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FCP > 4. Pathology > Flashcards

4. Pathology Flashcards

1
Q

Define pathology

A

The study of disease OR
The structural, biochemical, and functional changes in cells, tissues and organs that underlie disease

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2
Q

What are the 2 broad categories of pathology

A

General pathology
Systemic pathology

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3
Q

What is meant by general pathology

A

Basic responses of cells and tissues to insults and injuries, irrespective of the organs, systems, or species of animal involved

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4
Q

What is meant by systemic pathology

A

Pathology of organ systems
Alterations in specialized organs and tissues

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5
Q

When examining patients, what are the 2 types of pathology

A

Anatomic pathology
Clinical pathology

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6
Q

What is meant by anatomic pathology

A

Examination of tissues taken during life (biopsy) or after death (autopsy, necropsy)

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7
Q

What is meant by clinical pathology

A

Examination of blood and other body fluids, as well as cells (cytology) during life, laboratory diagnostics and technology

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8
Q

What is meant by inflammation

A

Vascular and interstitial tissue changes that develop in response to tissue injury and that are designed to sequester, dilute, and destroy the causal agent

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9
Q

What is meant by ‘healing’ and what 4 processes does it involve

A

Repair of injured tissue
Involves: angiogenesis, fibrosis, regeneration and epithelialisation

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10
Q

What is meant by the term thrombosis

A

Interaction of the blood coagulation system and platelets to form, within a vascular lumen, an aggregate of fibrin and platelets

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11
Q

How does thrombosis differ from normal clotting (Virchow’s triad)

A

Involves Virchow’s triad:
Vascular wall damage
Hypercoagulable state
Changes in blood flow

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12
Q

What is meant by the term neoplasia

A

New cellular growth
Leads to unrestrained mitosis and an expanding mass of uncontrolled cells that affects adjacent normal tissue.

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13
Q

2 mechanisms by which neoplasia affects normal tissue

A

Compression
Replacing them

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14
Q

What is meant by the word necrosis

A

Death of cells or tissue in the living animal

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15
Q

What Is meant by the word biopsy

A

Removal and examination of a tissue sample from a living animal body for diagnostic purposes

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16
Q

What do you need to include in a pathologic description of a lesion (x8)

A

Location
Number/extent
Demarcation
Distribution
Colour
Size
Shape
Consistency and texture

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17
Q

What are the 4 main aspects of disease

A

Aetiology
Pathogenesis
Molecular and morphologic changes
Clinical manifestation

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18
Q

What are the 2 aspects of a pathologic exam

A

Biopsy
Post mortem exam

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19
Q

What is a ‘clinical diagnosis’ based on

A

Based on data obtained from the case history, clinical signs and physical examination

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20
Q

What is a ‘clinical pathologic diagnosis’ based on

A

Based on changes observed in the chemistry of fluids and the haematology, structure, and function of cells collected from the living patient

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21
Q

What is a ‘morphologic diagnosis’ based on

A

Based on what is seen
Can be macroscopic or microscopic

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22
Q

What does a morphologic diagnosis describe

A

Describes severity, duration , distribution, location (organ or tissue), and nature (degenerative, inflammatory, neoplastic) of the lesion

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23
Q

What does a morphologic diagnosis describe

A

Describes severity, duration , distribution, location (organ or tissue), and nature (degenerative, inflammatory, neoplastic) of the lesion

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24
Q

What are the common post mortem changes which can be seen in tissues (x7)

A

Autolysis
Putrefaction
Rigor Mortis
Livor Mortis
Post Mortem clotting
Haemoglobin/bile imbibition
Pseudomelanosis

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25
Q

What is autolysis

A

Changes to a tissue due to ‘self digestion’

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26
Q

What is putrefaction

A

Colour and texture changes, gas production, and odours that are caused by post-mortem bacterial metabolism and dissolution of host tissues

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27
Q

What is rigor mortis, when does it start and how long for

A

Contraction of muscles occurring after death
Due to depletion of ATP and glycogen
Commences 1-6 hours after death
Persists for 1-2 days

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28
Q

What is Livor mortis

A

Gravitational pooling of blood in the animal

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29
Q

What is post mortem clotting

A

Evident in the heart and great vessels
Differs from thrombosis as not adhered to vessel wall

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30
Q

What is haemoglobin imbibition

A

Red staining of tissues by haemoglobin

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31
Q

What is bile imbibition

A

Bile from the gallbladder staining adjacent tissues yellow/green/brown colour

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32
Q

What is pseudomelanosis

A

Blue/green discolouration of tissue by iron sulphide

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33
Q

Are post mortem changes the same as a lesion

A

No

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34
Q

What are the 5 cardinal signs of acute inflammation

A

Redness
Heat
Swelling
Pain
Loss of function

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35
Q

What is the definition of acute inflammation

A

A redundant, complex, adaptative and protective response of vessels, resident cells and leucocytes to noxious stimuli.

