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Year 2 Semester 2 > Pathology > Flashcards

Pathology Flashcards

1
Q

What are the 4 types of amyloid?

A

AA (amyloid-associated) (seen in chronic inflammation)
AL (amyloid light chain)
B-amyloid protein
Islet amyloid polypeptide (cats)

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2
Q

What is platelet rolling mediated by?

A

P-selectin (on endothelium) or von Willebrand factor (on extracellular matrix)

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3
Q

For what 3 reasons may buccola mucosal bleeding time be abnormal?

A

Thrombocytopenia (check first)
Platelet dysfunction
Vascular disorders

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4
Q

When calculating buccola mucosal bleeding time, how soon after making the incision should pressure be applied?

A

10 mins

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5
Q

When performing a clot retraction test, an abnormal shrinkage result plus a normal platelet count is indicative of what?

A

Thrombocytopathia

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6
Q

What converts soluble fibrinogen to insoluble fibrin?

A

Thrombin

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7
Q

What are the 3 groups of coagulation factors?

What are they activated by?

A

Contact group (activated by contact with collagen)
Vitamin K dependant group (activated by other factors)
Highly labile fibrinogen group (activated by thrombin)

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8
Q

Where are most coagulation factors produced?

A

Liver

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9
Q

What is the average half life of most coagulation factors?

A

1-2 days

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10
Q

Which factor starts the intrinsic pathway?

A

XII

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11
Q

What is the end product of secondary hemostasis?

A

Cross-linked fibrin

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12
Q

What colour tube (and anticoagulant) is used most commonly for coagulation testing?

A

Blue top (citrate)

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13
Q

What test is performed for testing the extrinsic pathway?

A

Prothrombin time (PT)

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14
Q

What is the fibrinolytic pathway mediated by?

A

Plasmin

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15
Q

What can you measure that specifically indicates the breakdown of cross-linked fibrin?

A

D-dimers

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16
Q

Are clotting factors present in plasma or serum?

A

Plasma

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17
Q

What is albumin produced by?

A

Hepatocytes

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18
Q

What are globulins produced by?

A

Hepatocytes, B lymphocytes and plasma cells

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19
Q

Give 3 causes of decreased production of albumin

A
  1. Chronic liver disease (lack of hepatocytes to make albumin)
  2. Prolonged malnutrition (lack of precursor nutrients)
  3. Maldigestion (pancreatic enzyme deficiency; cannot digest precursor nutrients)
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20
Q

Give 3 causes of increased loss of albumin

A
  1. Kidney-glomerular leakage of albumin
  2. GI loss
  3. Burns
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21
Q

What happens to chylomicron remnants?

A

Travel to liver for uptake and degradation

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22
Q

Where is HDL formed?

A

Liver and intestinal epithelium

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23
Q

Lipaemia is primarily caused by increases in which two types of lipoprotein?

A

Chylomicrons

VLDLs

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24
Q

What are the functions of chaperones?

A

Interact with proteins
Aid with proper folding and transport
Facilitate degradation of proteins

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25
Q

What is the function of white blood cells (leukocytes)?

A

Destruction of microorganisms and removal of dead or damaged tissues

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26
Q

What is the function of platelets?

A

Haemostasis (stop bleeding)

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27
Q

Which blood cells live the longest?

A

Lymphocytes live weeks to years and may recirculate

RBCs live 1to >5 months

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28
Q

Which blood cell components have the shortest lifespan?
Why is it important to remember this?
Why should we care?

A

Neutrophils live 10 hours in the blood, and 24-48 hours in tissues
If there is a sudden arrest in haemopoiesis (formation of blood), neutropenia is the first thing we’d notice
A critical neutropenia may impair ability to fight infections

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29
Q 
How long do the following live for?
RBC
PLT
Lymphocytes
Monocytes
Neutrophils
A

RBC=1 to >5 months depending on species (160d cow, 150d sheep, 145d horse, 110d dog, 86d pig, 70d cat)
PLT=10 days
Lymphocytes=weeks to years, may recirculate
Monocytes=days
Neutrophils=10 hours in blood, 24-48 hours in tissues

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30
Q

What are the products of extravascular and intravascular lysis of RBCs?

A 
Extravascular= bilirubin
Intravascular= free haemoglobin
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31
Q

Give examples of haemopoietic tissue

A

Haemopoietic islands in yolk sac and aorta-gonad-mesonephros of embyro
Bone marrow
Liver, spleen, kidneys

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32
Q

Which cytokine plays a key role in growth, differentiation and activation of eosinophils?

A

IL-5 (interleukin-5)

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33
Q

What is the name of the hormone that controls erythropoiesis?

A

Erythropoietin (Epo)

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34
Q

Where is erythropoietin released from?

What does it stimulate?

A

Kidneys

Stimulates red bone marrow to produce RBCs

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35
Q

What name is given to juvenile red blood cells?

A

Reticulocytes

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36
Q

Which hormone mediates thrombopoiesis? (production of thrombocytes/platelets)
Where is it produced?

A

Thrombopoietin (TPO)

Liver

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37
Q

What effect does IL-6 (inflammation) and iron deficiency have on platelet production?

A

Increases it

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38
Q

When restraining an animal, why should you be quick and avoid the animal struggling?

A

To avoid platelet clumping and blood clots

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39
Q

What is the function of commensal bacteria?

Where are they found?

A

Prevent attachment of pathogenic bacteria and hence block their invasion and infection
Found on skin, and mucosal surfaces esp. GI and respiratory tracts

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40
Q

What name is given to the part of an antigen that the immune system recognises?

A

Epitope

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41
Q

Which 3 thymic hormones are produced in the cortex of the thymus?
Which cells produce them?

A

Thymosin, thymulin, thymopoietin

Producxed by reticular epithelial cells

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42
Q

Where does lymph flow?

A

Red bone marrow, lymphatic tissue and lymphatic vessels

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43
Q

What is the function of plasma?

A

Carries nutrients and waste products

Maintains fluidity

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44
Q

Which cell is the common precursor for all blood cells?

What does it immediately differentiate into?

A

Pluripotent stem cell

Lymphoid stem cell or myeloid stem cell

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45
Q

What cells are found in the storage pool?

A

Mature neutrophils

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46
Q

Which cells are found in the proliferative pool?

A

Monoblasts, myeloblasts, megakaryoblasts, rubriblasts

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47
Q

Which cells would you find in the maturation pool?

A

Monocytes, metamyelocytes, neutrophils, basophils, eosinophils, metarubricytes, reticulocytes, megakaryocytes

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48
Q

What is a metarubricyte?

A

Nucleated RBC

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49
Q

How are platelets produced?

A

Fragmentation of megakaryocyte cytoplasm and shedding into blood

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50
Q

A complete haemogram should include which 3 lab tests?

A

Centrifugation of microhaematocrit tube
Blood counts
Blood smear evaluation

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51
Q

Iron deficiency causes which type of anaemia?

A

Microlytic anaemia (small erythrocytes)

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52
Q

When does cell division of erythrocytes stop?

A

When optimal intracellular Hb concentration is reached

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53
Q

Why are smaller red blood cells produced in iron deficiency?

A

An extra cell division occurs before the critical cytoplasmic Hb concentration is reached that is necessary to stop DNA synthesis and cell division

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54
Q

Where is red bone marrow found in large mammals?

A

Spine, vertebrae, sternum and hip bones

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55
Q

What doe CFU stand for?

