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PVS > Pathology 3 > Flashcards

Pathology 3 Flashcards

1
Q

What is the predominant inflammatory cell type in acute inflammation?

A

Neutrophils

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2
Q

What are the predominant inflammatory cell types in chronic inflammation/

A

Macrophages, lymphocytes and plasma cells

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3
Q

What are the gross characteristics of acute inflammation?

A

Often abundant exudation of fluid, plasma proteins and leukocytes

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4
Q

What are the gross characteristics of chronic inflammation?

A

Fibrosis, tissue destruction and repair

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5
Q

What are potential causes of chronic inflammation?

A
  • Persistent infection
  • Prolonged exposure to toxic agents
  • Some foreign materials
  • Immune mediated inflammatory disease
  • Unidentified mechanisms
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6
Q

Give examples of microorganisms that may cause persistent infection

A
  • Ones that are difficult to eradicate

- e.g. mycobacteria, Histoplasma capsulatum

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7
Q

Give examples of toxic agents that may lead to chronic inflammation

A

Barbiturates or aflatoxins (causing chronic hepatitis)

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8
Q

Give examples of foreign materials that may lead to chronic inflammation

A
  • Occurs where these are indestructible

- e.g. plant material, asbestos fibres, some suture material

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9
Q

Give examples of immune mediated inflammatory diseases that may lead to chronic inflammation

A
  • Autoimmune disease e.g. masticatory myositis

- Immunodeficiencies e.g. hereditary defects in leukocyte function

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10
Q

Give an example of an unidentified mechanism that may lead to chronic inflammation

A

Granulomatous meningoencephalitis (GME)

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11
Q

Describe the morphological features of chronic inflammation

A
  • Tissue destruction
  • Attempts of healing: replacement of damaged tissue by connective tissue (fibrosis and angiogenesis) and tissue proliferation
  • Infiltration with mononuclear cells (macrophages, lymphocytes, plasma cells)
  • Thickening due to proliferation of epithelial cells
  • Nodular lesions
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12
Q

What nodular lesions may occur in chronic inflammation?

A
  • Abscesses

- Granulomas

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13
Q

Describe the appearance and cause of abscesses

A
  • Collection of pis circumscribed by fibrous capsule that is visible grossly
  • Pus composed mostly of leukocytes, exuded plasma and proteins
  • Most commonly caused by bacteria
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14
Q

Describe the development of a granuloma

A
  • Nodular aggregation of macrophages, surrounded by collar of mononuclear leukocytes mainly lymphocytes)
  • Macrophages may fuse to form multinucleated giant cells
  • Chronic inflammation walled off by fibrotic tissue
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15
Q

What agents may lead to granuloma formation?

A
  • Parasites
  • Fungi and algae
  • few bacteria e.g. Mycobacteria)
  • Few viral infections e.g. Porcine circovirus type 2)
  • Foreign body material
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16
Q

Where are monocytes found?

A

Blood

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17
Q

Where are Kupffer cells found?

A

Liver

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18
Q

Where are sinus histiocytes found?

A

Lymph nodes and spleen

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19
Q

Where are alveolar macrophages found?

A

Lungs

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20
Q

Where are microglia found?

A

Central nervous system

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21
Q

Where are osteoclasts found?

A

Bone

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22
Q

What do macrophages, Kupffer cells, sinus histiocytes, alveolar macrophages, microglia and osteoclasts have in common?

A

Are all derived from monocytes produced in the bone marrow. Differentiate when infiltrate tissue

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23
Q

Describe macrophage migration

A
  • Extravasation of monocytes controlled by adhesion molecules and chemokines
  • Reach tissues in similar way to neutrophils in acute inflammation (adhere to wall, emigrate)
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24
Q

What factors are required to activate macrophages?

A
  • Exogenous factors (microbial prodcts, foreign bodies)

- or Endogenous factors (cytokines e.g. IFN-y)

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25
Q

What are the actions of activated macrophages?

