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BVMS Module 2 > WEEK 1/2/3 > Flashcards

WEEK 1/2/3 Flashcards

1
Q

explain the roles of blood in transport of oxygen

A

transport of oxygen occurs via haemoglobin, nutrients, waste products, endocrine secretions, temp control, ICF water conc, electrolyte conc and acid base balance

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2
Q

erythrocytes

A

red blood cells haemoglobin, biconcave discs
produced in bone marrow,
1/3 non-circulating accumulate in spleen, removed by intravsaular haemolytic.

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3
Q

leukocytes

A

white blood cells, 2 types; granulocytes and agranulocytes, neutrophils, basophils, eosinophils. Lymphocytes and monocytes.

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4
Q

what is granulopoiesis?

A

the production of white cells

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5
Q

myeloblast

A

first recognisable granulocytic cell

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6
Q

Myelocyte

A

Proliferating Mitotic pool

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7
Q

what is left shift?

A

presence of immature cells within the blood cells in a sample of blood

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8
Q

platelets

A

small colourless fragments of cells that help for form blood clots and platelet plugs.

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9
Q

explain cat blood groups and how they work with antibodies

A

naturally curing isoantibodies; A, B, AB,
example; type A cats have a low conc of anti B antibodies and type b cats have low conc of anti A antibodies. important for blood transfusions.

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10
Q

explain how a blood clot forms?

A

when damage occur to the endothelium cells, construction of smooth muscle occurs and causes von willebrand factor to activate aggregates platelets to bind and form with collagen and a plug.

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11
Q
  1. Albumin
A

formed in liver and is a source of amino acids and maintain oncotic pressure.

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12
Q
  1. Globulin
A

formed in immune cells and liver – immune function.

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13
Q
  1. Fibrinogen
A

formed in liver – clotting.

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14
Q
  1. Erythropoietin
A

EPO, regulates the production of erythrocytes. When a decrease O2 levels in kidney, stimulates increased EPO production. EPO stimulates red blood cell production in bone marrow

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15
Q
  1. Plasma v Serum
A

In Viro – plasma + cells In Vitro – serum + cells. Serum doesn’t contain fibrinogen and plasma does. (used up in clotting process).

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16
Q
  1. Describe anaemia
A

reduction of erythrocytes number. Can be caused by red cell entering/leaving blood decrease production or increased turnover. Two types – regenerative (increased Turnover) or non-regenerative (lowered production). Lowered O2 – increased EPO – increased bone marrow production of RBC (3-5days) back to normal.

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17
Q
  1. Haemorrhage
A

increased loss of blood. Depends of servery of blood loss and location of blood loss (internal v external)

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18
Q
  1. Haemolysis
A

increased destruction of RBC, reduced red blood cell survival time, extravascular lysis and intervascular lysis. Casues – infectious agents, toxins, fragmentation etc.

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19
Q

what is fragmentation?

A

red cells, mechanical damage, passing through damaged/abnormal vasculature.

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20
Q

schistocytes

A

fragmentaged red cells

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21
Q

acanthocytes

A

red cell with asymmetrical anaemias

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22
Q

isoerthyrolysis

A

disease of the new born antibodies against body blood group antigens, causes destruction of neonatal RBC

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23
Q

canine autoimmune haemolytic anaemia

A

production of autoantibodies against own RBC - IgM/IgG, autoantibodies leads to phagocytosis.

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24
Q

extravascular lysis

A

phagocytes of RBS, iron and global reutilised, head converted to biliverdin converted to bilirubin and binds to albumin, causes jaundice or goes to liver an produces bile.

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25
Q

what is jaundice?

A

elevated bilirubin levels in plasma, shows excessive breakdown of RBCs and obstruction of liver and the bile duct.
yellow skin/mucous membranes

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26
Q

what is fibrinolysis?

A

clotting cascade activates thrombin and activates fibrinogen which leads to fibrin activating plasminogen and plasmin which leads soluble fibrin fragments leading to a blood clot

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27
Q

what do erythrocytes require for production?