A

Colony-forming unit

Give rise to blasts which eventually evolve into mature cells

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56
Q

Which cells are granulocytes?

A

Neutrophils, eosinophils, basophils

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57
Q

Name the 3 primary growth factors which cause differentiation of granulocytes and monocytes

A

GM-CSF (granulocyte and monocyte differentiation)
M-CSF (monocyte development)
G-CSF (granulocyte development)

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58
Q

If basophils are seen in circulation, what are they usually seen with?

A

Eosinophils

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59
Q

Describe the regulation of erythropoiesis

A

Hypoxia due to reduced RBC count, decreased availability of O2 to blood or increased tissue demand for O2.
Kidney releases erythropoietin
This stimulates red bone marrow to produce RBCs
Increases O2 carrying ability of the blood

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60
Q

How many days does it take from RBC stem cell to reticulocyte release?

A

5 days

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61
Q

Do juvenile RBCs contain a nucleus?

A

No, but they do contain residual RNA and organelles

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62
Q

Where do reticulocytes migrate to?

A

Through transient apertures in endothelial cells into venous sinuses
Mature after 24 hours in blood

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63
Q

What morphological changes would we see with accelerated erythropoiesis?

A

Polychromasia, reticulocytosis

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64
Q

How is thrombopoietin production and clearance controlled?

A

Produced constantly, mainly by liver
Cleared by receptor-mediated uptake and destruction by platelets and megakaryocytes
However, interleukin 6 can increase TPO synthesis, independent of PLT numbers. Iron deficiency increases thrombopoiesis independently of TPO

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65
Q

What is MCV?

A

Mean corpuscular volume

Average erythrocyte size

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66
Q

What is MCHC?

A

Mean corpuscular Hb concentration

Average erythrocyte Hb concentration

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67
Q

What is MCH?

A

Mean corpuscular Hb
Average erythrocyte Hb per cell
Hb/RBC

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68
Q

What kind of anaemia is present if there is raised MCV?

What about reduced MCV?

A 
Macrocytic anaemia (presence of larger cells which are usually juvenile RBCs-regenerative anaemia)
Microcytic anaemia (production of small erythrocytes, likely due to less haemoglobin available for erythropoiesis caused by iron deficiency)
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69
Q

What kind of anaemia is seen with reduced MCHC?

A

Hypochromic anaemia

Seen with regeneration (juvenile RBCS have lower Hb concentration) or iron deficiency

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70
Q

Which stains could you use to identify reticulocytes?

A

Routine Wright’s

New Methylene Blue (stains RNA in ribosomes)

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71
Q

How do you calculate an absolute reticular count?

A

% retic x RBC (10^12/L) x 10

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72
Q

Which values for absolute reticular count in dogs and cats are a sign of non-regenerative anaemia?

A

Dog

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73
Q

What is the general term for abnormal RBC shape?

A

Poikilocytosis

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74
Q

What are the causes of regenerative anaemia?

A

Blood loss

Haemolysis (destruction of RBCs)

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75
Q

What are the causes of non-regenerative anaemia?

A

Decreased production
Lack of erythropoietin
Chronic inflammation

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76
Q

What is blood loss anaemia?

A

Proportional loss of all blood components (plasma and cells)
Can be acute or chronic
1. Initial decrease of blood volume, while proportion of plasma and cells is maintained. Hct and TP are unchanged
2. Within a few hours, activation of mechanisms to maintain volaemia -> influx of H2O from extracellular space -> dilution -> reduction of Hct and total protein
(Hct-ratio of volume of RBCs to a given volume of blood)

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77
Q

What are 2 causes of blood loss anaemia?

A

Haemorrhage

Blood-sucking parasites

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78
Q

Presence of spherocytes is strongly supportive of what?

A

Immune-mediated haemolytic anaemia
Macrophages partially phagocytise RBCs at the part of the membrane where the antigen-antibody complex is, causing loss of the discoid shape

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79
Q

What is agglutination?

A

Antibody-mediated clumping of RBCs

Stongly supportive of immune-mediated haemolytic anaemia

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80
Q

What is rouleaux formation?
What is it caused by?
In which species is it normal?

A

Stacking of RBCs due to increased plasma proteins coating RBCs
Caused by inflammation, cancer
Horses and cats

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81
Q

How can you differentiate between agglutination and rouleaux formation?

A

Saline agglutination test

Add 9 drops of saline to 1 drop of blood. Rouleaux formation will disappear, whereas agglutination persists

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82
Q

Which values for WBC in a single field are indicative of leucopenia and leucocytosis?

A

If 50 WBC in a single LPF10x field then likely leucocytosis

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83
Q

What do we look for at the tail end of a blood smear?

A

Platelets

Erythrocytes will be ruptured here

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84
Q

Give some causes of neutropenia

A 
Severe inflammation 
Bone marrow disease eg neoplasia, immune-mediated destruction of precursors 
Overwhelming tissue demand
Reduced bone marrow production 
Increased destruction of neutrophils
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85
Q

What is left shift?

What causes it?

A

Increased number of juvenile neutrophils (band or earlier stages) released from bone marrow
Due to severe acute inflammation
(Also bacterial infection, immune-mediated disease (e.g. IMHA))

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86
Q

What causes monocytosis? (monocyte count above upper reference limit)

A

Chronic inflammation / tissue damage / necrosis (usually combined with neutrophilia)
‘Stress leucogram’ or steroid administration (combined with neutrophilia, lymphopenia and eosinopenia)
Leukaemia

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87
Q

What causes lymphocytosis? (Lymphocyte count above upper reference limit)

A

Chronic inflammation
Adrenaline release in cats
Leukaemia

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88
Q

What causes lymphopenia? (lymphocyte count below upper reference limit)

A 
Chronic inflammation (seen with neutrophilia)
Stress leucogram (effect of prolonged steroid in blood)
Viral disease eg FIV, FIP
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89
Q

What causes eosinophilia? (eosinophil count above upper reference limit)

A

Parasitic disease

Allergy

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90
Q

What is toxic change?

What is it due to?

A 
Increased basophilia (blue colour) of the cytoplasm, blue granules (Dohle bodies), vacuoles (foamy appearance)
Due to reduced maturation time because of intense stimulation of myelopoiesis. Seen in overwhelming inflammation
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91
Q

What is the average value for platelet count?

A

150-500 x 109/L

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92
Q

Platelet clumps are most common in which species?

A

Feline and bovine

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93
Q

Give 4 causes of thrombocytopenia

A 
Increased destruction
Increased consumption (intravascular coagulation)
Decreased production (destruction of megakaryocytes in bone marrow)
Redistribution/sequestration (splenomegaly-abnormal enlargement of the spleen-platelets are temporarily entrapped within the spleen but are still able to bind Thrombopoietin, so bone marrow is not stimulated)
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94
Q

What is immunomodulation?

Why would we want to use it?

A

Modification of the immune response

Reduce inflammatory response
Reduce allergic response
Treat neoplasia of the immune system
Enhance immune response to infection
Suppress inappropriate immune response (immune mediated diseases)
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95
Q

How does an immune mediated disease occur?

A

Something happens to prevent recognition of self-antigens
Immune response is directed towards own tissues
If no detected underlying cause, can be referred to as ‘autoimmune’

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96
Q

Which immune system does immunosuppressive drugs act on?

What do they do?