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36
Q

How long does acute inflammation last for

A

Hours to days

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37
Q

Name 6 causes of acute inflammation

A

Infections
Foreign bodies
Immune reactions (hypersensitivities)
Tissue necrosis
Trauma
Physical and chemical Injury

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38
Q

What are the 3 morphologic hallmarks of acute inflammation

A

Dilation of blood vessels
Activation and recruitment of leukocytes
Active oxidation of fluid in the extravascular tissues

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39
Q

What are the 6 steps of inflammation (6 R’s)

A

Recognition of injurious agent
Reaction of blood vessels
Recruitment of leukocytes
Removal of the agent
Regulation of the response
Repair/Resolution

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40
Q

Name the main 4 mediators in acute inflammation and give examples of each

A
  1. Vasoactive amines (histamine, serotonin)
  2. Inflammatory lipids (prostaglandins leukotrienes)
  3. Complement (C5a, C3a)
  4. Cytokines (IL-1, TNF, IL-6)
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41
Q

Which mediators are responsible for vasodilation in acute inflammation

A

Inflammatory lipids

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42
Q

Which mediators are responsible for increased vascular permeability in acute inflammation

A

Vasoactive amines
Complement
Inflammatory lipids
Cytokines

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43
Q

Which mediators are responsible for Leukocyte recruitment and activation in acute inflammation

A

Inflammatory lipids
Complement
Cytokines

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44
Q

Which mediators are responsible for Pain in acute inflammation

A

Inflammatory lipids

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45
Q

Which mediators are responsible for Tissue damage in acute inflammation

A

Neutrophil granule content
ROS

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46
Q

What is the sequelae of acute inflammation

A
  1. Complete resolution
  2. Scarring or fibrosis
  3. Progression to chronic inflammation
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47
Q

What is the acute phase response in acute inflammation

A

The acute phase response is characterized by different systemic effects of acute inflammation (and other conditions) including pyrexia, leucocytosis, metabolic changes.

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48
Q

How is pyrexia caused by acute inflammation

A

exogenous pyrogens and endogenous triggers
=> neutrophils and macrophages
=> endogenous pyrogens
=> PGE2
=> pyrexia

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49
Q

what are acute phase proteins

A

Biomarkers of inflammation
Can be positive or negative

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50
Q

Give 4 examples of positive acute phase proteins (increase during inflammation)

A

C reactive protein
Serum amyloid A
Fibrinogen
Complement

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51
Q

Give 4 examples of negative acute phase proteins (decrease during inflammation)

A

Albumin
Transferrin
Transthyretin
Retinol binding protein

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52
Q

Name 2 types of effusions

A

Transudates
Exudates

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53
Q

What is transudate and when is it present

A

Extravascular filtrate of protein and cell poor fluid
Due to increased hydrostatic pressure or decreased colloido-osmotic pressure

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54
Q

What is an exudate and when is it present

A

Extravascular fluid that has a high protein concentration and can contain leucocytes.
Implies existence of an inflammatory process that has increased permeability of blood vessels

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55
Q

Give 4 types of exudates

A

Serous
Fibrinous
Purulent
Haemorrhagic

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56
Q

What is serous inflammation

A

Inflammation with exudation of fluid with a low concentration of plasma protein and no to low numbers of leukocytes.

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57
Q

Give 3 examples of serous inflammation

A

Serous rhinitis
Acute allergic reactions
Cutaneous blisters

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58
Q

What is fibrinous inflammation

A

Inflammation with exudation of fibrinogen and fluid, and formation of thick, friable, loosely adherent fibrin.