A

amino acids, lipids and CHO. Iron for Hb production, folic acid for DNA and RNA synthesis.
Vit B12 for maturation of erythrocytes and formation of DNA (from Cobalt)

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28
Q

describe the main causes of Von Willebrands disease?

A

uncollected bleeding mainly in dogs, mainly a autosomal triat

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29
Q

describe factor VIII deficiency - Haemophilia

A

clinical signs show swelling at joints and very common in German Shepard’s. sex linked recessive

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30
Q

Describe factor IX deficiency - haemophilia B

A

Large subcutaneous haematoma - due to blood swelling, Most common in Cairn terriers, German Wire haired terriers, St Bernards, Coonhounds, Scottish terriers, Old english sheepdogs.
Factor IX -intrinsic coagulation pathway.
Clinical signs same as factot VIII deficiency.

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31
Q

what is haemophilia?

A

mostly inherited genetic disorder that impairs the body’s ability to make blood clots, a process needed to stop bleeding

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32
Q

what do R groups do on amino acids?

A

determines the characteristics (size, polarity, and pH) for each type of amino acid

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33
Q

what are the different levels of protein structure?

A

Primary 1o - amino acid sequences
Secondary 2o - hydrogen bonds within sequence
alpha helix and beta pleated shapes occur,
tertiary structures 3o - includes R group, responsible for folding and weak bonds present.
quantaertaery 4o - includes compels of 2 or more polypeptide chains example = haemoglobin.

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34
Q

what are some prion diseases?

A

scrapie, BSE, CWD, CJD.

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35
Q

describe the change that occurs in scrapie pion disease? PrPc = PrPSc

A

globular form changes to fibouris form, fibrous forms clump together and are insoluble. leads to plaques and holes in tissue, mainly seen in brain/nerve tissue.

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36
Q

describe collagen structure

A

is a triple helix and composed of glycine which occurs every 3 AA. include H bonds.

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37
Q

example of collagen disease - scurvy

A

scurvy is a vit C deficiency, insufienct hydroxylation of proline - leads to fewer H bonds so collagen is unstable due to diet

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38
Q

what is Michaelis-Menton kinetics and hyperbolic curve

A

low substrate concentration = lineal proportional to [S]
High [S], rate independent of [S]
Km= [S] when rate is half maximum (M, mM)

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39
Q

what is Km?

A

Low KM - low [S] when 1/2 Vmax
Indicates enzyme with high affinity for S

High KM - high [S] when 1/2 Vmax
Indicates enzyme with low affinity for S

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40
Q

what do allosteric enzymes do?

A

allosteric enzymes bind to an area not close to the active site and cause alteration of shape. allosteric enzymes, the affinity (Km) alters as more substrate binds to enzyme hlaemobgloin is a allosteric protein, that binds ligand oxygen and kinetics of interaction are similar to that observed with allosteric enzymes

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41
Q
  1. List important proteins associated with RBC membranes
A

Spectrin lies underneath the membrane (cytoskelteton), Interacts with Ankyrin, Actin, Protein 4.1. Helps with stability of membrane. Conatins 4 important integral membranes; Na/K ATP pump, Glut 1, Anion exchamger, Glycophorin A.

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42
Q

how is HCO3- generated?

A

CO2 from tissues enetrrs RBC – CO2 + H2O = H+ + HCO3- CARBONIC ANHYDRASE (CA) used as catalyst. Anion exhaner used to remove Cl- and bring in HCO3-.
The opposite reaction occurs in the lungs

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43
Q

why does RBC need NADPH

A

RBC carry O2 and is a strong oxidising agent. O2 becomes reduced n is now a Reactive oxygen species (ROS). ROS is produced during phagocytosis acting as a bacteria killer but ROS can damage lipids and proteins of cells.

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44
Q

what are the clinical signs of methemoglobinemia?