A

Adaptive

Reduce lymphocyte proliferation or limit their effect

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97
Q

What are the 3 main groups of immunosuppressive drugs?

A

Drugs which inhibit DNA synthesis
Drugs which inhibit IL-2 production/action
Drugs which inhibit cytokine gene expression

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98
Q

What is IL-2 produced by?

What does it do?

A

Th cells (CD4+)
Stimulates:
Clonal proliferation of T cells, humoral immunity (B cell activity) and innate immune cells (macrophages, NK cells)

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99
Q

What is cyclosporin used for?

What is it metabolised by? Excretion?

A

Immunosuppressive drug. Inhibits IL-2 and therefore causes decreased proliferation of cytotoxic cells, decreased B cell responses and decreased T cell function in hypersensitivity reactions.
Metabolised by liver (cytochrome P450). Metabolites excreted in bile.

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100
Q

Glucocorticoids are synthetic versions of what?

What do they do?

A

Cortisol
Stimulate neogenesis
Suppress inflammation. Immunosuppressive.
Reduce clonal proliferation of CD4+ cells (T helper cells)

Binds intracellular receptor which migrates to nucleus and modifies transcription-reduces transcription of IL-2 gene and other cytokine genes

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101
Q

Why must glucocorticoid treatment be withdrawn very slowly?

A

Glucocorticoids suppress the HPA (hypothalamus-pituitary-adrenal gland) axis; recovery of adrenal function can take months

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102
Q

What is the function of drugs which inhibit DNA synthesis?

Give 3 examples

A

Inhibit synthesis of purines and/or pyrimidines
Suppress B and T cells
Azathioprine (inhibits DNA and RNA synthesis-disrupts mitosis and cell metabolism)
MMF (mycophenolate mofetil) (selective suppression of B and T cell proliferation)
Leflunomide (inhibits T and B cell proliferation)

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103
Q

What is carprofen?

A

NSAID

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104
Q

What is histamine produced by?

What is its release caused by?

A

Basophils and mast cells

Release is caused by IgE binding to Fc receptors on mast cells

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105
Q

What is the function of COX-1 and COX-2?

A

Enzyme involved in prostaglandin biosynthesis. Converts free arachidonic acid to prostaglandin
Present at sites of inflammation. Promotes production of mucus in stomach and reduces acid secretion.
Inhibited by NSAIDs eg aspirin

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106
Q

What is the difference between COX-1 and COX-2?

A

COX-1 is produced under any conditions. It has protective uses like production of stomach mucus, secretion of bicarbonate and reducing gastric acid secretion. Found in the stomach, kidney, platelets.
COX-2 is only produced under certain conditions like inflammation. It causes production of prostaglandins which cause pain and inflammation, and pyrexia. Located in monocytes, macrophages, leukocytes.

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107
Q

Why would we want to inhibit COX enzymes?

A

COX enzymes convert arachidonic acid to prostaglandins
Prostaglandins play a key role in development of pain and inflammation
Therefore by inhibiting COX, we get relief from pain and inflammation

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108
Q

Give some examples of NSAIDs

A 
Oxicans (eg meloxicam)
Coxibs (eg celecoxib)
Propionates (eg carprofen)
Pyrazolones (eg phenylbutazone)
Salicylates (eg aspirin)
P-aminophenols (paracetamol)
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109
Q

What are the adverse effects of NSAIDs?

A

Stomach ulcers
GI bleeding
Anaemia

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110
Q

What is metastasis?

A

Movement of cancerous cells to other parts of the body

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111
Q

Why are smaller tumours more sensitive to chemotherapy?

A

Cells are dividing more quickly so are more sensitive

Larger tumours have more G0 cells (not dividing) so are less sensitive

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112
Q

Explain the 2 theories as to why some tumours are resistant to chemotherapy?

A
  1. Goldie-Coldman theory:
    Detectable tumours are heterogenous. High likelihood that some of the cells will be resistant. Chemo can’t kill the resistant cells, which then multiply and quickly make up the majority of the population
  2. Stem cell theory:
    Chemo kills daughter cells. Stem cells naturally resistant. Tumour proliferation rate greater than chemo kill rate due to required inter-treatment recovery interval
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113
Q

How do you measure drug dose intensity?

A

Drug dose per unit time

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114
Q

What are the 2 broad categories of chemotherapy?

A
  1. Damages DNA (cell cycle non-specific)

2. Inhibits DNA replication (cell cycle specific)

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115
Q

What are the general side effects of chemotherapy?

A

BAG
Bone marrow-lowest WBC count typically after 7-10 days
Alopecia- uncommon except in a few breeds
Gastrointestinal-usually lasts longer than the first 4 days

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116
Q

What is the function of alkylators (chemotherapy drugs)?
How are they metabolised?
Give some examples
Give some possible side effects

A

Bind DNA and insert an alkyl group, leading to a change in structure. Inhibits transcription and replication, leading to apoptosis if the lesion is not repaired.
Metabolised by liver, excreted by kidneys
Melphalan, Cyclophosphamide, Lomustine
Side effects: Low WBC count -> GI problems, cystitis (Cyclophosphamide), hepatic toxicity (Lomustine)

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117
Q

What is the function of vinca-alkaloids (chemotherapy drugs)?
How are they metabolised?
Give some examples
Give some possible side effects

A

Either bind to or inhibit formation of microtubules thus preventing the formation of the mitotic spindle. Cell cycle specific-cells die in M phase by are most sensitive in S phase.
Metabolised to active forms in liver, excreted in bile.
Vincristine, Vinblastine.
Side effects: GI effects, low WBC counts, perivascular irritation of drug goes outside the vein

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118
Q

What is the function of anti-tumour antibiotics (chemotherapy drugs)?
How are they metabolised?
Give some examples
Give some possible side effects

A

3 mechanisms of action:
1. Topoisomerase inhibition -> DNA strand breaks
2. Intercalation with DNA -> Prevents transcription
3. Free radical formation -> DNA damage
Cycle non-specific
Metabolised to active forms in the liver (via hydrolysis), excreted in bile
Doxorubicin, Epirubicin
Side effects: Anaphylaxis, GI problems, low WBC count, severe perivascular irritation if drug goes outside the vein, kidney damage (cats), cumulative cardiotoxicity (dogs)

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119
Q

What is the function of platinating agents (chemotherapy drugs)?
How are they metabolised?
Give some examples
Give some possible side effects

A

Insert a platinum group into DNA. Transcription and replication are inhibited, cells die if lesion is not repaired
Mainly excreted unchanged by kidneys
Carboplatin
Myelosuppression, occasional GI toxicity, rare kidney toxicity

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120
Q

What is the function of anti-metabolites (chemotherapy drugs)?
How are they metabolised?
Give some examples
Give some possible side effects

A

Interact with DNA production pathways. Cell cycle specific to S phase.
Cytosine arabinoside, Methotrexate.
Cytosine arabinoside is metabolised by liver, plasma and peripheral tissues. Excreted by kidneys.
Methotrexate is metabolised by normal and malignant tissues, peripheral tissues. Excreted by kidneys.
Side effects: myelosuppression, GI side effects, hepatic dysfunction (cytosine)

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121
Q

Give some examples of biotherapy (cancer treatment)

A

Glucocorticoids, NSAIDs, receptor tyrosine kinase inhibitors, immunotherapy

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122
Q

How does metronomic chemotherapy work?

