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Physiology > Immune system > Flashcards

Immune system Flashcards

1
Q

Erythropoiesis

A

Making of red blood cells in red bone marrow

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2
Q

How long do RBCs last?

A

120 days

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3
Q

Process of erythrocyte differentiation

A

Haematopoietic stem cells > Common myeloid progenitor > Proerythroblast > Reticulocyte > Erythrocyte
Reticulocyte loses its nucleus to become erythrocyte.

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4
Q

What happens to bone marrow as we age?

A

Red bone marrow is converted to yellow bone marrow, 100% red in children and 50% in adulthood

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5
Q

How is erythropoiesis regulated?

A

Kidneys produce erythropoietin in response to hypoxia

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6
Q

What does erythropoietin do?

A

Stimulates red bone marrow to produce red blood cells

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7
Q

What cells do all blood cells come from?

A

Haematopoietic stem cells

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8
Q

Where do innate immune cells come from?

A

Common myeloid progenitor cells, except natural killer cells which come from common lymphoid progenitor cells

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9
Q

Where do adaptive immune cells come from?

A

Common lymphoid progenitor cells

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10
Q

Where do basophils, eosinophils, neutrophils and monocytes come from?

A

Myeloblasts

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11
Q

Where do macrophages come from?

A

Monocytes

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12
Q

Where do platelets come from?

A

Megakaryocytes

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13
Q

Innate immune response

A

First response to infection - provides the first and second lines of defence
Involves physical and chemical barriers
Occurs quickly within the first 12 hours of infection

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14
Q

What are the proteins involved in the innate immune response?

A

CRP

Complement

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15
Q

What is CRP

A

C reactive protein, produced by the liver. It is an oponising protein

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16
Q

What are the physical barriers in the innate response?

A

Skin
Mucosal membranes
removal of particles by cilia

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17
Q

What are the chemical barriers in the innate response?

A

Normal flora in GI tract which occupy the biological niche
Lysozymes in tears
Stomach acid

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18
Q

What do mast cells do?

A

Degranulate to cause leaky tight junctions in endothelium. This allows other immune cells to enter and plasma to leave causing oedema. Release IL-1, TNF-alpha and CXC18 for chemotaxis

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19
Q

What do dendritic cells do?

A

Recognise PAMPs and DAMPs on their PRRs. Engulf pathogenic peptides and transport them to lymph nodes. Present peptides on MHC 2 molecules

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20
Q

What do neutrophils do?

A

Recognise PAMPs, carry out oxidative burst. Form a pseudopodia and then a phagosome around the pathogen. Granules are released to kill the pathogen.

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21
Q

What do macrophages do?

A

Clear up debris by phagocytosis.
Kupffer cells = liver
Langerhans = skin
Dust cells = alveoli

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22
Q

Adaptive immunity

A

Specific line of defence, but takes longer to occur. Works by recognising non-self from self antigens. Involved in development of immunological memory. Specific responses tailored to maximally eliminate a specific pathogen.

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23
Q

What are the 2 types of immunity that make up adaptive response?

A

Cell-mediated

Humoral

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24
Q

Extracellular pathogen response - TH2/ humoral response

A

Bacteria infect and proliferate the body
LPS of bacteria acts as a PAMP
activates the complement pathway
Activates the complement cascade
C3a and C5a cause degranulation of mast cells
release of histamine
causes inflammation
C3b opsonises
macrophages, dendritic cells and neutrophils carry out phagocytosis
Macrophages recognise PAMPs and release cytokines
C5a causes chemotaxis
so more immune cells are drawn to the site of infection
dendrites present pathogen peptide on their MHC 2 molecules and migrate to the local lymph node
Naive T cells are recruited to the lymph node and recognise the MHC 2 pathogen protein
T cells bind to the MHC 2 molecule
This causes the T cells to release IL-4
IL-4 causes TH2 cells to be formed
This is the humoral response
Plasma cells are formed and release IgM antibodies, then IgG and IgA antibodies.
Memory B cells are formed