A

elevated methaemoglobin in the blood. Cyanosis purple colour tongue/mucous membranes. Exercise intolerance. Vomiting. Choco brown blood. Anaemia.

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45
Q

myoglobin v haemoglobin?

A

myoglobin is heme in hydrophobic state. Outside polar AAs. Haemoglobin protein+heme group, Iron binds to 4 nitrogen’s in ring. Mygobin 1 heme group, Haemoglobin 4 heme groups. And allosteric protein.

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46
Q

what is an allosteric protein?

A

Hb is allosteric, 4 subunits that interact at 1 site shape of other sites. Myoglobin is not allosteric.

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47
Q

explain the oxygen dissociation curve?

A

Hb binding O2 does not follow MM kinetics. Is a sigmoid curve. This is because the 4 subunits interact and influence the affinity for O2 at each binding site (allosteric protein). When O2 level (pressure) is high in lungs, Hb becomes saturated and all Hb is in relaxed form – high affinity for O2. But as O2 pressure decreases as RBC move to tissues, affinity for O2 decreases and Hb releases O2

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48
Q

What is the effect of 2,3 BPG

A

2,3-BPG stabilizes the T state conformation, making it harder for oxygen to bind hemoglobin and more likely to be released to adjacent tissues. . If O2 deprivation – increases 2,3 BPG conc, stabilises deoxyg Hb, promote release of O2 in tissues.

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49
Q

what is sickle cell anaemia?

A

heridary disease effect in B-globin gene HbS – Deoxy HbS forms polyers and precipaoates inside RBC – sickle cell shape lyse readily. Detection of HbS gene, nucleotide base substitution A to T.

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50
Q

what is chronic inflammation?

A

prolonger inflammation weeks - years that may follow acute inflammation due to foreign body or infection by organism

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51
Q

what are some morphological features in chronic inflammation?

A

mononuclear cells as well as lymphocytes/plasma cells, attempts to heal by replacment connective tissue over damaged cells by proliferation

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52
Q

how do activated macrophages stimulate T cells in chronic inflammation?

A

macrophages become antigen-presenting cells and present antigens via secretion of infalmmaotky mediators

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53
Q

what does scarring and fibrosis result in?

A

substantial tissue destruction or where tissues cannot regenerate.

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54
Q

what is margination?

A

when vessels dilate they have reduced hydrostatic pressure and blood flow leukocytes exit the central region of lumen and go near to the endothelia cell surface.

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55
Q

what is adhesion activation?

A

controlled by inflammatory mediators including IL-8, IL-1 and TNF-alpha, activate neutrophils and endothelial cells which cause change to integrins allowing enchained binding to receptors.

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56
Q

what re macrophages

A

granulomatous inflammation, chronic inflammation, rule out if foreign bodies are presents, resolving lesions.

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57
Q
  • Mast cells
A

vasoactive amines - release histamine, produced in bone marrow, important when triggering acute inflammation, proteases, cytokines, chemokines. §

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58
Q
  • Basophils
A

linked with eosinophils, helps with allergy and parasites. Contains histamine, and cytokines.

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59
Q
  • Eosinophils
A

– inflammation, will NOT be present if any are shown - allergy, hypersensitive, parasite disease, fungal disease.

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60
Q
  • Neutrophils
A

most common in inflammation, kills microbes, kills neoplastic cells, eliminate foreign material.

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61
Q

Polymorphonuclear leukocytes

A

neutrophils, basophils, eosinophils)

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62
Q

mononuclear leukocytes

A

monocytes – macrophages, lymphocytes, plasma cells, mast cells.

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63
Q

what is Exudate

A

the leakage of fluid containing water, electrolytes , high protein and numerous inflammatory cells.

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64
Q

what is transudate

A

the leakage of fluid containing water and minerals but low proteins and cells.

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65
Q

what is vasodilation?

A

local increase in blood flow, heat, hyperaemia, slower blood flow, facilitated leukocytes migration, increased vascular permeability, fluid leukocytes plasma proteins

66
Q

what is inflammation?