A

Targets supporting cells of a tumour (not specific tumour cells)
Reduces new blood vessel formation, and numbers of regulatory T cells supporting the tumour
Most use a combination of an NSAID with cyclophosphamide (alkylator)

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123
Q

List 3 chemotherapy drugs which act in a cell cycle specific manner

A

Vinca-alkaloids eg Vinblastine, Vincristine

Anti-metabolites eg Methotrexate, Cytosine arabinoside

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124
Q

List 3 chemotherapy drugs which act in a cell cycle non-specific manner

A

Alkylators eg Melphalan, Cyclophosphamide, Lomustine
Anti-tumour antibiotics eg Doxorubicin, Epirubicin
Platinating agents eg Carboplatin

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125
Q

Which tumour type can L’asparaginase work against?
In which species is it more effective?
How does it work?

A

Lymphoma
Dogs
Converts L’asparaginase to to L’aspartic acid. Malignant lymphocytes are dependent on asparagine therefore it causes lymphocyte death

126
Q

What is the definition of immunity?

A

The process which allows the recognition and removal of non-self material which enters the body

127
Q

What is the difference between innate and adaptive immunity?

A

Innate: Non-specific. Body’s first line of defence. Rapid onset. Phagocyte-mediated. No protective immunity.
Adaptive: Shows specificity and memory. Slower. Lymphocyte-mediated. Protective immunity possible. Activated.

128
Q

What are defensins?

A

Small peptides secreted by cells, particularly in skin, which directly attack bacteria, viruses and fungi.
Part of innate immunity

129
Q

What are lysozymes?

A

Enzymes found in many bodily secretions. They are capable of digesting cell wall proteoglycans and thereby destroying microorganisms.
Part of innate immunity

130
Q

What is the function of the myeloperoxidase system?

A

Produces toxic oxygen and chlorine products which kill bacteria. Produced by phagocytes. Part of innate immunity.

131
Q

What are acute phase proteins?

A

A group of proteins whose serum concentration rises rapidly shortly after infection. For example, C-reactive protein which is produced by liver in response to release of endogenous pyrogen (IL-1) from macrophages. It binds to bacterial cell walls and can activate the complement cascade, thereby promoting bacterial destruction.
Part of innate immunity

132
Q

What are interferons?

A

A family of glycoproteins which are produced in response to viral infection. 3 types: IFNα, IFNβ and IFNγ. IFNα and IFNβ are produced by many cell types, whilst IFNγ is produced only by activated T cells.
Stimulate NK cell activity and promote differentiation of B lymphocytes.
Act as a link between innate and adaptive immune systems

133
Q

Mast cells have receptors for which antibodies?

134
Q

Macrophages and neutrophils have receptors for which antibodies?

135
Q

Which cells do NK cells kill?

A

Tumour cells, virally-infected cells, antibody-coated cells

Part of innate immunity

136
Q

What are antigens?

A

Molecules identified by the host as foreign, and to which the host reacts in an attempt to protect itself from infection and subsequent damage

137
Q

What is immunogenicity?

A

The ability of an antigen to stimulate an immune response

Related to its molecular size

138
Q

Where do B and T lymphocytes mature?

A

B lymphocytes: bone marrow (and Bursa of Fabricus in birds)

T lymphocytes: thymus

139
Q

What do B cells differentiate into?

A

Plasma cells, which synthesise and secrete antibodies. Humoral immunity.

140
Q

Give 3 examples of antigen-presenting cells

A

Macrophages
Dendritic cells
B cells

141
Q

Where do antigen fragments come from and how do they result in antigen-presenting cells?

A

Antigen fragments are produced by degradation of the antigenic organism/material. The most obvious site for this is in lysosomes in macrophages where components of the large antigen, mainly the proteins, are only partially digested. Peptide fragments are then returned to the macrophage cell surface where they are presented to lymphocytes.

142
Q

What are the primary lymphoid organs?
What are the secondary lymphoid organs?
What happens at each?

A

Primary=(Bursa of fabricus in birds), bone marrow and thymus. Here, T and B cells mature into Ag-recognising cells. Lymphocytes acquire Ag-specific receptors.
Secondary=spleen and lymph nodes. Here, Ag-driven lymphocyte proliferation and differentiation takes place.

143
Q

Describe the structure of the thymus

A

Connective tissue capsule. Internal framework of long thin processes of epithelial cells in which macrophages and dividing immature and mature T cells are scattered. The thymus is divided into an outer cortex where lymphocytes are densely packed, and an inner medulla where the epithelial-like cells predominate. The medulla also contains Hassall’s corpuscles. Invaginations of the connective tissue capsule divide the cortex, but not medulla, into lobes. The thymus is seeded with immature T cells from BM which mature and leave via postcapillary venules in the medulla.

144
Q

Why does the thymus degenerate with age?

A

The thymus loses its role once all secondary lymphoid tissues have been richly seeded with mature T cells, which are then capable of dividing

145
Q

Describe the flow of lymph through a lymph node

A

Lymph enters via many afferent lymphatic vessels, which penetrate the convex surface of the capsule. It then filters through the tissue of the node and is drained by a few efferent lymphatic vessels leaving from the concave surface

146
Q

What are trabeculae (in lymph nodes)?

A

Extensions of the capsule into the cortex to give mechanical support

147
Q

In which part of the lymph node do B and T cells congregate?

A

B cells: cortex

T cells: paracortical zone (junction of cortex and medulla)

148
Q

What are germinal centres in lymph nodes?

A

Pale-staining areas consisting of blast-like cells which are activated B cells.

149
Q

Describe the structure of the spleen

A

Capsule of connective tissue (or in some species such as cat, smooth muscle). Internal framework of reticular fibres containing macrophages and antigen-presenting cells. Trabeculae extend in from capsule to give internal support. Internal structure is divided into red and white pulp. Blood enters via trabecular arteries. Branches leave the trabeculae and enter the tissue of the spleen where they are immediately surrounded by a periarterial sheath (PALS). These arteries are called central arteries.Venous drainage is via trabecular veins.

150
Q

What is contained in the red pulp of the spleen?

A

Open sinusoids containing RBCs

151
Q

What is contained in the white pulp of the spleen?

A

Areas of lymphocytes aggregated in PALS around central arteries

152
Q

Name some permanent sites of lymphocyte aggregation

A

Tonsils (palatine, lingual, pharyngeal)

Peyer’s Patches in the ileum

153
Q

What are the 5 classes of immunoglobulin?

A

IgG, IgM, IgA, IgD, IgE

154
Q

What holds the heavy and light chains together in an immunoglobulin?

A

Disulphide bonds

155
Q

What are the 2 regions of an immunoglobulin?

A

Fab region: (fragment antigen-binding) variable region. Consists of 2 antigen binding sites, one at the end of each arm
Fc region: (fragment crystallisable) determines the biological activity, eg complement binding

156
Q

Antibody Switching
Which antibody is the first to be produced in response to an antigen?
Which is produced during the secondary response?

A

IgM (primary response)

IgG-has a higher affinity for the antigen and more biological activities than IgM. Secreted by memory cells

157
Q

Which is the main antigen in serum?

158
Q

Where is IgA found?

A

Mucosal surfaces and in mucosal secretions

159
Q

What are the functions of antibodies?