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25
Q

Intracellular immune response - TH1

A

The virally infected cell produces IFN-alpha
Neighbouring cells produce antiviral proteins to prevent them being infected
IFN-alpha attracts natural killer cells
NKs check the MHC 1 molecules and kill abnormal/ absent ones
After the cells burst and the viral particles are released the dendritic cells pick the viral particles up and take them to the local lymph nodes
Dendritic cells present the antigen on their MHC 2 and CD28 molecules
Dendritic cells produce IL-12 to form CD4 TH1 cells
TH1 cells release IFN gamma and IL-2 which activates CD8 cytotoxic cells
CD8 cells check MHC 1 molecules and kill the abnormal/ absent ones
They make holes in the cell using perforin and inject granzymes which kill the cells .

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26
Q

Clean up following an adaptive immune response

A

T regulatory cells are activated by TNF-beta and IL-10. They downregulate TH1 or TH2 cells depending on the type of infection. Macrophages and neutrophils clear away the debris.

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27
Q

What is isotype switching?

A

Change in the B cell’s production of an antibody from one class to another

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28
Q

Cytokines released by naive Th cell

A

Activate naive T helper cell produces IL-12 or IL-4, IL-12 produces TH1 cells and IL-4 produces TH2 cells.

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29
Q

What cytokines are released by TH1 cells

A

IFN-gamma which activates macrophages and NK cells and costimulates CD8 activation with Antigen presentation. TNF-beta activates macrophages and NK cells.

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30
Q

What are the stages of wound healing?

A

Haemostasis
Inflammation
Proliferation
Remodelling

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31
Q

Process of haemostasis

A
  1. Damage to vessel wall exposes underlying collagen and chemical factors from the damaged endothelium. Vascular spasm - blood vessels constrict in response to shock to reduce blood loss
  2. Platelet adhesion - platelets adhere to the damaged collage which involves von Willebrand Factor, it activates the platelets so they undergo a structural change that helps them adhere together.
  3. Activated platelets release Thromboxane, ADP and Serotonin which causes vasoconstriction and activates more sticky platelets
  4. Platelet plug is formed from platelets sticking together and the coagulation cascade is triggered
  5. Coagulation cascade converts fibrinogen into fibrin
  6. Fibrin reinforces the platelet plug and forms a mesh work that forms a clot
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32
Q

Why does the platelet plug not spread all the way along the vessel?

A

Prostacyclin and nitric oxide from intact endothelium inhibit platelet adhesion and aggregation

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33
Q

What are clotting factors?

A

Proteins in the blood that control bleeding. They are inactive unless needed.

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34
Q

How does the clotting cascade work?

A

Activated form of each factor acts as a catalyst for the next reaction in the cascade. Calcium ions and vitamin K are necessary for activation of some of the reactions

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35
Q

What is the purpose of the coagulation cascade?

A

To make thrombin which converts fibrinogen into fibrin to form a mesh .

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36
Q

Fibrin

A

Is factor 1, it is insoluble so doesn’t circulate in the blood as it would form blood clots so fibrinogen is the inactive soluble form

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37
Q

What are the pathways of the coagulation cascade?

A

Extrinsic = activated by tissue damage through release of tissue factors and causes the intrinsic pathway to kick in.
Intrinsic pathway = gets most of the coagulation done

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38
Q

Which stages of the coagulation cascade are vitamin K dependent?

A

II,VII, IX, X

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39
Q

where is vitamin K synthesised?

A

By bacteria in large intestine

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40
Q

Coagulation cascade

A

Learn the coagulation cascade!!!!