A

regulated response to physical/chemical injury or biological agent. Benefits, dilution of pathogens, toxins, killing forgeing bodies etc. provide healing, restrict movement for repair. Plasma protein mediators and cell derived mediators.

67
Q

main ways for transport in fluid compartments

A

diffusion, AT, bulk flow, endothelial/exocytosis

68
Q

diffusion

A

movement of moleucles from a high to low conc not requiring any eneery across a membrane.

69
Q

A.T

A

The movement of molecules from a low to high concentration requiring energy provided for ATP

70
Q

Bulk flow

A

Process by which small lipid-insoluble proteins move across the capillary wall.

71
Q

Endo/exocytosis

A

Exocytosis – the movement of insoluble molecules through a membrane layer, by fusing with the membrane and releasing the molecules across the junction. Endocytosis - is the process of actively transporting molecules into the cell by engulfing it with its membrane.

72
Q
  1. Osmosis
A

Osmosis is the movement of solutes and water across a membrane from a high to low water potential not requiring any energy

73
Q

what is osmolarity?

A

The measure of solute concentration; the number of solute particles per litre of solution

74
Q
  1. Tonicity
A

determines if a solution is hypertonic or hypotonic, depends on non-permeable solutes present if water will move or not.
If one solution is hypertonic it contains more nonpermeating solutes so low WC, water will flow in. If a solution if hypotonic it has less nonpermeating solutes so has a high WC. Water will flow out.

75
Q
  1. Oedema
A

The accumulation of excess water in tissues. Due to imbalance of starling forces.

76
Q

stallings forces

A

Capillary Hydrostatic pressure, interstitial hydrostatic pressure, oncotic pressure and oncotic pressure due to intestinal fluid proteins

77
Q

Hydrostatic pressue

A

causes intestinal fluid to be pushed out due to a higher pressure within the arteriole end than the venule end. There is Net Filtration. At the Venous end there is Net Absorption due, the oncotic pressure is greater due to plasma proteins which cause fluids to return to capillary

78
Q

What is the result of oedema when physical events occur?

A

Increase in cardiac output – arteriolar pressure increases - capillary pressure increase – increase in filtration

79
Q

How does heart disease cause a consequence of oedema?

A

Causes an increase in venous pressure, leads to increase in capillary pressure causing an increase in filtration.

80
Q

Neutrophilia

A

increased circulating neutrophils – occurs when excited/stressed/cortosteriods/inflammation. Physical response - Secondary to epinephrine release, short lived disease (30mins), young animals.

81
Q

what is Left shift

A

immature forms of neutrophils released from bone marrow storage. Regenerative left shift. Neutrophilia with mainly mature neutrophils with some immature forms (bands) seen. Degenerative left shift - More immature forms than mature neutrophils. Neutrophil count may be normal, mildly raised or reduced

82
Q

Toxic change

A

associated with inflammatory states, bacterial infections, marked tissue necrosis, neutrophils are being produced rapidly to meet the demand from tissue. Dohle bodies-small blue bodies in cytoplasm of neutrophil (rough ER), increased cytoplasmic basophilia, cell and nuclear swelling.

83
Q

Neutropenia

A

deficiency of circulating neutrophils. Increased when inflammation occurs. Severe overwhelming swelling. Decreased production – bone marrow disorder – toxins/drugs, infectious agents, neoplasia, immune-mediated destruction. RISK OF INFECTION

84
Q

Eosinophilia

A

increased number of circulating eosinophils. Response to IL-5 released by T cells + histamine by mast cells. Parasitic conditions.

85
Q

Monocytosis

A

increased number of circulating monocytes, excitement, stress/exogenous corticosteroids (dogs), inflammation, monocytoic leukaemia (rare)

86
Q

Eosinopenia

A

deficiency in circulating eosinophils. Endogenous or exogenous steroids inhibit mast cell degranulation and neutralise histamine. Eosinopenia by itself is of little diagnostic significance

87
Q

lymphocytosis

A

Increased numbers of circulating lymphocytes, Physiological (excitement), May occur in infectious disease, during recovery or in chronic disease Post vaccination in young animals, Lymphoid neoplasia.