A

Neutralise by preventing pathogen attachment, invasion of host cells, replication, toxin production
Activate complement system
Opsonisation by Fc receptors and complement receptors
Cytotoxicity of antibody-coated cellular antigens by killer lymphocytes

160
Q

What are the sites of action of IgG and IgM, IgA, IgE, and IgD?

A

IgG and IgM: function in lymphoid tissues, in the circulation and in tissues
IgA: works at mucosal surfaces which it almost coats, by preventing foreign antigens getting into tissues by preventing attachment to endothelial surfaces
IgE: found at v. low levels in circulation. Mostly attached to mast cells which have specific IgE receptors. When IgE meets its specific antigen, it causes mast cells to degranulate and release inflammatory molecules eg histamine
IgD: found in trace amounts. No known protective function

161
Q

What percentage of T cells survive the thymic journey?

A

5%

Removes most self-reactive T cells

162
Q

What are high endothelial venules (HEV)?

Where are they located in the lymph node?

A

Post-capillary cells in secondary lymphoid tissues
Enable lymphocytes to leave the blood supply and enter lymph tissues eg lymph nodes
Located in the paracortex

163
Q

Where is mucosa-associated lymphoid tissue located?

A

GI tract, respiratory tract, genito-urinary tract

Tonsils, Peyer’s patches, appendix

164
Q

Explain phagocytosis

A
  1. Attachment of eg bacteria by non-specific receptors to phagocyte
  2. Phagosome forms around the bacteria
  3. Lysosome fusion and killing. Digestion.
  4. Release of microbial products
165
Q

What are the 3 complement cascades?

A

Classical
Lectin
Alternative

166
Q

What is the central event in complement activation?

A

Cleavage of C3

167
Q

How is the lectin pathway (of complement) initiated?

A

Starts with mannan-binding lectin (MBL) or ficolin binding to certain sugars on bacteria, viruses and fungi. This binding leads to the cleaving of C2 and C4 to activate C3.
MBL is a pattern recognition receptor; a protein produced by the liver

168
Q

Explain the alternative pathway of complement

A

Surface components of certain bacteria and parasites are able to directly activate C3, resulting in C3b generation. This is then stabilised by factors B and D, and the activated C3b then acts as an enzyme, C3b convertase, which activates further C3 and converts it to C3b. This cycle is inhibited by factor H, however a number of foreign components including bacterial walls, helminths and endotoxins bind factor H and remove this inhibitor. As a result, C3 activation occurs, and membrane-bound C3b can cause C5-C9 activation, leading to cell lysis.

169
Q

Name some initiators of the alternative pathway of complement activation

A 
Pathogen components:
Many gram-negative bacteria
Lipopolysaccharides from gram-negative bacteria
Many gram-positive bacteria
Fungal cell walls
Some viruses and parasites

Non-pathogens:
Complexed IgG and IgA
Anionic polymers
Pure carbohydrates

170
Q

What are the biological effects of complement?

A

Cell lysis: C5-C9 MAC
Neutralisation of bacterial/viral attachment to host tissues, prevention of tissue invasion, presentation of pathogen replication, prevention of toxin release
Opsonisaton: antigens become coated with C3b, making them more likely to be taken up by phagocytes
Inflammatory response: C3a and C5 proteins increase vascular permeability at site of infection, activate neutrophils and cause mast cell degranulation, which releases vasoactive amines that induce smooth muscle contraction, leading to signs of inflammation eg redness, swelling, heat, pain
Clearance of immune complexes
However, can cause damage to host tissue eg if immune complexes are deposited

171
Q

Why is it good that C3a and C5 cause increased vascular permeability?

A

Increased permeability causes increased fluid leakage from blood vessels and leakage of immunoglobulins and complement molecules. Increased migration of PMNs and macrophages and their microbicidal activity.

172
Q

What are the control mechanisms for complement?

A

Lability (breaks down quickly)
All cells have surface protection by specific complement receptor molecules (Factor I and H cleave C3) (C3b receptor on RBCs)
C1 inhibitor binds C1r and so stops C2/4 binding

173
Q

What are PAMPs?

A

Pathogen-associated-molecular-patterns

Molecules on pathogens (mainly bacteria) recognised by receptors on cells of innate immune response (PPRs)

174
Q

What are PPRs?

Where are they found?

A

Pattern recognition receptors
Primitive part of innate immune system
Found on phagocytes and mast cells
Identify and bind PAMPs

175
Q

Where are T cells distributed?

What about B cells?

A

T cells: lymph node paracortex, spleen PALS

B cells: lymph node cortex, splenic follicles (germinal centres)

176
Q

What are the 2 types of T lymphocyte?

What percentage of each make up the total number of T cells>

A 
Th cells (T helper): CD4+, assist both antibody production and cytotoxic T cell effects. 65%
Tc cells (cytotoxic T cells): CD8+, kill infected host cells and tumours. 35%
177
Q

What are the 2 types of T cell receptor?

A

TCRαβ and TCRγδ (less common)

178
Q

What are the 2 classes of MHC gene?

A 
MHC class I: presents Ag to Tc cells (enables killing of infected host cells). Expressed on most nucleated cells.
MHC class II: presents Ag to Th cells (assists Ab production and Tc activity). Expressed on macrophages, APCs, B cells, activated T cells.
179
Q

Explain the 2 pathways for antigen processing

A 
Endogenous: HOST CELLS process infective agents and express on cell surface with MHC class I. Targeted by Tc cells-host cell killed.
Exogenous: MACROPHAGES etc digest infective agent and produce peptides to present on surface MHC Class II, or to be picked up by other cells eg dendritic cells to present to Th cells to activate them.
180
Q

Explain the 2 processes of T cell selection in the thymus

A

The first is positive selection where cells which recognise MHC antigens are allowed to survive and pass towards the medulla. Those which don’t die by apoptosis
The second is where T cells which have antigenic specificity for self-antigens are destroyed, again by apoptosis.
Eliminates 95% of T cells

181
Q

What are cytokines?

A

Intercellular hormones, secreted by one cell to influence another
Interleukins= from leukocytes
Control immune responses and inflammation

182
Q

What do antigen-presenting cells secrete to activate Th cells and encourage their proliferation?

183
Q

What are the 2 types of Th cells?

A

Th1: assist T cells functions eg macrophages, Tc cells. Used in intracellular infections (as antibodies can’t penetrate cell)
Th2: assist B cells to make antibodies. Used in extracellular infections

184
Q

What do NK cells recognise and induce?

A

Recognise cells without MHC Class I. Common with tumours, as tumour cells often lose MHC1 as they grow.
Induces apoptosis.

185
Q

Which 2 breeds have a complement deficiency?

A

Finnish Landrace Lambs
Brittany Spaniels-congenital autosomal recessive disease
C3 deficiency
Leads to bacterial infections, glomerulonephritis in lambs

186
Q

What are the 4 phases of the immune response?

A
  1. Recognition phase: Binding of foreign Ag to specific receptors on lymphocytes
  2. Activation phase: Lymphocyte proliferation, differentiation and migration
  3. Effector phase: Lymphocytes act to eliminate antigen. Production of antibodies, complement, cytokine production (to enhance function of phagocytes and stimulate inflammation)
  4. Memory phase: Lymphocytes with high affinity for antigen are in correct site if there is repeat infection
187
Q

What is the function of Tregs? (regulatory T cells)

A

has surface CD4+
Switches off immune responses
Prevents autoimmunity
Selected in thymus

188
Q

What is inflammation?

