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Medicine - Year 1 > Block 4 - The Immune System > Flashcards

Block 4 - The Immune System Flashcards

1
Q

How many litres of blood are there in the body?

How many litres can you lose and still recover?

A

4-6 litres

1-1.5 litres

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2
Q

What percentage of the blood is liquid and cells?

A

55% plasma liquid

45% cells (99% RBC, 1% WBC and platelets)

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3
Q

What is serum?

A

Plasma with clotting factors

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4
Q

Is straw coloured plasma clotted or not clotted?

A

NOT clotted

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5
Q

How does the bone marrow control production of blood cells?

A

Stromal cells and 3D mesh

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6
Q

What is the beginning of the haematopoesis lineage?

A

Haematopoetic stem cell –> Multipotent progenitor –> Common myeloid progenitor OR common lymphoid progenitor

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7
Q

What does the myeloid lineage give rise to?

A

Erythrocytes, Megakaryocyte, Thrombocytes
Mast cells, Basophils, Neutrophils, Eosinophils, Monocytes, Macrophages, Dendritic cells

PHAGOCYTES

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8
Q

What does the lymphoid lineage give rise to?

A

Dendritic, Natural killer, B lymphocyte, T lymphocyte

LYMPHOCYTES

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9
Q 
What controls the production of:
Erythrocytes
Platelets
Immune cells of the myeloid lineage
Immune cells of the lymphoid lineage
A

Erythrocytes: EPO
Platelets: TPO
Immune cells of the myeloid lineage: Granulocyte Colony Stimulating Factor
Immune cells of the lymphoid lineage: Interleukins

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10
Q

How is the porphyrin ring of Hb excreted?

A

Bilirubin

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11
Q

What does hypoxia lead to?

A

Kidneys increase EPO

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12
Q

How does EPO increase the production of erythrocytes?

A

It binds to erythropoetin kinase linked receptors on progenitor cells

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13
Q

Erythrocyte production flow chart (8)

What is special about the nucleus in RBC?

A

Haemocytoblast (stem cell) –> Proerythroblast (committed cell) –> Erythroblast –> Nomoblast –> Reticulocyte –> Erythrocyte

When the cell is a nomoblast the NUCLEUS IS EJECTED

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14
Q

What do platelets secrete?

A

Platelet derived growth factor

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15
Q

Where is TPO produced?

A

Kidney and liver

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16
Q

How are plaelets produced (lineage - 4)

What type of mechanism is used to produce platelets - what does this allow to occur?

A

Myeloid stem cell –> Megakaryoblast –> Megakaryocyte –> Platelet
‘Budding off mechanism’ - proliferation

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17
Q

What are neutrophils involved in? What is their lifespan?

A

Phagocytosis and inflammation

1-2 days

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18
Q

What are eosinophils involved in? What is their lifespan?

A

Phagocytose and helminths

2-5 days

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19
Q

What are basophils involved in? What is their lifespan?

A

Allergies

1-2 days

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20
Q

What are monocytes involved in? What is their lifespan?

A

Phagocytes and turn into macrophages

1-7 days

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21
Q

What are natural killer cells involved in? What is their lifespan?

A

Kills viruses

14 days

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22
Q

Define leukocyte

A

White blood cell

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23
Q

2 types of lymphocytes
Characteristics (4)
Lifespan?

A

B and T cells
Small, large nucleus, different markers, many subdivisions
Weeks - years

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24
Q

What does the haematocrit test do?

A

Measures the proportions of centrifuged blood to see if anything is wrong

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25
Q

How are WBC levels measured?

A

Flow cytometry

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26
Q

What type of disorder is myelofibrosis?
What happens during it?
What is it caused by?

A

Myeloproliferate disorder
Increased WBC and platelets, decreased RBC
JAK2 mutation

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27
Q

What type of disorder is polycythaemia vera?
What is another name for it?
What happens during it?
What is it caused by?

A

Myeloproliferate disorder
Primary polycythaemia
Increased levels of all blood cells
JAK2 mutation

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28
Q

What type of disorder is essential thrombocythaemia?
What is another name for it?
What happens during it?
What is it caused by?

A

Myeloproliferate disorder
Secondary polycythaemia
Increased platelets, other cells normal
JAK2 mutation

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29
Q

Three treatments for polycythaemia

A

Aspirin
Venesection (removal of blood)
Chemotherapy (to decrease the speed of proliferation)

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30
Q

Explain what JAK2 does normally and what changes when it gets mutated?
What can it be used to diagnose and treat?