88
Q

Lymphopenia

A

Deficiency of circulating lymphocytes, Occurs in acute inflammation Migration to tissues or back to lymph nodes, Bacterial or viral infections Endotoxemia, Endogenous or exogenous corticosteroids, Stress leukogram
Transient altered distribution of lymphocytes between blood and lymphoid tissue more common that lymphocytosis, can be seen as part of stress leukogram and sometimes the only component.

89
Q

Leukaemia

A

Primary site in bone marrow, moves into blood and becomes secondary into tissues. Maturation and defects occur. Can be diagnosed by routine haematology report

90
Q

what are the 2 classes of leukaemia?

A

Classification 1 – involves immature and mature cells. Presence or absence of neoplastic cells in the blood
No neoplastic cells being released into blood => subleukaemic leukaemia (aleukaemic)
Leukaemia classification 2 – Lymphoid – most common, B or T cells. Myeloid, The stage at which a mutation occurs in this hierarchy determines which cell type the tumour represents.

91
Q

what are the consequences of leukaemia?

A

– Replacement of bone marrow population by neoplastic cells
– Deficiencies in other cells lines → cytopenias
– Extramedullary haematopoeisis
Splenomegaly/hepatomegaly
Haemodynamics
– If very high WBC, blood is thicker impairing blood flow through microvasculature
Hyperviscosity syndrome

92
Q

what is innate immunity?

A

includes, physical barrieers secretions enzymes, complement, phagocytouc cells

93
Q

what is intrinsic immunity?

A

restriction factors, TRIM5, APOBECS, Tetherin, SAMHD1, etc

94
Q

what is adaptive immunrtity?

A

Antibody, helper T-cells, cytotoxic T cells etc

95
Q

name cells that are involved in myeloid lineage?

A

myeloid lineage, neutrophils, eosinophils, basophils, mast cells, macrophages, monocytes.

96
Q

name cells that are involved in lymphoid lineage?

A

NK cells, Th cells, Tc cells, B cells, Plasma cells, dendritic cells

97
Q

what is complement?

A

a system of plasma proteins that can be activated by pathogens leading to a cascade of reactions that occur on surface of pathogens.

98
Q

how does complement C3 split?

A

Enzyme C3bBb complex splits C3 = C3a + C3b, C3b promotes local inflammation
and C3a and C5a both attract leukocytes to site of infection. (chemotaxis)

99
Q

what is C3b coated in?

A

coated in Microbe and is phagocytosed, causes lysis to be triggered.

100
Q

what is oxygen dependent killing?

A

involves the use of reactive oxygen-coating molecules

example - OD production of a superoxide, which is an oxygen rich bacteria killing substance.

101
Q

what is oxygen independent killing?

A

involves the use of a non-oxygen coating molecules when killing.
example; lysozyme - destruction of bacteria cell wall
OR lactoferrin - collation of iron.

102
Q

what is an antibody and what does it consist of?

A

Antibody is an immunogloibn protective protein that is produced by the immune system to help fight of infection. it consists of 2 light chains and 2 heavy chains.
hinge region and variable domain, Fab and Fc fragments
fragments crystallisable.

103
Q

what do antibodies do?

A

they bind ‘antigen’, epitope area at which the AB bind to Ag,

104
Q

name the different types of Ab?

A

IgM, IgG, IgA, IgE, IgD, IgY

105
Q

IgM

A

pentameric structure, involved in primary response to antigen, often low affinity but high avidity.
Nutralises antigen, fixes complement.

106
Q

IgG

A

involved in secondary repose to antigen, Fc receptor binding, neutralises the antigen and fixes complement, high affinity due to affinity maturation

107
Q

IgD

A

expressed on B cells surface during development, surface receptor for antigen, immunity to respiratory bacteria.