A

A complex reaction to injurious agents such as microbes and damaged (usually necrotic) cells that consists of vascular responses, migration and activation of leukocytes and systemic reactions

189
Q

What are virus-neutralising antigens?

A

Antigens which produce a virus-neutralising antibody response
Generally structured viral proteins
Found on the outer surface of a virus
Important for reduction of infectivity

190
Q

What are the mechanisms of virus-neutralising antigens?

A

Prevention of virus attachment
Morphological damage to virus
Inhibition of virus uncoating
Inhibition of virus replication

191
Q

What are the 2 types of virus?

A

Live-can be attenuated, a genetic modification, or a naturally-occurring avirulent strain
Killed- unactivated products

192
Q

What are the advantages and disadvantages of using live vaccines?

A

Advantages: humoral and cell-mediated immune responses are stimulated, more rapid protection
Disadvantages: can cause the disease, reversion to virulence

193
Q

What are the advantages and disadvantages of using killed vaccines?

A

Advantages: humoral immunity (antibodies), adjuvants (enhance ability to protect against infection), no reversion to virulence
Disadvantages: less immunogenic (less likely to produce an immune response)

194
Q

Give some reasons why a vaccine might have a lack of efficacy

A

Disease may be produced by a pathogen not in the vaccine
Vaccine production failure
May have been stored or administered incorrectly
Vaccines not 100%
Immunosuppression
Interference from MDA
Overwhelming infection
Animal is already a carrier and is showing chronic or recrudescent disease

195
Q

Give some reasons why a vaccine may have adverse reactions

A

Vaccine given by wrong route
Lack of attenuation or inactivation
Reaction to adjuvant
Immunocompromised animal may react to attenuated strain
Animal may already be incubating disease at time of vaccination

196
Q

What is an adjuvant?

How does it work?

A

A substance that enhances the body’s immune response to an antigen.
It works by increasing cytokine synthesis (enhanced T cell activity) and enhancing antigen presentation (enhanced B and Tc cell activity), leading to enhanced immunity

197
Q

Which immunoglobulins are the main protective antibodies stimulated by vaccination?

A

IgG and IgA

198
Q

What are the critical properties of vaccines?

A

Stimulation of antigen-presenting cells
Both T and B cells stimulated
Helper and effector responses to several epitopes
Vaccine antigen should persist in appropriate sites in lymphoid tissues

199
Q

What is the difference between active and passive immunity?

A

Passive: can be natural (maternally-derived in colostrum or via placenta) or artificial (injection of antibodies from resistant to susceptible animal). No cell-mediated immunity; antibodies only. Immediate protection but only for a few weeks as antibodies wane in recipient. Risk of hypersensitivity with foreign serum.
Active: can be from natural infection or artificial immunisation. Cell-mediated immunity.

200
Q

When should you not vaccinate?

A

If there is poor/artificial immunity
Immunity does not stop infection (ie get disease carriers)
Antibodies contribute to disease
Causes disease by infection
Vaccine antigens interfere with serodiagnosis

201
Q

What are some pros and cons of living vs inactivated vaccines?

A

Living vaccines: few inoculating doses required, adjuvants unnecessary, relatively cheap, less chance of hypersensitivity, induction of interferon
Inactivated vaccines: stable on storage, unlikely to cause disease through residual virulence, unlikely to contain contaminating organisms, safer than live vaccines, have to be administered more often

202
Q

What are the 5 kinds of virus vaccines?

A 
Modified live virus
Inactivated virus
Purified subunits
DNA vaccine
Recombinant product (broken down)
203
Q

How do DNA vaccines work?

A

Cloned microbial DNA is inserted into plasmid
Cloned DNA integrates into cell genome
Cell synthesises microbial antigen
Antigen is processed and presented to T cells

204
Q

Around birth, activity of which cell type is impaired and why?

A

Macrophage, due to increase in glucocorticoids

205
Q

What is meant by tolerance to a disease (by a foetus)?

Give some examples of such diseases

A

Lack of immune response to specific antigens, as foetus thinks they’re part of its own body
eg BHV, BVD, bluetongue

206
Q

What % of transfer of immunity to offspring is via placenta and colostrum in:
Dogs and cats
Ruminants, pigs and horses

A

Dogs and cats: 5% placental, 95% colostral

Ruminants, pigs and horses: 100% colostral

207
Q

What is the main colostral antibody?

The content of which antibody increases as colostrum production changes to milk?

208
Q

How do Igs end up in colostrum?

A

Active transfer of Igs from blood to mammary gland under hormonal influence (oestrogen and progesterone) and local production

209
Q

What is the primary immunoglobulin in non-ruminant milk?

210
Q

Calves and foals need a minimum of how much colostrum in which time period?

A

1L within 6 hours of birth

211
Q

Explain the species differences between absorption of Igs in colostrum of ruminants vs horses and pigs

A

Ruminants: all Igs absorbed by intestine
Horses and pigs: IgG and IgM are selectively absorbed; IgA stays in intestine (acts like an antibiotic lining)
Intestine is only permeable for a short period, declines after 6 hours, by 24 hours almost nil absorption

212
Q

When are the peak levels for circulating Igs reached in the neonate?

A

12-24 hours after birth

213
Q

What do IgG and IgA prevent?

A

IgG prevents septicaemia

IgA prevents enteric disease

214
Q

Why do non-suckled calves make antibodies sooner than suckled calves?

A

Maternally-derived antibodies inhibit Ab production

215
Q

How can you assess neonate Ig levels?

A

Zinc sulphate turbidity test (cloudier=precipitated protein of immunoglobulin)
Measure serum levels of Igs by radial immunodiffusion

216
Q

What is the difference between hyperplasia and hypertrophy?

A

Hyperplasia=increase in organ size due to increase in number of cells
Hypertrophy=increase in organ size due to increase in size of cells

217
Q

What is meant by metaplasia?

A

Reversible change-replacement of one adult cell type by another
Due to reprogramming of stem cells

218
Q

What are chaperones?

A

Interact with proteins, aid proper folding, transport and degradation of proteins

219
Q

What is haemosiderin a storage form of?

A

Iron

In tissues, ferritin is transferred to haemosiderin granules

220
Q

What are the causes of jaundice?

A

Excessive haemolysis
Severe hepatic injury
Obstructed bile flow

221
Q

What is hypercalcaemia seen with?

A 
Increased PTH secretion
Destruction of bone tissue
Vitamin D intoxication 
Renal failure (secondary hyperparathyroidism)
222
Q

What is an amyloid?

A

A pathological proteinaceous substance deposited between cells

223
Q

What factors cause cell injury?

A

Decreased O2 availability
Infectious agents
Immunological dysfunctions
Chemicals and toxins
Physical agents (trauma, temperature, pH, radiation)
Nutritional deficiencies
Genetic derangement (specific enzyme derangement)

224
Q

What are the effects of oxygen free radicals in cell injury?

A

DNA fragmentation
Protein cross-linking and fragmentation
Membrane lipid peroxidation

225
Q

Which enzymes are activated by increased intracellular Ca2+?

What are the consequences?