A
  • Eliminate injurious agents
  • Initiate process of repair
  • Responsible for much of tissue injury in chronic inflammation
  • Some products are toxic to microbes and also host cells (ROS, NOS), potentiate inflammation (e.g. cytokines) or healing by inducing fibrosis and angiogenesis
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26
Q

What is the connection between lymphocytes ad macrophages?

A
  • Act in bidirectional way
  • Recruit and activate each other
  • May lead to very chronic and severe reactions
  • T cells secrete IFN-y
  • Macrophages secrete T cell cytokine IL-12
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27
Q

What is the role of plasma cells in chronic inflammation?

A
  • Activate B lymphocytes

- Produce antibodies direct against persistent foreign or self antigens

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28
Q

What is the role of eosinophils in chronic inflammation

A
  • Present in parasitic and some fungal infections

- Some hypersensitivity reactions

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29
Q

What is the role of neutrophils in chronic inflammation

A
  • Characteristic of acute inflammation, but still present in some forms of chronic inflammation
  • e.g. abscesses
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30
Q

Outline regeneration in wound healing

A
  • Proliferation of cells and tissues to replace lost structures
  • Complete resolution of lost structures
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31
Q

Outline repair in wound healing

A

Combination of regeneration and scar formation by deposition of collagen

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32
Q

What is the proportion of regeneration vs scarring dependent on?

A
  • Ability of the tissue to regenerate (i.e. labile vs permanent tissue)
  • Extent of the damage
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33
Q

What are the 3 stages of cutaneous wound healing?

A
  • Blood clot and inflammation
  • Proliferation and granulation tissue
  • Remodelling and maturation
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34
Q

Describe the blood clot and inflammation phase of cutaneous wound healing

A
  • Occurs within 24 hours
  • Activation of coagulation pathways
  • Blood clot formation
  • Neutrophils appear
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35
Q

Describe the proliferation and granulation tissue phase of cutaneous wound healing

A
  • Occurs between 2-7 days
  • Macrophages replace neutrophils, clean and promote proliferation
  • Proliferation of epithelial cells
  • Fibroblasts and endothelial cells proliferate to form granulation tissue
  • Macrophages produce FGF to stimulate fibroblasts to produce collagen to carry out fibrosis
  • Fibroblasts and connective tissue grow parallel to wound surface and perpendicular to proliferating capillaries
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36
Q

Outline the process of remodelling and maturation in cutaneous wound healing

A
  • Weeks
  • Leukocytes and increased vascularity disappear during second week
  • Granulation tissue converted into pale, avascular scar composed mainly of fibroblasts and dense collagen)
  • Wound contraction occurs in large wounds
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37
Q

Define clinical pathology

A

The practice of pathology as it pertains to the care of patients

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38
Q

What is the importance of the development, application and interpretation of clinical pathology laboratory procedures?

A

Can be used for:

  • Establishing diagnosis and/or prognosis
  • Monitoring treatment of sick animals
  • Monitoring animal health
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39
Q

How can clinical pathology be used in healthy animals?

A
  • Monitoring production/performance e.g. metabolic profile of dairy herd
  • Monitoring during critical periods e.g. anaemia in piglets, subclinical fatty liver in recently calved cows
  • Special purposes e.g. transport/export, selling, animal exhibition, prior to slaughter
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40
Q

What is involved in clinical pathology?

A
  • Haematology, clinical biochemistry, cytology

- Blood, urine, FNAs, effusions, cerebrospinal fluid, lavages, synovial fluid, faeces, ruminal fluid

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41
Q

What is meant by anatomic pathology?

A
  • Biopsy

- Necropsy

42
Q

What factors may induce variability in clinical pathology results?

A
  • Laboratory quality (pre-analytical, analytical, post-analytical)
  • Biological variables
  • inter-individual factors
  • Intra-individual factors
  • Pre-instrumental factors
43
Q

Give examples of pre-analytical factors that may affect laboratory quality

A
  • Something biological in the patient unrelated to the disease
  • Patient preparation
  • Sample preparation (e.g. choice of collection tube)
  • Shipping (temperature of sample)
44
Q

Give examples of analytical factors that may affect laboratory quality

A
  • Appropriate equipment/reagents used?