108
Q

IgA

A

lives in mucous areas on body and helps with digestion by secreting mucous from cells

109
Q

IgE

A

involved in allergy response and hypersensitivity, triggered release of histamine from mast cells, High affinity for IcE is expressed on mast cells and basophils

110
Q

IgY

A

thought to be an ancestor of IgG and IgE in birds, reptiles, lungfish.

111
Q

how are antibodies produced?

A

B cells are made and matured in the bone marrow while T cells are made in bone marrow and matured in the thymus. they are served firm hematopoietic stem cells.
example:
Lymphoid progenitor - lymphoblast - small lymphocyte - B lymphocyte

112
Q

how does clonal section work?

A

when an antigen enters the body they float round naive B cells, MHC T cells and lymphocytes. the cells that match with the Ag will bind and fees. orm memory and effector cells. Mass replication called clonal expansion occurs in which daughter cells proliferate and expand in number to fight off antigen.

113
Q

what are ‘Virgin’ B cells

A

newly formed B cells that are short lived - over 75% do not reach circulation and die by apoptosis and are phagocytosed in bone marrow by macrophages

114
Q

what are gene rearrangements and where do they occur?

A

gene rearrangements are when the variable region gene change to generate the VDJ (heavy chain) and the VJ (light chain) the occurs in bone marrow and lymphoid tissue

115
Q

what gene rearrangements occur in lymphoid tissue?

A

isotope class switching, occurs after stimulation of B cells with antigen. Affinity maturation - further mutation of variable region, selection

116
Q

what is the primary immune response?

A

pathogen enters body, causes phagocytosis to occur. macrophages then become antigen presenting cell displaying antigen on surface on membrane.
leads to an immune response from acquired immunity, B and T cells contain complementary Ab on surface and when they come in contact an Ag-Ab complex will form, this causes B cells to produce B plasma and B memory cells. Helper T cells aid activation of B cells. Cytotoxic T cells kill virus infected cell and antibodies remove the infection. IgM abs are presents at 1o repose due to high avidity but low affinity. (has 10 weak binding sites but lots of them)

117
Q

what is the secondary immune response?

second exposure

A

IgG is reasonable for the 2o response high Affinity but low avidity (2 very strong binding sites)
second exposure causes a stomper antibody response, re-exposure to antigen produces a high titre of IgG

118
Q

what is B cell trafficking?

A

B cell leaves bone marrow, expressing IgM and IgD, enters lymph node, into B and T cell area and then into afferent lymphatic duct then efferent lymphatic duct. They then enter the high endothelial venue (HEV) and the germinal centres. they are then drained into the venous system.

119
Q

what is a germinal centre?

A

B cell encounter with Ag, secondary lymphoid follicle enters germinal centre, T helper cells are present, centrocyte and centroblast and follicular demerit cells are present. helps B cello mature and differentiate their antibodies.

120
Q

what is the adaptive immune response?

A

thymus maturing T cells. most cells are produced before puberty and the thymus decrease in size after 25y/o No longer needed to produce vast amounts of T cells due to previous years.

121
Q

what would happen is there was no thymus present?

A

cause defective antibody formation (no CD4+ helper T cells) no cell mediated immune repossess for CD4+ and CD8+ T cells, no delayed-type hypersensitivity. (requires CD4+ T cells)

122
Q

describe the process of T cell maturation in the thymus?

A

T cells interact with interdiggiating cells which present self-peptides. If T cells recognise these cells they are eliminated. undergo apoptosis and are phagocytosed by macrophages. T cells that travel though HEV and finish devoplment in lymph node. T cells react with antigen present cells through T cell receptors and MHC

123
Q

explain the structure of the thymus?

A

the thymus consist of a capsule, which contains a cortical, sub-cortical and medullary epithelial cell wall, with a trabeculae membrane in the capsule. The thymus contains, macrophages, dendritic cells, thymocytes, Hassall’s corpuscle.

124
Q

where is MHC 1 expressed?