A

A signalling receptor that acts downstream of EPO receptors
Activates receptors without EPO by phosphorylation causing excessive proliferation of erthyroid, myeloid and megakaryocyte cells

Polycythaemia vera

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31
Q

What are the ABO antigens?

What

A

Carbohydrate structures on glycoproteins/lipids of RBC

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32
Q

What are the main carriers of the ABO antigens?

A

N-glycosylated glycoproteins, anion exchanger (band 3) and glucose transporter (GLUT1)

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33
Q

What do the ABO genes code for and what does this gene do?

What is the difference between the enzyme for A, B and O

A

The enzyme glucosyl-transferase which adds the carbohydrate chain to the cells
A: N-acetylgalactosaminyltransferase
B: Galactosyltransferase
C: No transferase

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34
Q

What are the 5 rhesus antigens and the 2 genes that encode them

A

Antigens: D,C,E,c,e
Genes: RHD, RHCE

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35
Q

What is kernicterus?

A

A complication of severe jaundice which can cause brain damage/deafness

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36
Q

What happens during Anti-D therapy

A

The mother is given a drug which binds to the rhesus antigens on the baby’s cells, preventing the formation of antibodies

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37
Q

What is pallor?
What is tachycardia?
What is glossitis?
What is koliohychia?

What are these all signs of?

A

Pallor: Lack of red in the eye
Tachycardia: Increased pulse
Glossitis: Swollen and painful tongue
Koliohychia: Spoon nail due to iron deficiency

Anaemia

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38
Q

10 symptoms of anaemia

Which ones are severe?

A

Weakness, tiredness, shortness of breath, confusion, thirst

Severe: Jaundice, enlarged liver and spleen, angina, fever, cardiac faliure

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39
Q

What are the types of anaemia

A

Microcytic: Iron-deficiency, Sideroblastic, Thalassemias
Normocytic: Haemolytic, Bone marrow disorders, Trauma, Changes in RBC number
Macrocytic: Vitamin deficiency, Reticulocytosis

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40
Q

What is the difference between the multipotential and erythroid stage of RBC development?

A

Multipotential: Forms the progenitors and regulated by stem cell cytokines in the bone marrow
Erythroid: Forms the red blood cells and regulated by EPO in the bone marrow and blood

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41
Q

What is pure red cell aplasia?

A

Conditions that affect erythropoesis in the bone marrow

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42
Q

What is pancytopenia?

Example

A

Conditions that affect other cells (e.g. WBC and platelets)

Virus attacks stem cells, stopping their ability to self-renew

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43
Q

What is haemolytic anaemia?

A

When RBC are destroyed prematurely

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44
Q

What is allo-immune haemolysis?
Example
What type of anaemia is it?

A

When the immune system attacks foreign erythrocytes (e.g. rhesus disease)
Haemolytic

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45
Q

What is auto-immune haemolysis?
What is it usually a result of? (2)
What type of anaemia is it?

A

When the immune system attacks your own erythrocytes
Usually as the result of an illness/ idipoathic
Haemolytic

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46
Q

What are microspherocytes?

A

Smaller erythrocytes

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47
Q

What type of condition is sickle cell?

What is is caused by?

A

Autosomal co-dominant

Mutation in the beta globulin gene

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48
Q

What four molecules regulate RBC production and haem metabolism?

A

Fe, B12, B6, folate

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49
Q

What 4 things make it hard to absorb iron?

A

Tea, coffee, calcium and PPI’s

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50
Q

What happens during sideroblastic anaemia?

What are the resulting cells called?

A

Haem is not incorporated into erythrocyte precursor cells due to mutations in genes which regulate haem synthesising
Sideroblasts

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51
Q

Full blood count:

Hb, RBC, MCV, RDW, MCH, MCHC, HCT

A 
Hb: Haemoglobin 
RBC,: Red blood cell 
MCV: Mean cell volume 
RDW: RBC distribution width 
MCH: mean cell Hb 
MCHC: MCH concentration 
HCT: Haematocrit
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52
Q

What bones does the majority of blood cell production occur in an adult?

A

Pelvis, sternum, vertebrae, cranial bones

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53
Q

What type of organisation does bone marrow have?

A

Local-organisation

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54
Q

What does the secondary lymphoid tissue do?

