- Instinctive, first line of defence
- *non-specific,* does not depend on lymphocytes,
- *present from birth*
- Slow response
- no memory
adaptive
= - Specific ‘Acquired/learned’ immunity,
- r*equires lymphocytes*,
- *antibodies*
- Response specific to antigen
- Quicker response
    - Cell-mediated response (T-cells)
    - Humoral response (B-cells)
-> has passive and active memory and cell-mediated immunity
60
Q

What cell type is described below?

‘These are the most abundant white blood cell in humans and are characterised by the multi-lobed shape of their nucleus.’

A

Macrophages

61
Q

Which antigen presenting cell is considered a professional at activating lymphocytes?

A

Dendritic cells

62
Q

Give examples of live attenuated vaccines in the UK (2)

A

MMR

BCG (TB)

63
Q

Give examples of diseases that polysaccharide vaccines treat? (3)

A

Pneumococcal disease

Salmonella Typhi

Meningococcal disease

64
Q

Influenza vaccine is targeted towards ‘at risk’ groups in the UK. Which are classified as ‘at risk’? EDITTTTTT

A

6 months of age and over

65
Q

Which of the following is not an organ-specific auto-immune disease?

Type 1 diabetes mellitus
Graves disease
Ulcerative colitis 
Hashimoto’s thyroiditis
Sjogren's syndrome
A

Ulcerative colitis

66
Q

PAMPs: define?

Give examples of classical PAMPs
5

A

Pathogen Associated Molecular Patterns

Specific characteristics that occur on pathogens but not on cells of the body
Macrophages can recognise these

Flagellin, a protein found in bacterial flagella

Lipopolysaccharide (LPS) from the outer membrane of gram-negative bacteria

Peptidoglycan, found in bacterial cell walls

Lipoarabinomannan of mycobacteria

Endotoxins

Double stranded RNA

67
Q

Complements are the proteins that are involved in the clearance of antigen/bacteria. Which of the following is not part of the Elimination phase of complement activation?

Opsonisation
Production of interferons
Target cell lysis
Chemoattraction of leukocytes
Phagocytosis
A

Production of interferons

68
Q

What are the 3 main outcomes of complement system activation?

A
  1. Pathogen lysis. (Membrane attack complex)
  2. To act as Opsonins and coat organisms -> fork (for phagocytosis by …)
  3. Activation of leukocytes. (Attracting more leukocytes to site of infection)
69
Q

How are the 3 different complement pathways triggered?

Name the 3 diff complement pathways

A

Lectin pathway and alternative pathway - triggered directly by pathogens

Classical pathway - triggered by Ag-Ab complexes

70
Q

Is production of interferons (anti-viral proteins) part of the elimination phase of complement activation?

A

No

71
Q

What are the consequences of complement deficiency?

A

Impaired opsonisation of encapsulated bacteria.

72
Q

Give 4 functions of antibodies.

A
  1. Neutralise toxins.
  2. Opsonisation.
  3. Activate classical complement system.
  4. Agglutination
  5. Attach t receptors and block other antigens from binding
73
Q

Describe ab structure:

A

FAB. Region - the variable that binds to ag

FC region - binds to B cells

Complementarity determining region (CDR).- reversible bonding between antibodies and antigens - Hydrogen bonds and VDW’s etc form cumulative weak interactions that together form a strong force. -

74
Q

What immunoglobulin do naive antibodies express?

A

IgM

75
Q

Which compound is responsible for signalling when an antigen binds to an antibody?

A

Tyrosine kinase

76
Q

Name 5 types of cytokines.

A
  1. Interferons.
  2. Interleukins.
  3. Colony stimulating factors.
  4. Tumour necrosis factors.
  5. Transforming Growth Factors
77
Q

What is the main function of Toll Like Receptors?

A

TLR’s send signals to the nucleus to secrete cytokines and interferons. These signals initiate tissue repair. Enhanced TLR signalling = improved immune response.

78
Q

What is the main function of Nod Like Receptors?

A

NLR’s detect intracellular microbial pathogens. They release cytokines and can cause apoptosis if the cell is infected.

79
Q

interferons (IFN) : function and produced by?

A

Interferons produce antiviral proteins.

Interferons are produced by virus infected cells

80
Q

Interleukins (IL) : function?

Lots of qs from ek in notion

A

They cause cell division and differentiation

produced by many cells, over 30 types

81
Q

Colony Stimulating Factors (CSF): function?

A

Bind to surface receptors on haematopoietic stem cells - causing them to differentiate and proliferate]]

(Causes division and differentiation of bone marrow stem cells.)

82
Q

Tumour Necrosis Factors (TNFa&b): function?

A

Binds to receptors on some cells eg tumour cells and cause cels to die

TNF mediates inflammation and cytotoxic reactions.

83
Q

Transforming Growth Factors (TGF); function?

A

Help CD4+ THcells become regulate cells

84
Q

How do pro-inflammatory cytokines initiate an inflammatory response?

A

Vasodilation

Increased vascular permeability

Localised endothelial cell activation

85
Q

What other systems do cytokines activate?

A

Mast-cell degranulation

Clotting system activation

Kinin system

86
Q

Chemokines: function?