- Analytical sensitivity, specificity, precision

45
Q

Give examples of post-analytical factors that may affect laboratory quality

A
  • Results given for the correct patient
  • Appropriate interpretation
  • Diagnostic sensitivity and specificity
46
Q

Give examples of biological variables that may induce variability in clinical pathology results

A
  • Species, breed, age and sex

- Intra-individual variation

47
Q

What is meant by inter-individual factors in relation to clinical pathology?

A
  • Inherent differences between groups of animals due to
  • Species e.g. cat PCV < dog PCV
  • Breed (akitas have lower mean cell volume)
  • Age (growing dogs have lower PCV and total protein concentration than adult dogs)
  • Sex (males usually have higher PCV values)
48
Q

What is meant by intra-individual factors in relation to clinical pathology?

A
  • Transient differences in the ame animal due to usually environmental or external factors
  • Can induce outlier results when compaed to usual reference ranges for disease-free animals
  • Can be minimised by standardising procedures e.g. fasting before sampling
49
Q

Give examples of factors that may lead to intra-individual variation

A
  • Fasting/post-prandial samples very different
  • Diet: low protein diet = low blood urea
  • Excitement/anxiety: increase glucose and lymphocytes in cats, adrenergic response increases PCV in horses
  • Reproductive status: lactation leads to reduced serum Ca
  • Drugs/therapy e.g. glucocorticoids increase ALP and ALT in dogs
  • Method of blood sampling
  • Sampling site e.g. mammary vein has less glucose vs jugular in lactating cows
50
Q

Give examples of pre-instrumental factors that may affect the clinical pathology of a blood sample

A
  • Poor sampling method e.g. pumping of syringe punger
  • Haemolysed, lipaemic or icteric plasma
  • Incorrect tube choice
  • Wrong anticoagulant :blood ratio
  • Transportation of specimen
  • Storage of specimen
51
Q

What is the difference between serum and plasma?

A
  • Serum: forms 3 layers, blood at bottom, gel in middle, serum at top. No proteins
  • Plasma: need to centrifuge blood to get plasma. Contains proteins
52
Q

What are the advantages of serum?

A
  • Plasma not recommended for some analyses e.g. direct bilirubin, bile acids, haptoglobin, protein electrophoresis
  • Autoanalysers may work better with serum
  • Most “normal values” are for serum
53
Q

What are some disadvantages of serum?

A
  • Separation times time for clots for form (unless serum accelerator used, can interact with some assays)
  • Separation may be more likely to result in haemolysis, lower yield
  • Cannot be used to measure fibrinogen
54
Q

Why must plasma and serum be separated from blood as soon as possible?

A
  • Some compounds may not be stable in whole blood (e.g. glucose)
  • Red cells can haemolyse
  • Haemoglobin coloured, will affect test results where colour is assessed
55
Q

Describe appropiate storage and transportation of serum/plasma samples

A
  • Separated from blood asap
  • Closed tubes, cool and dark
  • Get sample to lab without delay
  • Storage: freeze serum (-20) and plasma (-70)
56
Q

What is the anticoagulant used in clinical pathology haematology?

A

EDTA

57
Q

What samples are used in clinical chemistry for clinical pathology?

A
  • Li-heparin plasma
  • EDTA plasma
  • Plain serum
58
Q

What sample type is used for glucose tests in clinical pathology?

A

Fluoride oxalate

59
Q

What sample type is used to assess haemostasis/coagulation for clinical pathology?

A

Citrate

60
Q

When should EDTA not be used?

A

When measuring potassium and ionised calcium values, as K-EDTA increases K and decreases Ca (binds out calcium to block clotting cascade)

61
Q

Describe the appearance of haemolysed, icteric, and lipaemic blood samples

A
  • Haemolysed: red
  • Icteric: yellow
  • Lipaemic: opalescent/cloudy
62
Q

What is the effect of haemolysis in a sample on laboratory tests?