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41
Q

Coagulation cascade drugs

A

Thrombolytics
Antiplatelets
Anticoagulants

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42
Q

Thrombolytic drugs

A

Break down fibrin

e.g. tPA, Urokinase

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43
Q

Antiplatelet drugs

A

Aspirin - inhibits COX
Clopidogrel - inhibits platelet aggregation
Ticagrelor

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44
Q

Anticoagulants

A

Heparin - makes anti-thrombin very active, low molecular weight heparin acts on thrombin and unfractionated heparin works on Xa
Warfarin - vitamin K agonist (acts on 10,9,7 and 2)
These have to be stopped before surgery

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45
Q

Hemophilia

A

Type A = . factor VIII deficiency, X-linked recessive disease
presentation depends on severity. Presents early in life or after surgery/ trauma.

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46
Q

what can Excessive bleeding do?

A

Into joints can cause arthropathy and into muscles can cause hematomas
increase in pressure can cause nerve palsies and compartment syndrome

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47
Q

Treatment of hemophilia

A

Avoid NSAIDs and intramuscular injections
minor bleeding - pressure and elevation
major bleeding - give recombinant factor VIII

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48
Q

Type B hemophilia

A

Factor IX deficiency and behaves clinically like type A

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49
Q

Liver disease

A

Liver makes vitamin K and so liver disease causes a complex bleeding disorder with the decreased synthesis of clotting factors. Decreased absorption of vitamin K and abnormalities in platelet function.

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50
Q

Malabsorption of vitamin K

A

Less uptake of vitamin K

Treat with IV vitamin K

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51
Q

Inflammation

A

Non-specific defensive response to tissue damage .

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52
Q

How does inflammation occur

A

Damaged cells release cytokines and histamines causing vasodilation. Neutrophils phagocytose bacteria and debris. Macrophages carry out debridement/ matrix turnover. Tissue fluid moves into the area providing cells and nutrients.

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53
Q

Scab

A

Blood clot and dead macrophages

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54
Q

Signs of inflammation and their causes

A

Heat - capillary widening causing increased blood flow
Redness - increased permeability causing fluid release into tissues
Swelling - increased permeability causing fluid release into tissues
Tenderness - Attraction of leukocytes and extravasation (movement) of them to site of injury
Pain - systemic response, fever and proliferation of leukocytes

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55
Q

Acute inflammation

A

Usually lasts <3 weeks
Accumulation of neutrophils
Purulent = pus (bunch of dead neutrophils)
Increases ESR (sedimentation rate) and CRP

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56
Q

Chronic inflammation

A

Defined as lasting longer than 6 weeks
Significant tissue destruction - a typical feature
CRP will be less raised
Accumulation of macrophages and leukocytes

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57
Q

Proliferation of wound healing

A

Days to weeks timescale
Angiogenesis - oxygen needed for growth
Fibroplasia - fibroblasts move to the site and grow - forms collagen
Epithelialisation - making new skin
Contraction - fibroblasts form myofibroblasts, which produce contractile proteins which pull the edges of the wound together

58
Q

What is the dominant cell type at wound edges in the first week?

A

Macrophages/ mast cells

59
Q

What is granulation tissue?

A

Collagen and proteoglycans deposited by fibroblasts which hold epidermal cells together

60
Q

Remodelling

A

Formation of new granulation tissue stops
Collagen composition changes from type 3 to 1
Fibrous scar forms due to collagen cross linking
The new blood vessels formed are no longer required and so are removed by apoptosis

61
Q

What local factors impair wound healing?

A 
Poor blood supply
infection
oedema
movement
foreign material 
moisture
62
Q

What systemic factors impair wound healing?