3 examples

A

Turn on the acquired response

Spleen, lymph nodes, mucosal associated lymphoid tissue

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55
Q

What are the two parts of the thymus?

A

Medulla: dark and dense
Cortex: light and less dense

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56
Q

Where are lymph capillaries not found?

A

CNS. epidermis and cartilage

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57
Q

What route do superficial lymphatics follow? Where does the fluid drain?

A

Route of superficial veins

Fluid drains into lymph nodes in the auxillary, inguinal or cervical areas before draining into the deep lymphatics

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58
Q

What route do deep lymphatics follow? Where does the fluid drain?

A

Route of main vessels from organs

Drain into para/pre-aortic lymph nodes

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59
Q

What do lymphs in the URQ drain into
What do lymphs in the other 3 quadrants drain into?
How?

A

URQ: R brachiocephalic vein

Other quadrants: L brachiocephalic vein (via thoracic duct)

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60
Q

The lymph node fluid supply

A

Arterial and venous supply
Afferent and efferent lymphatic supply

Blood enters via artery and leaves via vein
Lymphocytes enter via artery and leave via efferent lymphatic

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61
Q

main parts of the lymph node

A

Medullary sinus (middle)
Marginal sinus (outside)
Germinal centre and lymphoid follicle (B cells)
T cell area

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62
Q

How is the efficiency of a lymph node increased?

A

Compartamentalism

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63
Q

What type of lymphoid organ is the spleen?

A

Secondary

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64
Q

What type of infections does the spleen alert of?

A

Blood infections

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65
Q

What are the two types of pulp in the spleen?

A

Red and white

66
Q

What is hypersplenism

A

Presence of erythrocytes with nuclear fragments in the spleen

67
Q

What directs the structure and behaviour of gut-associated lymphoid tissue?

A

Non-haematopoetic ‘stromal’ cells

68
Q

Give 5 examples of physical defence barriers to pathogens

A

Epithelial cells joined by tight junctions
Cilia and longitudinal flow of air
Decreased pH
Enzymes (pepsin, lysozome in saliva degrades cell walls)

69
Q

3 routes that start the complement cascade

A

Alternative and Lectin pathway: Direct interaction between the complement and pathogen
Classical pathway: Needs antibodies

70
Q

What do the complement molecules do?

A

C3a and C5a: Inflammation via chemotactic signals and recruitment of mast cells
C3b: Helps phagocytes interact with pathogens
C5a: Starts the cascade forming C6-C9 –> membrane attack complex

71
Q

What do mast cells release?

What does this molecule do?

A

Histamine

Allergies and increases blood vessel permeability

72
Q

What is opinisation?

A

A ligand on C3b that binds to the pathogen and receptor on the phagocytes –> recognition

73
Q

What do phagocytes have on their surface?

A

Receptors that detect pathogens or C3b

These are linked to intracellular pathways that produce cytokines and chemokines

74
Q

Name 6 microbial mechanisms of phagocytes

A

Acidification, antimicrobial peptides, competitors, enzymes, toxic oxygen derived products, toxic NOx

75
Q

How do phagocytes activate the acquired response

A

They activate other cells (e.g. dendritic cells, monocytes, macrophages and neutrophils)
These can enter the lymph nodes

76
Q

What cells can commit suicide after trapping bacteria in their DNA?

A

Neutrophils

77
Q

What are cytokines and chemokines?

What are they also known as?

A

Hormones of the immune system

Interleukins

78
Q

How do you prevent septic shock?

A

Release cytokines and chemokines in low concentrations for localised contact
These chemicals are also short-acting

79
Q

How are antibodies found in relation to the B cell?

A

Released from the B cell

Bound to the B cell through the transmembrane region

80
Q

How many domains do the light and heavy chains of an antibody have?

A

Heavy chain: 3 domains

Light chain: 2 domains

81
Q

Define affinity

A

Goodness of fit and interaction strength

82
Q

Define avidity

What increases it?

A

Increased interaction stability

Increased if there are more antibodies

83
Q

What can antibodies do aside from bind to pathogens?

A

Bind to toxins produced by pathogens
Regulate the immune response indirectly
Terminate the immune response
Cell recruitment

84
Q

What is Fab?

A

Fragment antigen binding

Made from the variable region

85
Q

What is Fc?