Produced by?

A

Help cells move towards the site of inflammation

  1. Leukocyte chemoattractants

Produced by TH cells & send signals to migrate to inflamed area

87
Q

Which cells express MHC2?

A

Antigen presenting cells ONLY e.g. macrophages, B cells, dendritic cells.

(MHC2 - CD4+ TH cells can bind to)

88
Q

Live Vaccine: pros and cons?

Examples of these vaccines?

A

Pros:

  1. Very effective, prolonged and comprehensive.
  2. Immunological memory produced.
  3. Often only 1 vaccine is needed.

Cons:

  1. Immunocompromised patients may become ill.
  2. Vaccines often need to be refrigerated which can be a problem in remote areas.

Eg:

  • TB-BCG
  • MMR
  • Varicella-zoster
  • Oral poliovirus vaccine (OPV)
  • Yellow fever virus vaccine
89
Q

Inactivated Vaccines: pros and cons?

Examples of these vaccines?

A

Pros:

  1. There is no risk of infection.
  2. Storage is less critical.

Cons:

  1. Inactivated vaccines tend to only activate the humoral response; there is a lack of T cell involvement.
  2. The response is often weak.
  3. Boosters are needed and so patient compliance may be poor.

Eg:

  • Inactivated poliovirus vaccine (IPV)
  • rabies vaccine
  • hepatitis A virus vaccine.
  • Influenza
90
Q

What is the role of an adjuvant?

A

An adjuvant is a substance added to a vaccination to stimulate an immune response. They convince your immune system that you’re infected.

91
Q

Subunit (acellular), recombinant, polysaccharide, and conjugate vaccines:
Definition?

Examples of these vaccines?

A

only has the antigenic part (most immunogenic pieces of pathogen)

do not contain any whole bacteria or viruses at all. Instead they contain some components, such as polysaccharides (sugars) or proteins, from bacteria or viruses.

Eg:

  • Pneumococcal Disease (polysaccharide)
  • Salmonella Typhi (polysaccharide)
  • Meningococcal Disease (polysaccharide)
  • Haemophilus influenzae type b vaccine
  • Hep B
  • HPV
92
Q

Toxoid vaccines: define?

And give examples?

A

Some bacteria release toxins (poisonous proteins) when they attack the body.
Some vaccines are made with inactivated versions of these toxins. They are called “toxoids” because they look like toxins but are not poisonous.

Eg:

  • diphtheria
  • tetanus
93
Q

Passive immunity:
Definition?
Pros vs cons?

A

transfer of preformed Ab to circulation [naturally via maternal transfer or artificially)

Pros:

  1. Immediate effect.
  2. Useful treatment for acute dangers e.g. snake venom. (Kills the toxin before it kills youuu)

Cons:

  1. no immunological memory created
  2. so no long term protection - is short term
  3. possible reaction to the anti-sera
94
Q

Active immunity:
Definition?
Pros vs cons:

A

manipulating the immune system to generate protective response to a pathogen via a vaccine w/ decreased infection risk, resulting in safely mimicking the natural infection & immunological memory.

Pros:

  1. Induces immunological memory.
  2. Produces high affinity antibodies.
  3. It produces a persistent protective response against pathogens.

Cons:

95
Q

Describe the first immune response to initial exposure.

A
  1. Innate immune response.
  2. IgM predominates. (Then IgG replaces it)
  3. Low affinity.
96
Q

Describe the second immune response following exposure to a pathogen encountered before.

A
  1. Rapid and larger than the first.
  2. High affinity IgG.
  3. Adaptive immunity, T cell help.
97
Q

Hypersensitivity: 5 possible treatments for allergy and hypersensitivity.

A
  1. Avoid allergens.
  2. Desensitisation (immunotherapy, some risks).
  3. Prevent IgE production (interfere with TH2 pathway).
  4. Prevent mast cell activation.
  5. Inhibit mast cell products (e.g. histamine receptor antagonists).
98
Q

Type 1 hypersensitivity: describe?

Cause?

A

Cause: allergies (Pollen, cat hairs, peanuts etc. )

IgE mediated hypersensitivity.

Acute anaphylaxis, hay fever

IgE becomes attached to mast cells, IgE cross linking leads to mast cell degranulation -> histamine.

  1. Initial exposure to the antigen leads to some antibody synthesis and the production of B memory cells (mediate active immunity)

In those with atopy and type 1, particular antigens that elicit type 1 reactions stimulate the production of type IgE antibodies.
Production of IgE requires the participation of a particular type of T helper cell that are activated by the allergens presented by B cells.

activated T helper cells trigger the mast cell to secrete inflammatory mediators, including histamine & chemokines which then initiate a local inflammatory response

99
Q

Type 2 Hypersensitivity: describe?

Cause ?

A

IgG binding to cell surface antigens so IgG mediated cytotoxicity/IgM

e.g. transfusion reactions, autoimmune diseases, Goodpastures (term used if alveoli are involved) (an anti-Glomerular Basement Membrane disease), eg haemolytic disease of foetus and newborns
Eg transplant rejections

100
Q

Type 3 Hypersensitivity: describe?