A 
Diabetes
atherosclerosis 
nutrients
immunosuppression 
connective tissue disorders
smoking
age 
alcohol
drugs - steroids and antiplatelets
63
Q

Maggots

A

Can be used to differentiate between live and dead tissue in a wound as they eat the dead tissue - allows debridement without surgery

64
Q

Core body temperature

A

36.5 - 37.5
can be altered by menstrual cycle and circadian rhythms
Hypothermia = <35
Hyperthermia = >38 - pyrexia/ fever

65
Q

Thermoreceptors

A

Cold receptors - in the peripheries, it is conducted by myelinated A fibres (fast)
Warm receptors - central in hypothalamus
Pain receptors - nociceptors

66
Q

Response mechanisms to temperature changes

A

Physiological, behavioural, neurological and hormonal

67
Q

Behavioural responses to temperature change

A

Voluntary actions to increase muscle activity

Moving out of the environment you are in

68
Q

Physiological responses to temperature change

A

Involuntary effecting heat loss and production

69
Q

Hormonal responses to temperature change

A

Thyroxine, T3 and adrenaline will increase metabolism to generate heat

70
Q

Nervous system responses to temperature change

A

Activation of either the sympathetic or parasympathetic NS and motor system can cause shivering

71
Q

Responses to cold

A

Cold receptors in skin signal to hypothalamus.
Heat loss is reduced by warm clothing and vasoconstriction
Heat production is increased by thyroxine/ T3 release, shivering and catecholamine release (adrenaline) .

72
Q

Responses to hot

A

Warm receptors detect it in the hypothalamus .
Heat loss is increased by sweating, vasodilation and exposure
Heat production is decreased by decreased activity

73
Q

How to treat heat stoke?

A

Ice cold IV saline

74
Q

Who is at high risk of hypothermia?

A

Neonates

People who have experienced near drowning, major trauma or those who have taken drugs/ alcohol

75
Q

Why are neonates at greater risk of hypothermia?

A

They have a high surface area to weight ration and cannot make behavioural changes. They have brown fat found between the scapulae that is especially to be metabolised to produce heat and doesn’t produce ATP as oxidative phosphorylation is uncoupled

76
Q

Why are people who experience major trauma at risk of hypothermia?

A

Blood loss is replaced with cold fluids

Hypothermia impairs blood clotting

77
Q

Why are people who nearly drown at risk of hypothermia?

A

Heat loss via conduction to water

78
Q

Why are intoxicated people at risk of hypothermia? (Drugs/ alcohol)

A

They cannot make behavioural changes

79
Q

Function of lymph

A

Draining excess interstitial fluid
Transport of dietary lipids and lipid soluble vitamins
carrying out immune response
returns lost plasma proteins into circulation

80
Q

What allows transport of lymph?

A

Skeletal muscle pump
Respiratory pump - pressure changes
When you breath in pressure in the abdomen increases, drawing lymph into thorax

81
Q

Lymphatic capillaries

A

Larger than blood capillaries
When pressure in interstitial spaces is higher than the capillaries the cells fluid enters the lymph system due to anchoring filaments being pulled.
Endothelial cells overlap = one way valve

82
Q

Passage of lymph

A 
Capillaries
Vessels
Nodes
Trunks
Ducts
83
Q

What are the 5 trunks and what do they drain?

A 
Jugular - head and neck
Subclavian - upper limbs
Bronchomediastinal - thoracic wall, lungs and heart
Intestinal
Lumbar - lower limb and pelvic organs
84
Q

What drains the right upper quadrant of the body?

A

The right lymphatic duct:

  • right jugular
  • right bronchomediastinal
  • right subclavian
85
Q

What drains most of the body?

A

Thoracic duct:

  • lumbar
  • intestinal
  • left jugular
  • left subclavian
  • left bronchomediastinal
86
Q

Venous angle

A

Site where the lymph drains into the venous system

It is the junction of the subclavian and internal jugular vein bilaterally .

87
Q

virchow’s node

A

In left supraclavicular area that drains lymph from the gut. When it is enlarged it can be an early sign of intra-abdominal malignancy. It is located at the venous angle .

88
Q

Primary lymphatic organs

A

stem cells which become immune cells

red bone marrow

89
Q

Secondary lymphatic organs

A

Essential for an efficient immune response and surveillance

e.g. peyers patches, spleen, tonsils and MALT and lymph nodes

90
Q

Thymus

A

soft triangular organ in the mediastinum, enlarges during childhood then atrophies. T cells mature in the thymus, where they undergo tolerance .