A

Fragment crystallisation
Made from the constant region
Many phagocytes have receptors for this region

86
Q

3 ways to increase the genetic diversity of antibodies during production

A

Germ line diversity: Different genes code for different parts
Combitoral diversity: Difference in how the segments are joined
Junctional diversity: A change in the ‘glue’ –> different structure

87
Q

What is somatic hypermutation and where does it occur?

A

When B cells select for increased affinity

In the germinal centre

88
Q

What happens during somatic recombination?

What happens if the enzymes that carry out this cannot mature?

A

Sections of DNA are looped and cut out to make different antibodies
Immunodeficiency diseases

89
Q

Where are the genes for light and heavy chains found?

A

On separate chromosomes

90
Q

How do the different classes of antibodies arise?

What are they?

A

Different CONSTANT region

IgA, IgD, IgE, IgG, IgM

91
Q

What are the two structures of antibodies?

What does a secretory piece allow?

A

Pentameric structure: 5 antibodies held together in a pentagon by a J chain

Dimeric structure: 2 antibodies held by a J chain with a secretory piece that allows transport into the mucosa without breakdown by digestive enzymes

92
Q 
What is class switching?
What 2 things does it involve the recognition of?
A

B cells change their antibody isotope but keep the antigen binding site the same
It involves recognition of cytokines and T cells

93
Q

Four things that can control B cell production

A

Cytokines, chemokines, dendritic cells and microenvironment

94
Q

How do T cells control B cell production?

A

Helper T cells stick to B cells at an immunological synapase before they produce antibodies

95
Q

What process do T cells go through before they are released?

A

Thymic selection

96
Q

What molecule turns tertiary molecules to linear ones?

A

Phagocytes

97
Q

What are the 2 chains of a T cell receptor?
How many polypeptide chains?
How many domains?

A

Alpha chain and Beta chain
2 polypeptide chains
2 domains

98
Q

What defines why everyone’s immune system is different?

A

Major incompatibility molecules

99
Q

What is the role of MHC’s and what are the 2 types and the differences between them?

A

Transport linear peptides to T cells

Class 1: Capture from the CYTOPLASM, expressed on nucleated cells and present to CD8+ cells

Class 2: Capture from PHAGOSOMES, expressed on antigen presenting cells and present to CD4+ cells

100
Q

2 ways in which T cells can be signalled - differences in what they singal them to do

A

‘Go no go’ signal from a T cell receptor (how and when to respond)
Cytokines released from phagocytes –> costimulatory signals (what response)

101
Q

What is cancer immunotherapy based on?

A

Costimulatory signals

102
Q

Where do phagocytes reside?

A

Bone marrow

103
Q

What 4 things do dendritic cells do?

A

Capture and process antigens
Co-stimulation signal
Cytokines to turn on T cells
Pattern recognition receptors

104
Q

What immune cell contains MHC-2 molecules?

A

Dendritic cells

105
Q

What causes secondary polycythaemia vera?

3 examples

A

A consequence of something else

e. g. hypoxia (need more cells to increase oxygen levels to cells)
e. g. EPO secreting tumours
e. g. newborn babies due to maternal blood cell transfusion

106
Q

What is relative polycythaemia vera?

A

When there is a decrease in plasma volume relative to RBC proportion

107
Q

Type 1 hypersensitivity:
What type of antibody response is it?
What antibodies are involved?
Why does it happen immediately? (2)

A

Misdirected
IgE
Mast cells have receptors for the fc part of IgE antibodies –> fast degranulation of histamine
IgE is a preformed antibody

108
Q

Type 2 hypersensitivity:
What antibodies are involved and what do they do?
Two types of tissue cytotoxicity caused?

A

IgG or IgM

ADDC: Antibody dependent cellular toxicity
CDC: Complement dependent cytotoxicity (causing cell death)

109
Q 
Type 3 hypersensitivity:
What antibodies are involved?
What other molecules are involved?
What is created?
Where?
How does damage occur and what does this cause?
3 reasons why the complexes are formed
A

IgG and soluble molecules
Protein complex that precipitates forming tissue deposits
In the kidneys, blood vessels and synovial joints due to increased pressure
Damage through complement/phagocytosis –> Systemic diseases
Complexes formed due to infection, environment or autoantigens

110
Q

Type 4 hypersensitivity:
Explain the primary and secondary response
What is a Hapten?
What class of diseases also come under this?