Causes?

A

Immune complex deposition; immune complexes have not been adequately cleared by innate immune cells, giving rise to an inflammatory response.
/ activation of complement / IgG

e.g. hypersensitivity pneumonitis, lupus

Causes: fungal

Type III hypersensitivity occurs when there is accumulation of immune complexes (antigen-antibody complexes) that have not been adequately cleared by innate immune cells, giving rise to an inflammatory response and attraction of leukocytes. Such reactions may progress to immune complex diseases.

101
Q

Type 4 Hypersensitivity: describe?

Causes?

A

mediators: T-cells (lymphocytes) and macrophages
e. g. TB, stevens-johnson’s syndrome, sarcoidosis ,contact dermatitis

the overreaction of the helper T cells and overproduction of cytokines damage tissues, cause inflammation, and cell death.
These cytokines act as inflammatory mediators and also activate macrophages to secrete their potent mediators

102
Q

Give 4 risk factors for hypersensitivity.

A
  1. Protein based macromolecules.
  2. Female > male.
  3. Immunosuppression.
  4. Genetic factors.
103
Q

Anaphylaxis:
Define?

Which cells and which immunoglobulin is commonly involved?

Anaphylactic systemic effects.

A

Anaphylaxis is a severe, life-threatening, generalised or systemic hypersensitivity reaction.

  • Mast cells and basophils.
  • IgE.
  • CV: vasodilation, lowered BP, inc vascular permeability
  • Resp: bronchial SM contraction, mucus.
  • Skin: rash, swelling.
  • GI: pain, vomiting.
104
Q

Give 6 features of anaphylaxis.

A
  1. Rapid onset.
  2. Blotchy rash.
  3. Swelling of face and lips.
  4. Wheeze.
  5. Hypotension.
  6. Cardiac arrest if severe.
105
Q

Anaphylaxis: treatment?

The effect of the main medication?

A
  1. Commence basic life support (ABC).
  2. Stop infusion of drug.
  3. Give adrenaline and anti-histamines.
    —-> Adrenaline 1mg (10mls of 1:10,000 (IV)) 1ml IV increments
    note: if cardiac arrest then may need to give cardiac massage in order to get drugs circulating
    —-> IV Anti histamine (Chlorphenamine 10mg)
    ——> IV Hydrocortisone (100 to 200mg) - note: unlikely to cause harm
    in excess so can’t really give too much

Effect of adrenaline:
Vasoconstriction, bronchodilation & increased cardiac output

106
Q

Transplant Rejection:

Transplant cascade?

Why do organs transplanted from donors pose a threat to hosts immune system?

A

Donor -> organ preservation -> implantation -> re-perfusion -> organ function.

Organs transplanted from donors pose a threat to the host immune system due to the presence of different major histocompatibility antigens (MHA) on the surface on the organs

107
Q

Transplants: why are immunosuppressive agents needed?

A

Immunosuppressive drugs are used to prevent graft rejection as transplanted organs are recognised as non self and therefore are seen as a threat.
Graft v host disease; T-cells destroy graft cells.

Or else can cause a type 2 hypersensitivity reaction

108
Q

Give 6 ways of preventing transplant rejection?

A
  1. Manage risk factors.
  2. Tissue typing.
  3. Cross match.
  4. Immunosuppressive agents.
  5. Sensitisation and desensitisation.
  6. Tolerance.
109
Q

Define tolerance with regards to transplant immunology.

A

a state in which the immune system of the recipient of a tissue or organ transplantation does not attack the transplanted tissue.

Tolerance is the acquired modification to host immunity leading to drug free transplant survival with full immunocompetence.

110
Q

Describe the immune responses to detection of graft antigens.

A

X

  1. Innate immune response is activated.
  2. T cell mediated cytotoxicity.
  3. Ab mediated cytotoxicity.
  4. Hypersensitivity.
  5. Tolerance.
111
Q

Thymic tolerance: define

A

T-cell development in the thymus plays an important role in eliminating T cells capable of recognising peptides from self-proteins
/ baso is the process of eliminating anydevelopingTorB lymphocytesthat are reactive to self.

End result = population of lymphocytes that are not reactive to self-antigens but may be able to recognize foreign, non-self antigens, depending on the randomly arranged receptor

112
Q

Peripheral tolerance:

Define

A

Its main purpose is to ensure that self-reactive T and B cells which escaped central tolerance do not cause autoimmune disease.

To prevent large amounts of self-antigen from gaining access to antigen-presenting cells, debris from self-tissue breakdown is rapidly cleared & destroyed by apoptosis thereby preventing the widespread spilling of cell contents
Self-antigens and lymphocytes are also kept separate by the restricted routes of lymphocyte circulation which limit naive lymphocytes to secondary lymphoid tissue and the blood

113
Q

Anergy: define

A

a condition in which the body fails to react to an antigen.

114
Q

Give the classes of drug used to treat i) arterial thrombosis ii) venous thrombosis (2)

A

Arterial thrombosis is anti-coagulants eg

Venous thrombosis is anti-warfarins eg warfarin, heparin, NOAC

med 2a (13 decks)

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