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59
Q

Give 2 examples of fibrinous inflammation

A

Fibrinous peritonitis
Fibrinous bronchopneumonia and pleurisy

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60
Q

What is purulent inflammation

A

Inflammation with production of pus, viscous to creamy liquid, an exudate consisting of degenerated and necrotic neutrophils, debris and fluid
Typically associated with bacterial infections

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61
Q

Give 2 examples of purulent inflammation

A

Purulent pleurisy (pyothorax)
Purulent lymphadenitis and cellulitis

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62
Q

What is haemorrhagic inflammation

A

Inflammation with vascular damage, loss of integrity of endothelium and/or extensive tissue necrosis, with leakage of red blood cells. Reflects a severe inciting stimulus.

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63
Q

How long after acute inflammation does chronic inflammation start

A

24-72 hours after acute inflammation

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64
Q

How long can chronic inflammation persist for

A

Weeks/months/years

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65
Q

What is the main cell type involved in chronic inflammation and what are the different classes

A

Macrophages - M1 or M2
M1 = turn arginine => nitric acid = highly toxic to phagocytoses organisms
M2 = non inflammatory, turn arginine => orthinine => proline

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66
Q

What do activated macrophages produce in chronic inflammation and give examples

A

Pro inflammatory cytokines
E.g. IL-1, IL-6

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67
Q

What do pro-inflammatory cytokines cause

A

Pyrexia
Lethargy
Stimulate acute phase proteins

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68
Q

What causes granulomas to form

A

Persistent stimulus e.g. inert irritant or a pathogen

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69
Q

What cell types are present in pyogranulomatous lesions

A

Macrophages and neutrophils

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70
Q

Give 2 disease examples with pyogranulomatous lesions

A

Feline infectious peritonitis
Johnes disease in cattle

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71
Q

What are the 2 types of chronic inflammation

A
  1. With a clear pathogen
  2. Without a clear pathogen
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72
Q

Define neoplasia

A

The process of abnormal proliferation of cells

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73
Q

Define neoplasm

A

An abnormal mass of tissue that occurs as result of abnormal cell proliferation (can also be called cancer or tumour)

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74
Q

What is the difference between benign, pre-malignant, and malignant neoplasms

A

Benign - Do not invade/spread to surrounding tissues or around the body
Pre-malignant - Characterised by criteria of malignancy, can become malignant
Malignant - Harmful, will invade locally and metastasise

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75
Q

What is ‘oncogenesis’

A

Process of gradual stepwise tumour development
Cancer develops gradually from normal tissue

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76
Q

Name the 3 steps of oncogenesis

A
  1. Initiation (mutagenesis)
  2. Promotion
  3. Progression into malignancy
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77
Q

Give the different types of initiation/mutagenesis in the process of oncogenesis (x4)

A

Chemical or physical
Inherited or spontaneous
Viruses or bacteria
Reactive oxygen species (ROS)

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78
Q

Benign vs malignant differentiation

A

Benign - Well differentiated, similar to tissue or origin, little to no anaplasia
Malignant - lack of differentiation, atypical structure, variable anaplasia

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79
Q

Benign vs malignant growth rates

A

Benign - slow, progressive, rare and normal mitotic features
Malignant - slow to rapid, many abnormal mitotic figures

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80
Q

Benign vs malignant local invasion level

A

Benign - no invasion, cohesive growth, capsule often present
Malignant - local invasion, infiltrative growth usually no capsule

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81
Q

Benign vs malignant metastasis level

A

Benign - no metastasis
Malignant - frequent metastasis

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82
Q

Benign vs malignant host consequences

A

Benign - space occupying lesion, effect depends on location
Malignant - Life threatening

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83
Q

Benign vs malignant cellular morphology

A

Benign - Minimal to mild anisocytosis (variation in cell size and shape)
Malignant - marked anisocytosis

84
Q

Benign vs malignant nuclear to cytoplasmic ratio

A

Benign - normal to reduced
Malignant - increased

85
Q

Benign vs malignant nuclear morphology

A

Benign - Minimal to mild anisokaryosis (variation in nuclear size and shape)
Malignant - marked anisokaryosis with frequent binculeation and multi nucleation