A

Primary: Sensitisation and memory cell production when APC presents Haptens (sensitising agents that bind to self-proteins in the epidermis –> neoantigens)

Secondary: APC with hapten presents to CD4+ cells –> T cell and macrophage activation

Autoimmune diseases

111
Q

Example of a primary immunodeficiency disorder

What causes it and what happens during it?

A

Chronic Granulomatomus disease
Genetic disorder in PHOX genes
Stops phagocytes killing
Granuloma’s form as the body works harder to kill the pathogen

112
Q

Example of a secondary immunodeficiency disorder

How does it show the difference in T cell activation between diseases?

A

HIV/AIDS

Some diseases do not form until the T cell count is really low meaning they are not usually fought off by T cells

113
Q

Example of a cancer where there are too many B/T cells

A

Acute lymphoblastic leukaemia

114
Q

How can B and T cells help with cancer?

A

They can kill the tumour cells

115
Q

What is auto-inflammation?

A

Prolonged and unwanted activation of the innate response leads to uncontrollable phagocytosis

116
Q

What can bacterial cells do that can trigger autoimmune disease?

A

Turn on cells that shouldn’t be turned on

117
Q

What can form if a blood clot dislodges?

A

Embolism

118
Q

What are the three stages of haemostasis?

A
  1. Vascular Spasm: Decreased blood flow to the area
  2. Platelet Plug Formation: Platelets bind and form a plug (Primary haemostasis)
  3. Coagulation: Stable clot forms (Secondary haemostasis)
119
Q

How is a clot made?

What is the structure of the fibres in a clot?

A

By converting fibrinogen to fibrin

Cross-linked

120
Q

What are the macrophages called which destroy platelets?

A

Kupfer cells

121
Q

What do alpha secretory granules contain?

A

Adhesive proteins: Fibrinogen, fibronectin, vWf
Specific proteins
Membrane proteins: Receptors for the molecules released from platelets

122
Q

What do dense secretory granules contain?

A

Vasoconstrictive agents: Serotonin
Platelet agonists: Increase platelet activation (e.g. ADP)
Ca and Mg for cell surface proteins

123
Q

Are there more alpha or dense secretory granules in a platelet?

A

Alpha

124
Q

How do platelets bind to the sub-endothelium?
What increases adhesion?
How are platelets activated and what do they do?

A

Bind to vWf on the collagen sub-endothelium
Blood flow rolls the pltelet –> increased adhesion and associations with vWf
Firmer adhesion activates platelets –> granule release and strong adhesion

125
Q

Explain how a platelet plug forms

2 examples of platelet agonists

A

A platelet monolayer causes the release of platelet agonists (e.g. thromboxane and fibrinogen) which increases the number of platelets attracted to the plug
These platelets create spindles which form fibrinogen cross-bridges

126
Q

Define ‘coagulation factors’

A

A group of inactive precursors of enzymes called ‘zymogens’ which are found in the plasma and work in the coagulation cascade

127
Q

What factor does the extrinsic pathway activate?

A

Factor 3 (tissue factor)

128
Q

What factor does the intrinsic pathway activate?

A

Factor 12

129
Q

Name the coagulation cascade

What happens to the factor when it is activated?

A

Intrinsic: 12 –> 11 –> 9 –> 8a+9a –> 10
Extrinsic: 3 –> 7 –> 3a+7a –> 10
Final common pathway: 10 –> 5 –> (Prothrombin to thrombin) –> (Fibrinogen to fibrin) –> 13

It has an ‘a’ on the end

130
Q

What do tissue factor inhibitors and anti-thrombin’s do?

What disorders to tissue factor inhibitors target?

A

Tissue factor inhibitors: Inhibits interaction between factor 7 and factor 3
(Target for haemophiliac disorders)
Anti-thrombin: Inhibits factor 5,9 and 11

131
Q

Explain how a coagulation test works

A

Plasma with no platelets in a machine with a metal ball that spins to a magnetic stirrer
Add a reagent to activate coagulation, the plasma turns to jelly and the metal ball stops moving
Measure the time taken for the ball to stop moving

132
Q

Which pathway does prothrombin time and partial prothrombin time measure?

A

Prothrombin time: Extrinsic pathway

Partial prothrombin time : Intrinsic pathway

133
Q

What are the two types of Haemophilia?
What are their causes?
Which one is more common?

A

Type A: Decrease in factor 8 (more common)

Type B: Decrease in factor 9 (less common)

134
Q

How does immune thrombocytopenia occur?