A
  • Increases palsma/serum values for some compounds/enzymes due to higher concentration within RBC
  • Decreases plasma/serum values of compounds due to lower concentration in RBCs and being diluted
  • Interferes with determination by colour interferences or chemical interactions
63
Q

Give examples of compounds that are found in higher concentrations within RBCs vs plasma

A
  • K+ in horses, inorganic phosphate

- Enzymes e.g. lactate dehydrogenase, AST

64
Q

Give examples of compounds that are found in lower concentrations in RBCs vs plasma

A
  • Ca
  • Glucose
  • Mg in cattle
65
Q

Give examples of the interfering effect of haemolysis on colour determination and chemical interactions in a sample

A
  • Bilirubin falsely increased due to similar absorbance range to haemoglobin
  • Chemical interaction: creatinine (Jaffe colorimetric method) falsely decreased in ketotic plasma
66
Q

How can lipaemia in a sample be avoided?

A

Fast patients appropriately prior to sampling

67
Q

What are the main changes in a sample, associated with lipaemia?

A
  • Increase in total lipid, TAG and cholesterol

- many determinations either cannot be carried out or results significantly affected

68
Q

How does lipaemia increase or decrease values of some compounds in plasma/serum?

A
  • Presence of extra lipid fractions

- Turbidity caused by the lipids

69
Q

What is the importance of vaildation methods and techniques in clinical pathology?

A

Aim is to remove/account for instrumental variation

70
Q

How are instrumental factors causing variation in results controlled?

A
  • Validation of techniques used (assay parameters, machine set up, analytical range) - must be known before analysis starts
  • Quality control must be performed regularly
  • Can batch samples or have continuous analysis, but QC important for both
71
Q

What factors are included in the validation of a clinical pathology technique?

A
  • Precision (repeatability, reproducibility)
  • Accuracy (measuring right thing correctly)
  • Specificity (ability of a technique to measure one single analyte in a complex solution)
  • Sensitivity (range and linearity, interval between lowest and highest concentrations method can measure)
  • Other
72
Q

In what 2 situations are imprecise and accurate results possible in clinical pathology?

A
  • Where there are wide differences between physiologic and pathologic state
  • Where the use of mean of repeated measures used to increased precision
73
Q

Explain how post-instrumental or analytical factors may affect clinical pathology interpretation?

A
  • Validation of the result (analytical and biological), is the clinical interpretation of the result
  • Transfer of the result to the final user: verbal vs written, easy to make mistakes
  • Archiving the result and storing the specimen provides opportunity for reexamination
74
Q

What is meant by test precision?

A
  • Repeatability/reproducibility

- The ability of a technique to give the same result when the same specimen is analysed several times

75
Q

How is repeatability of a test assessed?

A
  • Is the within assay precision
  • Consecutive measurements within a series of tests
  • Usually assessed by replicate QCs in an assay
  • Gives intra-assay coefficient of variation
76
Q

How is reproducibility of a test assessed?

A
  • Is the between assay precision
  • Different series of measurements, usually assessed by running same QCs across different assays
  • Inter-assay coefficient of variation produced
77
Q

Define test accuracy

A
  • The ability of the test to measure the right thing correctly
  • I.e. the agreement between the true value and the observed value
78
Q

How is test accuracy assessed?

A
  • Measurements are repeated in order to minimise the influence of imprecision
  • Given as percentage: (true value-mean of measurements)/true value
79
Q

Define assay specificity

A
  • The ability of a technique to measure one single analyte in a complex solution
80
Q

What may affect the specificity of an assay?

A

Presence of similar molecules e.g. testing for cortisol, but also picks up other similar shaped steroids = low specificity

81
Q

Give examples of specificity interfering substances

A
  • Substances that interact with analytical techniques e.g. drugs, detergents, anticoagulants, pollutants
  • Ascorbate (vit C, reducing agent) interferes with glucose oxidase reaction of urine test strips
  • EDTA (anticoagulant) interferes with calcium, magnesium, iron and potassium
82
Q

Define assay sensitivity

A
  • Interval between lowest and highest concentrations the method can measure
  • The analytical range of a technique is the range of values between which a measurement of the concentration of the analyte is possible with a known imprecision
83
Q

What is the formula for coefficient of variation?