A

ATPase: decreased ATP
Phospholipase: decreased phospholipids
Endonuclease: nuclear chromatin damage
Protease: disruption of membrane and cytoskeletal proteins

226
Q

Give 4 potential causes of cell membrane damage that lead to irreversible injury

A

Progressive loss of membrane phospholipids due to activation of phospholipase by Ca2+
Cytoskeletal abnormalities due to activation of proteases and cell swelling
Toxic oxygen radicals after restoration of blood flow
Lipid breakdown products from phospholipid degradation
ULTIMATELY A MASSIVE INFLUX OF CALCIUM

227
Q

What is the difference between apoptosis and necrosis?

A 
Apoptosis= programmed cell death. Phagocytosis of apoptotic cells and fragments. No inflammation. Cells shrink. Plasma membrane stays intact. Cellular contents stay intact.
Necrosis= enzymatic digestion and leakage of cellular contents. Cells swell. Plasma membrane is disrupted. Cellular contents undergo enzymatic digestion.
228
Q

What are the 4 types of necrosis?

A

Coagulative necrosis: Hypoxic cell death, preservation of cell outline
Liquefactive necrosis: Enzymatic digestion, complete digestion of cells -> liquid mass
Caseous necrosis: Complete obliteration of tissue architecture, surrounded by inflammatory cell border
Fat necrosis: focal destruction of adipose tissue, released fatty acids combine with calcium

229
Q

Describe the morphology of apoptosis

A

1) Cell shrinkage
2) Chromatin condensation
3) Formation of cytoplasmic blebs and apoptotic bodies
4) Phagocytosis of apoptotic cells (by adjacent parenchymal cells and/or macrophages)

230
Q

Why do neurones have to die in an apoptotic way?

A

We don’t want inflammation of neurones in the brain. Instead they shrink and microglia quickly remove them.

231
Q

What is involved in primary haemostasis?

A

Formation of a platelet plug

232
Q

The release of what induces rolling of platelets and leukocytes?

A

P-selectin (from endothelial cells) on the endothelium

von Willebrand factor on the extracellular matrix

233
Q

What does von-Willebrand factor bind to?

A

Platelets and collagen

234
Q

Platelets adhere to endothelium via what?

A

GPI to von Willebrand factor or collagen

235
Q

How do platelets aggregate with other platelets?

A

GPIIb/IIa through fibrinogen or vWF bridges

236
Q

What do platelets release after activation?

A

Thromboxan, serotonin, factor V, ADP, ATP and plasminogen

237
Q

Give some examples of platelet agonists?

A

ADP, thrombin, collagen, PAF

238
Q

Secreted vWF serves as a carrier for which factor?

A

Factor VIII

239
Q

Where is vWF released from?

A

Endothelial cells

240
Q

The platelet plug is stabilised by strands of what?

241
Q

When doing a platelet count, how many platelets per hpf is considered normal?

242
Q

What is inflammation?

A

A complex reaction to injurious agents such as microbes and damaged (usually necrotic) cells that consists of vascular responses, migration and activation of leukocytes and systemic reactions

243
Q

What are virus-neutralising antigens?

A

Antigens which produce a virus-neutralising antibody response
Generally structured viral proteins
Found on the outer surface of a virus
Important for reduction of infectivity

244
Q

What are the mechanisms of virus-neutralising antigens?

A

Prevention of virus attachment
Morphological damage to virus
Inhibition of virus uncoating
Inhibition of virus replication

245
Q

What are the 2 types of virus?

A

Live-can be attenuated, a genetic modification, or a naturally-occurring avirulent strain
Killed- unactivated products

246
Q

What are the advantages and disadvantages of using live vaccines?

A

Advantages: humoral and cell-mediated immune responses are stimulated, more rapid protection
Disadvantages: can cause the disease, reversion to virulence

247
Q

What are the advantages and disadvantages of using killed vaccines?

A

Advantages: humoral immunity (antibodies), adjuvants (enhance ability to protect against infection), no reversion to virulence
Disadvantages: less immunogenic (less likely to produce an immune response)

248
Q

Give some reasons why a vaccine might have a lack of efficacy

A

Disease may be produced by a pathogen not in the vaccine
Vaccine production failure
May have been stored or administered incorrectly
Vaccines not 100%
Immunosuppression
Interference from MDA
Overwhelming infection
Animal is already a carrier and is showing chronic or recrudescent disease

249
Q

Give some reasons why a vaccine may have adverse reactions

A

Vaccine given by wrong route
Lack of attenuation or inactivation
Reaction to adjuvant
Immunocompromised animal may react to attenuated strain
Animal may already be incubating disease at time of vaccination

250
Q

What is an adjuvant?

How does it work?

A

A substance that enhances the body’s immune response to an antigen.
It works by increasing cytokine synthesis (enhanced T cell activity) and enhancing antigen presentation (enhanced B and Tc cell activity), leading to enhanced immunity

251
Q

Which immunoglobulins are the main protective antibodies stimulated by vaccination?

A

IgG and IgA

252
Q

What are the critical properties of vaccines?

A

Stimulation of antigen-presenting cells
Both T and B cells stimulated
Helper and effector responses to several epitopes
Vaccine antigen should persist in appropriate sites in lymphoid tissues

253
Q

What is the difference between active and passive immunity?

A

Passive: can be natural (maternally-derived in colostrum or via placenta) or artificial (injection of antibodies from resistant to susceptible animal). No cell-mediated immunity; antibodies only. Immediate protection but only for a few weeks as antibodies wane in recipient. Risk of hypersensitivity with foreign serum.
Active: can be from natural infection or artificial immunisation. Cell-mediated immunity.

254
Q

When should you not vaccinate?

A

If there is poor/artificial immunity
Immunity does not stop infection (ie get disease carriers)
Antibodies contribute to disease
Causes disease by infection
Vaccine antigens interfere with serodiagnosis

255
Q

What are some pros and cons of living vs inactivated vaccines?

A

Living vaccines: few inoculating doses required, adjuvants unnecessary, relatively cheap, less chance of hypersensitivity, induction of interferon
Inactivated vaccines: stable on storage, unlikely to cause disease through residual virulence, unlikely to contain contaminating organisms, safer than live vaccines, have to be administered more often

256
Q

What are the 5 kinds of virus vaccines?

A 
Modified live virus
Inactivated virus
Purified subunits
DNA vaccine
Recombinant product (broken down)
257
Q

How do DNA vaccines work?

A

Cloned microbial DNA is inserted into plasmid
Cloned DNA integrates into cell genome
Cell synthesises microbial antigen
Antigen is processed and presented to T cells

258
Q

Around birth, activity of which cell type is impaired and why?

A

Macrophage, due to increase in glucocorticoids

259
Q

What is meant by tolerance to a disease (by a foetus)?

Give some examples of such diseases

A

Lack of immune response to specific antigens, as foetus thinks they’re part of its own body
eg BHV, BVD, bluetongue

260
Q

What % of transfer of immunity to offspring is via placenta and colostrum in:
Dogs and cats
Ruminants, pigs and horses

A

Dogs and cats: 5% placental, 95% colostral

Ruminants, pigs and horses: 100% colostral

261
Q

What is the main colostral antibody?

The content of which antibody increases as colostrum production changes to milk?

262
Q

How do Igs end up in colostrum?

A

Active transfer of Igs from blood to mammary gland under hormonal influence (oestrogen and progesterone) and local production

263
Q

What is the primary immunoglobulin in non-ruminant milk?

264
Q

Calves and foals need a minimum of how much colostrum in which time period?