A

Antibodies bind to platelet proteins forming a complex which is then cleared in the liver

135
Q

What is Glanzmann’s Thrombasthenia?
What do the mutations do and what does this lead to?
What are the two types of mutations and how do these cause different severities of the disorder

A

An autosomal recessive bleeding disorder which decreases the number of megakaryocytes
Mutations change the fibrinogen receptors leading to decreased aggregation

Stop/missense –> no protein and haemorrhage
Point –> different protein and mild bleeding`

136
Q

What is the difference between acute and chronic inflammation
Examples

A

Acute: Sudden event e.g. cut or allergic reaction
Chronic:Long term e.g. persisting infections, transplants, autoimmune diseases

137
Q

5 examples of inflammation driven by the immune system

A 
Infection
Allergies
Graft vs Host disease
Transplant rejection
Autoimmune disease
138
Q

Mediators of the inflammatory response (11)

A

Histamine, serotonin, complement
Basophils, neutrophils, macrophages, cytokines,
Platelets, prostaglandins, factor 12, leukotrines

139
Q

What happens at the end of the inflammatory response?

3 molecules which also help?

A

Fibroblasts –> collagen

Lipoxins, resolvins and protectins

140
Q

How is Arachidonate Acid produced?

A

Metabolised from phospholipids by phospholipase 2

141
Q

What does Arachidonate Acid produce? (5)

A

Prostaglandins, thromboxanes and prostacyclins

Lipoxins and leukotrines

142
Q

What does COX 1 produce?

A

Prostacyclin for the stomach

Prostaglandin and thromboxanes for platelets

143
Q

What does COX 2 produce?

How is it activated?

A

Prostaglandins, proteases (free radicals) and hydrogen peroxide for inflammation
Prostacyclin to switch platelets off and vasodilate

Activated by inflammation

144
Q

How does high levels of Aspirin increase the risk of a myocardial infarction?

A

COX 2 produces prostacyclin which switches platelets off and vasodilates; when this is blocked platelets are switched on and the vessels are vasoconstricted –> clots

145
Q

How does Aspirin actually work?

A

Stops platelets from metabolising arachidonate acid to thromboxanes
Arachidonate acid is therefore metabolised to lipoxins which solve the response

146
Q

What are steroids produced from?

What enzyme controls their production?

A

Cholesterol

ACTH

147
Q

What is the role of the complement system?

A

Coordinate the response and return it to normal after

148
Q

What three symptoms does histamine cause and how?

A

Reddening: Vasodilation of arterioles
Wheal: Increased permeability of venules
Flare: Stimulation of nerves and vasodilation

149
Q

What receptors does Histamine act on in the stomach?

5 things it does

A

H1, H2, H3, H4

Cardiac stimulation, gastric secretion, smooth muscle contraction, vascular permeability and vasodilation

150
Q

What 3 things cause hypersensitivity reactions?

A

Infection, self-antigens and the environment

151
Q

What do hypersensitivity reactions cause?

A

Tissue damage

152
Q

Define allergen
What do they contain?
3 ways they can enter the body
What immune cell do they stimulate?

A

Antigens that cause allergy
Proteases
Inhaled, injected, drugs
Helper T cells

153
Q

Define Allergy

A

An immune response that occurs due to repeated exposure to an allergen
Sensitisation and activation of IgE antibodies

154
Q

Define Atopy

A

When there is a predisposition to develop an IgE immune response

155
Q

What are the 6 mediators which are released immediately during a Type 1 hypersensitivity reaction?
Explain briefly what they do

A

Cytokines: Change in vasculature and inflammation
Enzymes: e.g Tryptase activates complement
Histamine: GI, vasculature, airways, red and itchy skin
Interleukins: Activate helper T cells
Leukotrines: Contraction of gut and airways; chemotaxis
Prostaglandins: Vasculature change, smooth muscle contraction

156
Q

Which mediator is released hours after the initial response during a Type 1 hypersensitivity reaction?
Explain briefly what it does

A

Migration of eosinophils

Peroxide and mediator release

157
Q

What is the spectrum for autoimmune diseases?

A

Organ specific to systemic

158
Q

What are many autoimmune diseases caused by?

A

MHC 2 gene expression

159
Q

An alternatives to organ transplant

A

Mechanical maintenance

160
Q

How is transplant an investment?

A

It costs a lot to instate but you save money in the long term due to a decrease in mechanical maintenance

Medicine - Year 1 (20 decks)

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