A

on every cell in your body, but cytotoxic T cell with CD8+ interact with MHC 1

125
Q

where is MHC 2 expressed?

A

Helper T cells with CD4+ interact with MHC 2

126
Q

why do puppies not get vaccinated straight after they are born?

A

high levels of maternally derived abs can nurtaise the pathogen (coating virus to prevent replication, marking it for phagocytosis and binding complement) therefore puppy will not have time to achieve acquired immunity, it will have been dealt with by passive immunity, and the passive immunity will not last long.

127
Q

what is the immunity gap?

A

time during which the levels of antibody are not high enough to protect from infection but still high enough to interfere with vaccination.

128
Q

what are NK cells?

A

recognise “Stress” receptors on surface of virus-infected ad malignant cells. able to detect reduced MHC expression, NK cells can kill infected cells by ADCC (Antibody-dependent cell-mediated cytotoxicity) also rich in Fc receptor expression.

129
Q

what do cytotoxic T cell contain on surface membrane?

A

CD8+ and TCR receptors.
CD8+ checks for MHC1 receptors on infected cell.
TCR checks for specific antigen. the infected cell will express MHC1 or MHC2

130
Q

how does MHC1 processing occur?

A

in the ER, a proteasome enters and is expressed into the MHC1 with a specific antigen. moves through Golgi apparatus and into endosome. then expressed surface of infected cell and the cytotoxic t cell will bind with TCR and CD8+ and destroy the cell.

131
Q

how does MHC2 processing occur?

A

T helper cells with CD4+ receptors on the APC. in the ER, ribosomes produce MHC2 proteins. MHC2 proteins bound with a receptor released from ER. travels through golgi, binds with broken down bacteria (peptides) The MHC2 receptor with antigen binds to activated T helper cell which has CD4+, CD4+ checks for MHC2 and Tcr checks the antigen.

132
Q

what is PAMP

A

pathogen-assocaited molecules patterns

133
Q

what’s is PRR

A

pathogen recognition receptors.

134
Q

what is a vaccination?

A

a vaccination is a dead/weakened pathogen that causes an immune response to triggered memory cells for the next time the body comes into contact with it

135
Q

what is a killed/inactive vaccination?

A

more longer able to replicate following treatment with formalin, heat or irradiation. protection is limited, related to the short-lived nature of the antibody response produced

136
Q

what is a live attenuated vaccination?

A

usually more potent than killed vaccines as limited viral replication. antigen is proceed by both exogenous and endogenous pathways conformational epitopes are persevered. derived form live virus that has mutated so no longer pathogenic.

137
Q

what is a subunit vaccination?

A

used to replace live/inactive vaccines. they are protective virus neutralising antibodies tend to be directed against particular surface of the virus

138
Q

what are Adjuvants?

A

mechanisms that non-specifically enhance the immune response, involves substances that induce inflammation by antigen-independent mechanisms.

139
Q

give some examples of adjuvants?

A

Freund’s incomplete and complete
Alum (aluminium hydroxide)
ISCOMS (immune stimulating complexes, saponin isolated from Quillaja Saponaria mixed with cholesterol and phospholipid)

140
Q

what is Fruend’s incomplete and complete? Adjuvants?

A 
incomplete = oil in water leads to a delayed release of antigen, enhanced uptake of APC
complete = oil in water and killed mycobacteria leads to delayed release of antigen, enhanced uptake of APC and activates macrophages
141
Q

give an examples of successful live vaccine in dogs?

A 
canine distemper virus vaccine, first developed in 1938, should be vaccinated at 6 weeks old until 16 weeks old, symptoms include, nasal discharge, fever, eye discharge, lethargy, sneezing, coughing. immunity should last up to 3 years, log lasting issues may include
 seizures
Muscle twitching
Jaw spasms
Nerve damage
Brain damage
142
Q

give examples of a live vaccine in humans?

A

ATTENUVAX,
MUMPSVAX,
MERUVAX

143
Q

give some examples of subunit vaccines?