91
Q

Spleen

A

Main storage site of T independent B cells, e.g. the T independent B cells that produce the IgG2 antibody - eliminates encapsulated bacteria.
Contains fixed macrophages.
Huge network of capillaries with a long transmit time through the organ so encapsulated bacteria are exposed to the spleen’s fixed macrophages for a longer time so the body has a greater chance of defending itself.

92
Q

Why are encapsulated bacteria difficult to fight?

A

They are difficult to recognise as non-self pathogens because of their thick capsule.

93
Q

Tolerance

A

Mechanism to remove immune cells that attack self tissue - autoimmunity.
T cells undergo central and peripheral tolerance.

94
Q

Positive selection

A

Makes sure T cells can recognise MHC molecules - MHC I = CD8 and MHC II = CD4

95
Q

Negative selection

A

Occurs after positive selection. If the cells bind strongly to self peptides being displayed on MHC molecules they will undergo apoptosis to remove them.

96
Q

Lymphatic drainage of bladder

A

External iliac

97
Q

Lymphatic drainage of prostate

A

Internal iliac

98
Q

Lymphatic drainage of penis

A

superficial inguinal

99
Q

Lymphatic drainage of Scrotum

A

superficial inguinal

100
Q

Lymphatic drainage of testes

A

para aortic - enlargement is a sign of testicular cancer

101
Q

Lymphatic drainage of Ovaries

A

Lateral and pre-aortic

102
Q

Lymphatic drainage of Uterus

A

Fundus = para-aortic

Body and cervix = internal and external iliac

103
Q

Lymphatic drainage of Vagina

A

Upper 1/3 = external and internal iliac
Middle 1/3 = internal iliac
Lower 1/3 = superficial inguinal

104
Q

Antibodies

A

5 classes

all have the same basic structure

105
Q

What do antibodies do?

A

Prevent toxins from damaging tissue
prevent pathogens from entering cells
highlight the pathogen to phagocytes and help phagocytosis
important for encapsulated bacteria and viruses
antibodies can cause activation of complement so activate mast cells

106
Q

What are the different types of immunity?

A

Natural passive
Artificial passive
Natural active
Artificial active

107
Q

What are the different antibody classes?

A 
IgG
IgA
IgM
IgD
IgE
108
Q

IgG

A 
monomer
important in secondary response
pass through the placenta to the fetus
have the ability to traverse the blood vessels to tissues 
most abundant of circulating antibodies
109
Q

IgA

A

found in GI tract and respiratory tract - mucus membranes
high concentration in breast milk
help in transferring immunity to the new born infants

110
Q

IgM

A

Produced in the primary immune response. They are restricted to the blood stream due to high mass . They are important in the primary response .

111
Q

IgD

A

Present on the surface of B cells where they function as receptors for antigens .

112
Q

IgE

A

Important in protection against parasites. They are involved mainly in the development of allergic responses. They release histamine which causes contraction of smooth muscles and stimulates secretion of mucus .

113
Q

What are the different types of pathogens?

A

Bacteria, viruses, fungi, protozoa, metazoa and prions

114
Q

What are prions?

A

Misfolded proteins with the ability to transmit their misfolded shape onto normal variants of the same protein

115
Q

Bacterial replication

A

DNA is replicated
DNA is pulled to separate poles of the bacterium as it increase in size to prepare for splitting
The growth of a new cell wall begins to separate the bacterium
New daughter cells have tightly coiled DNA, ribosomes and plasmids, DNA gyrase and polymerase

116
Q

Spores

A

Allow the bacteria to exist in a dormant state
complex multi-layered coat that is resistant to heat, drying, alcohol and UV
bacteria are able to return to a vegetative state when conditions are favourable

117
Q

Biofilms

A

Community of bacteria attach to surfaces in extracellular polymeric substances
It protects them against desiccation and chemical attack
can occur on living or inanimate structures

118
Q

Why are viruses easier to remove from the environment than bacteria?