A

Standard deviation/mean

84
Q

Compare the Gaussian curves of a precise and an imprecise technique

A
  • Precise: narrower curve, more results around the mean

- Imprecise: wider curve, wider distribution of results around the mean

85
Q

Outline the distribution of fluid in the body

A
  • 60% water
  • 2/3rds intracellular, 1/3rd extracellular
  • Extracellular: 80% interstitium, 20% in plasma
86
Q

Give examples of how abnormal fluid distribution may occur

A
  • Imbalance between intracellular and interstitial compartments may lead to swelling/shrinkage, potential for serious cell injury
  • Imbalance between intravascular and interstitial components may lead to oedema
87
Q

What are the main mechanisms of oedema?

A
  • Increased microvascular permeability
  • Increased intravascular hydrostatic pressure (high BP)
  • Decreased intravascular osmotic pressure
  • Decreased lymphatic drainage
88
Q

What might cause increased microvascular permeability in oedema?

A
  • Inflammation
  • Toxins
  • Anaphylaxis
  • Clotting abnormalities
89
Q

What may cause increased intravascular hydrostatic pressure?

A
  • Portal hypertension
  • Pulmonary hypertension
  • Localised venous obstruction
  • Fluid overload
  • Hyperaemia
90
Q

What may cause decreased intravascular osmotic pressure?

A
  • Decreased albumin production (liver disease)
  • Increased albumin loss
  • Water intoxication
91
Q

What may cause decreased lymphatic drainage in oedema?

A
  • Lymphatic obstruction/compression
  • Lymphangitis
  • Lymphangiectasia
  • Lymphatic aplasia/hypoplasia
92
Q

What are some effects of oedema?

A
  • Decreased wound healing/clearance of infection
  • Pulmonary oedema leads to decreased oxygen diffusion
  • Brain oedema is acutely life threatening
93
Q

What is haemostasis?

A

Arrest of bleeding

94
Q

Outline the process of haemostasis

A
  • Formation of platelet plug (primary haemostasis)
  • Formation of fibrin meshwork (secondary haemostasis)
  • Removal of platelet/fibrin plug (fibrinolysis, thrombus retraction)
95
Q

Outline the formation of the platelet plug (primary haemostasis)

A
  • Transient arteriolar vasoconstriction
  • Platelet adherence and activation
  • In minimal vascular injury, platelet plugs alone may resolve the damage
96
Q

Outline the formation of the fibrin meshwork

A
  • Local activation of coagulation results in fibrin polymerisation
  • Fibrin “cements” platelets into definitive secondary haemostatic plug
97
Q

Outline the removal of the platelet/fibrin plug

A
  • Release of tissue factors: thrombomodulin (stops the clotting cascade) and tPA (tissue plasminogen activator, stimulates fibrinolysis)
  • Fibrin-platelet thrombus dissolved after healing of the vessel (thrombolysis)
  • Fibrin dissolution (fibrinolysis) initiated immediately on vessel injury by plasmin
98
Q

What are the 2 pathways of the coagulation cascade and what is the result?

A
  • Extrinsic
  • Intrinsic
  • Both activate factor X, both produce proteolytic enzymes that initiate fibrin formation
99
Q

Outline the extrinsic coagulation pathway

A
  • Occurs outside the blood vessel wall when shed blood contacts tissue debris
  • Thromboplastin plays major role
  • Produces tissue factor VIIa
100
Q

Outline the intrinsic coagulation pathway

A
  • Triggered by effects of abnormal surfaces on components normally present in blood
  • All coagulation factors are present in normal plasma
  • Leads to cascade of complex enzymatic reactions until factor X activated

PVS (23 decks)

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