A

feline leukaemia virus vaccine based on recombinant gp70, hepatitis B vaccine based on HBSAg and HPV vaccines based on the capsid protein L1

144
Q

what is tolerance?

A

to accept without an immunological reaction an antigen that normally produced one

145
Q

what is autoimmunity?

A

the state by the presence of with auto-antibodes or of lymphoid cells sensitised against some constituent of the subject own issues.

146
Q

give some examples of autoimmune conditions and the antigens targeted?

A

Addison’s disease - attack of adrenal glands, means not enough production of steroid hormones cortisol and aldosterone.
Rheumatoid arthritis
Myasthenia gravis

147
Q

explain myasthenia gravis autoimmune condition?

A

Myasthenia gravis - autoantibodies to acetylcholine receptor. mainly cat and dog, inherited in jack Russells., springer spaniels and fox terries. clinical signs ) may display skeletal muscle weakness, megaoesophagus and in severe cases, aspiration pneumonia and collapse.

148
Q

explain Rheumatoid arthritis autoimmune condition?

A

autoantibodies to collagen and immunoglobulin. Immune complexes deposited in membrane leads to complement fixation and local inflammation with cartilage degeneration and bone de-mineralisation.

149
Q

what is the ELISA test?

A

use dfor detection of collagen-specific antibody in canine SLE.

150
Q

how does the ELISA test work?

A

sample is dated with antigen and test sample serum - wash the wet throughly to remove unbound conjugate - add antibody-enzyme conjugate specific for the antibody in test serum - wash well again to remove unbound conjugate - add chromogenic substate for enzyme and read absorbance on microplane reader.

151
Q

what is the rapid immunomigration test and how does it work?

A

FelV antigen detection.
FeLV antigen in plasma placed into sample area. Anti-FelV antibody -1 + gold - migration to test are and binds to anti-FeLV antibody -2.
if FeLV antigen is present detection will occur.

152
Q

define an allergic respsone?

A

over reaction of the immune system to a harmless antigen.

153
Q

what are the four types of hypersensitivity?

A

Type I
Type II
Type III
Type IV

154
Q

what is type I hypersensitivity?

A

antigen is soluble, includes mast cell degranulation (granules include, histamine, heparin, TNF-a cytokines)
examples = asthma, allergic rhinitis

155
Q

type I hypersensitivity in horses?

A

sweet itch, recurrent dermatitis - allergy to salvation of biting insects such as culicoides, sand flies etc.

156
Q

what is type II hypersensitivity?

A

mal molécules binfing T cell surface modify the ntigenicty of the moeleuc rendering then immunogenic. B cell respond to antigen and destroy. IgG binds to novel antigen complement cascade triggered IgG binds to surface. autoimmunity.

157
Q

what is type III hypersensitivity?

A

soluble protein antigens bind to immunoglobulin forming immune complexes, despot small blood vessels triggering complement cascade and inflammation.

158
Q

example of type III hypersensitivity?

A

Arthurs reaction, serum sickness, farmers lung, many infections disease have immune complex component e.g) feline infectious peritonitis (FIP)

159
Q

what is type IV hypersensitivity?

A

antigen-specific effector T cells, soluble antigen cell associated antigens, mechanisms, macrophages ,eosinophils.
reaction: chronic asthma, allergic rhinitis, contact dermatitis, tuberculin reaction
Requires 100-1000x more antigen than type I

160
Q

what is cancer chemotherapy?

A

cytotoxic drugs used to target rapidly dividing cells. can also effect other dividing cells in git and bone marrow. can immunosupressrion from toxic effect.

161
Q

list/summary on the vaccine?

A

The vaccine contains an Ag. The Ag goes off to a lymph node. Ags are processed in dendritic cells and presented to the immune system. B cells are sensitised and helper T cells help them to multiply. Abs are produced by plasma cells. Class switching occurs when the concentration of antigen decreases since only the best B cells are selected for.

BVMS Module 2 (1 decks)

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