86
Q

Benign vs malignant mitotic count

A

Benign - low
Malignant - high

87
Q

Benign vs malignant necrosis level

A

Benign - minimal or absent
Malignant - frequently present

88
Q

Benign vs malignant individualisation and invasiveness of cells

A

Benign - absent
Malignant - invasiveness to surrounding tissues

89
Q

What 4 types of neoplastic lesions are common and give examples

A

Mesenchymal - lymphoma, haemangioma, lipoma, leiomyosarcoma
Epithelial - melanoma, andeocarcinoma
Nervous - ganglioneuroma, astrocytoma
Other - germ cell tumour e.g. teratoma

90
Q

How are metastases formed

A

Formed by cancer cells that have left the primary tumour and travelled through blood and lymphatic vessels

91
Q

What are the main 2 causes of cancer related morbidity and mortality

A

Invasion
Metastasis

92
Q

What are the 8 steps in the metastasis cascade

A
  1. Primary tumour formation
  2. Localised invasion
  3. Intravasation
  4. Transport through circulation
  5. Arrest in microvessels of various organs
  6. Extravasation
  7. Formation of micrometastasis
  8. Colonisation
93
Q

Name the 3 pathways of metastasis

A
  1. Transcoelomic
  2. Lymphatic
  3. Haematogenous
94
Q

Name 4 types of tumours which metastasise to the lungs

A

Osteosarcoma
Hemangiosarcoma
Melanoma
Mammary tumours

95
Q

Name 2 types of tumours which metastasise to the liver, spleen and kidney

A

Mast cell tumours
Hemangiosarcomas

96
Q

Name 3 types of tumours which metastasise to the bone

A

Mammary gland tumours
Prostatic carcinomas
Urinary bladder tumours

97
Q

Name the common sites of metastasis

A

Lungs
Liver, spleen and kidney
Bone
Brain, adrenal glands

98
Q

Name the direct effects of neoplasias

A

Space occupying
Displaces and puts pressure on surrounding tissues
=> atrophy, necrosis or death of surrounding tissues

99
Q

Name the indirect effects of neoplasias

A

Normally caused by tumour cell products
Haematological, endocrinological and metabolic complications
Such complications may be the main presenting sign

100
Q

Define cachexia

A

Weakness and wasting of the body due to severe chronic illness

101
Q

How does cancer cause cachexia

A

Results from altered carbohydrate, protein and lipid metabolism
Complex pathogenesis due to TNF-a, IL-1, IL-6 and prostaglandins

102
Q

How is a fever caused by tumour/cancer

A

Caused by tumour-induced production of cytokines (IL-1)

103
Q

What is an endocrine neoplasm, give an example and what can they cause

A

Functioning endocrine tumour
Hypoglycaemia - caused by insulinoma

104
Q

What is a non-endocrine neoplasm, give examples and what they can cause

A

Can produce hormonally active substances not normally found in the tissue of tumour origin
E.g. lymphoma, multiple myeloma, adenocarcinoma
Cause hypercalcaemia, many tumours produce PTH related protein

105
Q

What is hypertrophic pulmonary osteopathy, and what tumours are they commonly associated with

A

Rapid periosteal new bone growth affecting distal limbs
Lung tumours

106
Q

What is myelofibrosis

A

Overgrowth of nonneoplastic fibroblasts in the bone marrow, which impairs normal haematopoiesis

107
Q

Name some common paraneoplastic syndromes

A

Alopecia
Epidermal necrosis
Vascular and haematological disorders

108
Q

Name the intrinsic and extrinsic causes of neoplastic transformation

A

Intrinsic - DNA damaging metabolites e.g. ROS and organic acids
Extrinsic - Chemical environmental agents, physical environmental agents, oncogenic viruses

109
Q

What is the difference between a mutagen and a carcinogen

A

Mutagens = agents that create the DNA damage and gives rise to mutation
Carcinogens = agents that can cause cancer
(Many mutagens are carcinogens)

110
Q

What are the two types of chemical environmental agents (extrinsic factors for neoplasms)

A

Direct acting chemical carcinogens - effective in the form the enter the body
Indirect acting chemical carcinogens - procarcinogens

111
Q

Give 3 categories of physical environmental extrinsic factors for neoplasms and how they act

A

Complete carcinogens - initiation and promotion
Ionising radiation - DNA damage and ROS generation
UV radiation - formation of hallmark pyrimidine dimers and ROS generation

112
Q

What is a proto-oncogene

A

Unmutated gene which are involved in growth factor pathways
When they are mutated, they will lead to uncontrolled cell proliferation