A

1L within 6 hours of birth

265
Q

Explain the species differences between absorption of Igs in colostrum of ruminants vs horses and pigs

A

Ruminants: all Igs absorbed by intestine
Horses and pigs: IgG and IgM are selectively absorbed; IgA stays in intestine (acts like an antibiotic lining)
Intestine is only permeable for a short period, declines after 6 hours, by 24 hours almost nil absorption

266
Q

When are the peak levels for circulating Igs reached in the neonate?

A

12-24 hours after birth

267
Q

What do IgG and IgA prevent?

A

IgG prevents septicaemia

IgA prevents enteric disease

268
Q

Why do non-suckled calves make antibodies sooner than suckled calves?

A

Maternally-derived antibodies inhibit Ab production

269
Q

How can you assess neonate Ig levels?

A

Zinc sulphate turbidity test (cloudier=precipitated protein of immunoglobulin)
Measure serum levels of Igs by radial immunodiffusion

270
Q

What is the difference between hyperplasia and hypertrophy?

A

Hyperplasia=increase in organ size due to increase in number of cells
Hypertrophy=increase in organ size due to increase in size of cells

271
Q

What is meant by metaplasia?

A

Reversible change-replacement of one adult cell type by another
Due to reprogramming of stem cells

272
Q

What are chaperones?

A

Interact with proteins, aid proper folding, transport and degradation of proteins

273
Q

What is haemosiderin a storage form of?

A

Iron

In tissues, ferritin is transferred to haemosiderin granules

274
Q

What are the causes of jaundice?

A

Excessive haemolysis
Severe hepatic injury
Obstructed bile flow

275
Q

What is hypercalcaemia seen with?

A 
Increased PTH secretion
Destruction of bone tissue
Vitamin D intoxication 
Renal failure (secondary hyperparathyroidism)
276
Q

What is an amyloid?

A

A pathological proteinaceous substance deposited between cells

277
Q

What factors cause cell injury?

A

Decreased O2 availability
Infectious agents
Immunological dysfunctions
Chemicals and toxins
Physical agents (trauma, temperature, pH, radiation)
Nutritional deficiencies
Genetic derangement (specific enzyme derangement)

278
Q

What are the effects of oxygen free radicals in cell injury?

A

DNA fragmentation
Protein cross-linking and fragmentation
Membrane lipid peroxidation

279
Q

Which enzymes are activated by increased intracellular Ca2+?

What are the consequences?

A

ATPase: decreased ATP
Phospholipase: decreased phospholipids
Endonuclease: nuclear chromatin damage
Protease: disruption of membrane and cytoskeletal proteins

280
Q

Give 4 potential causes of cell membrane damage that lead to irreversible injury

A

Progressive loss of membrane phospholipids due to activation of phospholipase by Ca2+
Cytoskeletal abnormalities due to activation of proteases and cell swelling
Toxic oxygen radicals after restoration of blood flow
Lipid breakdown products from phospholipid degradation
ULTIMATELY A MASSIVE INFLUX OF CALCIUM

281
Q

What is the difference between apoptosis and necrosis?

A 
Apoptosis= programmed cell death. Phagocytosis of apoptotic cells and fragments. No inflammation. Cells shrink. Plasma membrane stays intact. Cellular contents stay intact.
Necrosis= enzymatic digestion and leakage of cellular contents. Cells swell. Plasma membrane is disrupted. Cellular contents undergo enzymatic digestion.
282
Q

What are the 4 types of necrosis?

A

Coagulative necrosis: Hypoxic cell death, preservation of cell outline
Liquefactive necrosis: Enzymatic digestion, complete digestion of cells -> liquid mass
Caseous necrosis: Complete obliteration of tissue architecture, surrounded by inflammatory cell border
Fat necrosis: focal destruction of adipose tissue, released fatty acids combine with calcium

283
Q

Describe the morphology of apoptosis

A

1) Cell shrinkage
2) Chromatin condensation
3) Formation of cytoplasmic blebs and apoptotic bodies
4) Phagocytosis of apoptotic cells (by adjacent parenchymal cells and/or macrophages)

284
Q

Why do neurones have to die in an apoptotic way?

A

We don’t want inflammation of neurones in the brain. Instead they shrink and microglia quickly remove them.

285
Q

Platelets adhere to endothelium via what?

A

GPI to vWF or collagen

286
Q

Platelets aggregate with other platelets via what?

A

GPIIb/IIa through fibrinogen or vWF bridges

287
Q

Platelets can release what after activation?

A

Thromboxan, serotonin, factor V, ADP, ATP and plasminogen

288
Q

Name some platelet agonists

A

PAF, collage, ADP, thrombin

289
Q

What are vWF and P-selectin produced by?

A

Endothelial cells

290
Q

Define secondary haemostasis

A

Formation of the fibrin clot

291
Q

What are the 2 products of the coagulation cascade?

A

Thrombin (factor IIa) and insoluble fibrin

292
Q

The steps of the coagulation cascade are carried out in the presence of what?

293
Q

Which is the only factor involved in the extrinsic pathway of the coagulation cascade?

294
Q

What is the intrinsic pathway activated by?

A

Intravascular causes- exposed damaged endothelium

295
Q

What is the extrinsic pathway activated by?

A

Tissue factor released from damaged tissue

296
Q

Which factor (combined with free calcium ions) causes cross-linking of fibrin?

297
Q

Which coagulation factors are vitamin-K dependant?

A

II, VII, IX, X

2, 7, 9, 10

298
Q

Which coagulation factors are in the contact group?

A

XI, XII

11 and 12

299
Q

Which coagulation factors are in the highly labile fibrinogen group?

A

I, V, VIII, XIII

1, 5, 8, 13

300
Q

What is the preferred anticoagulant? Why?

A

Citrate as it forms an ionic bond with calcium that new added calcium can override

301
Q

Which lab tests can we do to test the intrinsic pathway?

A

PTT, ACT (more letters for more factors)

302
Q

Which lab tests can we do to test the extrinsic pathway?

A

PT (less letters for less factors)

303
Q

Which lab tests can we do to test the common pathway?

A

PTT, ACT, PT

TT

304
Q

Name some natural anticoagulants

A

Intact endothelium
Protein C
Antithrombin III

305
Q

What does antithrombin III limit?

A

Fibrin formation

Inhibits thrombin

306
Q

What can you measure that is evidence of fibrinolysis?

A

FDPs

Fibrin Degradation Products

307
Q

What is the difference between labile, stable and permanent cells?

A 
Labile= continuously dividing eg epidermis 
Stable= low levels of replication (G0), however, in response to stimuli undergo rapid division (G1) eg hepatocytes 
Permanent= non-dividing eg neurones
308
Q

What is the difference between agenesis and aplasia?

A 
Agenesis= absence of an organ or body part- no associated primordium (first trace of a structure)
Aplasia= failure of an organ to develop
309
Q

What is the difference between benign and malignant tumours?

A 
Benign= tumour remains localised and cannot spread. Slow growth.
Malignant= can invade and destroy adjacent structures and spread to different sites (metastasis) to cause death. Fast growth
310
Q

What do the suffix’s -oma and -sarcoma mean?

A
  • oma = benign tumour
  • sarcoma = malignant mesenchymal tumour (bigger and badder)
  • carcinoma = malignant epithelial tumour
311
Q

What is the difference between gram-positive and gram-negative bacteria?

A

Gram-negative have an outer membrane but gram-positive don’t

Year 2 Semester 2 (16 decks)

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