A

They don’t form spores or biofilms

119
Q

Cleaning

A

Removal of physical debris from a surface that microorganisms might be supported by. Involves handwashing .

120
Q

Disinfection/ antiseptics

A

Removal of microorganisms
doesn’t remove everything
antisepsis = disinfection of living tissues

121
Q

Sterilisation

A 
Process of destroying all micro-organisms
destroys spores
pressure and heat in an autoclave
blast with gamma rays
super fine filters
gas
122
Q

Gram staining

A

Flood with crystal violet
Flood with iodine
Decolourise with gram’s alcohol
flood with safranin counterstain

123
Q

Interpreting gram staining

A

Purple = gram postive
Pink = gram negative
oblong shape = rod
Sphere = cocci

124
Q

PCR

A

Makes it possible to detect pathogenic viruses or bacteria

125
Q

Process of PCR

A

95 degrees - denaturation
55 degrees - Annealing
72 degrees = Taq polymerase joins free nucleotides to template

126
Q

What is the bacteria that commonly causes UTIs

A

Enterbacteriacae

127
Q

When does testing for microorganisms need to be done?

A

From site of infection when the patient is acutely ill - start of the infection

128
Q

When does testing antibodies need to be done?

A

When the patient is recovering, later on and from the blood .

129
Q

What are the 4 main classes of receptor?

A

Endocrine
Paracrine
Synaptic
Contact-dependent

130
Q

Endocrine signalling

A

hormones produced by endocrine cells
secreted into the bloodstream
act on distant tissues and cells

131
Q

Paracrine signalling

A 
hormones/ signals are released by various types of cells 
secreted locally (not into bloodstream) and diffuses between cells
act on cells in near vicinity - short distance
132
Q

what are the 3 types of surface receptors?

A

Ion channel coupled receptors
G protein coupled receptors
receptor tyrosine kinases - enzyme linked

133
Q

Ion channel coupled receptors

A

Ligand binds to receptor (ion channel)
causes a conformational change
allows movement of specific ions
change in relative ion concentration across the cell may cause other changes

134
Q

G protein coupled receptors

A

Absence of the ligand - GPCR is inactive
GPCRs bind to G proteins which are a trimeric protein - alpha, beta and gamma subunits
G proteins bind GDP when the GPCR is inactive but GTP when active.
When GTP binds the trimeric protein splits into 2 signals
The G protein hydrolyses the GTP to GDP to inactivate GPCR

135
Q

Enzyme linked receptors

A

Ligand binds to 2 adjacent receptors which then dimerise
Receptors phosphorylate each others intracellular domain
Initiates a downstream signalling cascade
Most receptor tyrosine kinases activate Ras which cause GDP to become GTP
This initiates downward signalling

136
Q

Contact dependent signalling

A

requires direct contact between 2 cells e.g. through gap junctions or through cell surface molecules .

137
Q

Gap junctions

A

Hexameric channels that allow diffusion of small molecules between the 2 connected cells
usually smaller molecules - ions
all coordinated contraction of cardiac muscle cells

138
Q

Cell-surface molecules

A

signalling molecule is not secreted, it is bound to the surface of the signalling cell
there is a receptor on the surface of the target cell
cells need to be in close vicinity to make a molecular contact

139
Q

what is the difference between gram positive and negative bacteria?

A

Gram positive has a thick peptidoglycan cell wall and no outer lipid membrane but gram positive bacteria has a thin peptidoglycan cell wall and an outer lipid membrane . The gram positive retain the crystal violet stain, making them purple, but the gram negative are only coloured by the safranin counterstain as they cannot retain the crystal violet.

140
Q

What is peyers patches

A

Small masses of lymphatic tissue found in the small intestine. They monitor intestinal bacteria

Physiology (46 decks)

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