113
Q

What is an oncogene

A

Mutated proto-oncogene
Promote autonomous growth
Can encode for specific proteins (oncoprotein)

113
Q

What is an oncoprotein

A

Have a mutation and have no internal regulatory elements
Ability to promote cell growth
Cells expressing them don’t have normal check points and control

114
Q

Name 3 direct mechanisms the oncogenic viruses have and explain them

A

Dominant oncogene mechanism - mutated gene in a virus which drives tumour development
Insertional mechanism - viruses which don’t have their own oncogene, insert viral DNA which activates target cell oncogene
Hit and run mechanism - Viral genome causes neoplasm by transient resistance in target cells

115
Q

Name 2 indirect mechanisms of oncogenic viruses

A

Suppression of animals immune system
Stimulation of target cell proliferation

116
Q

2 methods of diagnosing neoplasms

A

Cytopathological examination
Histopathological examination

117
Q

What method of extraction do we use for cytopathology of a neoplasm

A

Fine needle aspiration

118
Q

Why do we need to do histopathology on a neoplasm as well as cytopathology

A

Give additional info needed which can direct the therapeutic plan
Helps to provide microscopic description
Gives tumour grade

119
Q

Importance of surgical margins tissue biopsies

A

Crucial for exiciokal tissue biopsies where the entire mass is removed
Allows microscopic evaluation of the margins to make sure you got the whole thing

120
Q

Define cytology

A

The study of cell number and type in a tissue mass or fluid accumulation, to investigate its cause

121
Q

Name 4 common cytological specimens

A

FNA
Touch imprints
Body fluids
Lavages

122
Q

What does cytological examination allow (4 things)

A

Differentiation of inflammation from tissue growth
Differentiation of types of inflammation
Detect neoplasia
Differentiation of different fluid

123
Q

Give the main advantages of cytology

A

Quick, safe and inexpensive
Demands little equipment
Quickly available results

124
Q

Give the main limitations of cytology

A

False negatives - Failure to sample tumour tissue, extensive necrosis/inflammation present
False positives - Dysplasia which can mimic neoplasia can occur in inflammatory diseases
Have to do histopathology anyway

125
Q

Name 3 lesion types which are identifiable by cytology and give examples

A

Inflammation - Neutrophillic, eosinophilic, granulomatous
Cystic lesions - epidermal, serum, haematoma
Neoplastic - epithelial, round, mesenchymal, benign vs malignant

126
Q

Cell types identifiable by cytology

A

Epithelial
Spindle/mesenchymal
Round

127
Q

What can cytology tell us about cells

A

Inflammatory - sterile vs septic
Non inflammatory - Cystic, hyperplastic, neoplastic

128
Q

Name 4 types of inflammation (based on cell type)

A

Neutrophillic inflammation
Pyogranulomatous inflammation
Granulomatous inflammation
Eosinophillic inflammation

129
Q

Give specific examples of epithelial skin tumours (6)

A

Trichoblastoma (basal cell tumour)
Trichoepithelioma (hair follicle tumour)
Squamous cell carcinoma
Sebaceous cell tumours-adenoma, carcinoma, epithelioma
Anal sac apocrine adenocarcinoma
Perianal gland (hepatoid) adenoma

130
Q

Where do mesenchymal skin tumours arise from

A

Connective tissue, muscle, bone, cartilage, nerve and endothelial cells

131
Q

Give examples of mesenchymal skin tumours

A

Lipoma and liposarcoma
Melanoma
Haemangioma/haemangiosarcoma

132
Q

Give characteristics of a lipoma

A

Adipocytes with small nucleus and abundant cytoplasm
free fatty droplets
Appears identical to subcutaneous fat cytologically

133
Q

Give examples of round cell tumours

A

Mast cell tumour
Lymphoma
Plasmacytoma
Histiocytic tumours

134
Q

what is clinical pathology (tests involved)

A

combination of haematology, clinical biochemisrty, cytology

135
Q

What anticoagulants are used for: haematology, clinical chemistry, glucose and haemostasis

A

Haematology - EDTA
Clinical chemistry - Lithium heparin, EDTA
Glucose - Fluoride-oxalate
Haemostasis - citrate

136
Q

If a sample is contaminated with EDTA, what electrolyte levels will be affected

A

Calcium - will be very low
Potassium - will be very high

137
Q

How to to avoid haemolysis of a blood sample

A

Choose appropriate gauge needle
Don’t dispense blood back through the needle

138
Q

What are the effects of haemolysis on a blood sample

A

Increases in plasma/serum values of some compounds due to higher conc. in RBC
Interferes if using colorimetry and chemical interactions

139
Q

What are the effects of lipaemia on a blood sample

A

Can alter values of compounds due to presence of extra lipid fractions
If doing colorimetry turbidity caused by lipids can affect this
Increases in total lipid, triglycerides and cholesterol

140
Q

3 sources of variation and errors in lab results and give examples

A

Pre-analytical - patient and sample prep, shipping
Analytical - Appropriate equipment, quality control
Post analytical - appropriate interpretation, diagnostic sensitivity and specificity

141
Q

When looking at validation of an analytical techniques, what does PASS stand for

A

Precision
Accuracy
Specificity
Sensitivity

142
Q

What is an internal quality control

A

Done with patient samples

143
Q

What is an external quality control

A

Non contemporaneous - at a different time

144
Q

3 aspects of urinalysis

A

Physical analysis
Chemical analysis
Microscopy/ sediment examination

145
Q

What do you look at in a physical exam of urine

A

Colour, turbidity, odour
USG

146
Q

What do you look at in a chemical exam of urine

A

pH
Protein, glucose, ketones, bilirubin
Blood

147
Q

What do you look at in a microscopy/sediment exam of urine

A

RBC, Leukocytes
Epithelial cells
Bacteria
Casts
Crystals

148
Q

What is measuring USG actually measuring

A

Urine osmolality

149
Q

If urine is isosthenuric in a dehydrated/azotaemic patient what does this suggest

A

Shows the tubules are not secreting or absorbing
Suggests a problem with the kidney
Concentrating ability is impaired around 60-70% of nephron loss

150
Q

What do you have to do to determine if there is a problem with concentrating ability alongside USG

A

Needs correlation with hydration status and/or azotaemia

151
Q

3 mechanisms causing proteinuria and describe

A

Pre-glomerular - Too high quantities of protein in the filtrate to be reabsorbed
Glomerular - basement membrane has failed due to inflammation, immune attacks or accumulation of content
Tubular - damaged tubular cells cannot reabsorb filtrate protein as well as they should

152
Q

Which type of proteinuria causes blood albumin to fall and cause “nephrotic syndrome”

A

Glomerular proteinuria

153
Q

Causes of glomerular proteinuria

A

Inflammation in the glomeruli (glomerulonephritis)
Damage to glomeruli - diabetes, hypertension, kidney diseases

154
Q

Which 3 chemical readings on urinalysis are not reliable/applicable in dogs and cats

A

Leukocytes
Urobilinogen
Nitrites

155
Q

What do casts in urine suggest

A

Tubular damage/disease

156
Q

Name 4 types of casts in urine

A

Hyaline - protein
Cellular
Granular
Waxy

157
Q

Name 4 types of crystals that can be seen in urine

A

Calcium carbonate
Struvite - magnesium ammonium phosphate
Calcium oxalate monohydrate and dihydrate
Urates (ammonium and amphorus)

158
Q

Two approaches to cytology of tissue

A

Unknown mass
Known tissues

159
Q

How to classify cavity effusions with cytology

A

Protein content, cell count and classification
Protein poor transudate vs protein rich transudate vs exudate (inflammatory)

160
Q

Name 3 cytological criteria of malignancy

A

Cellular
Nuclear
Cytoplasmic

161
Q

Give 4 reasons why lymph nodes may be enlarged

A
  1. Reactive hyperplasia
  2. Lymphadenitis
  3. Metastatic neoplasia
  4. Lymphoma
162
Q

What are we looking for when looking at red cell parameters

A

Red cell mass
Evidence of erythropoiesis
Red cell size and variation
Red cell colour (haemoglobinisation)
Red cell shapes and inclusions

163
Q

How to assess red cell mass (3 methods)

A

PCV
RBC count
Hgb levels

164
Q

Causes of high haemoglobin

A

Haemolysis of the blood sample
Lipaemia

165
Q

Causes of misleading mean cell value results

A

Swelling in transport
Misidentification
Cell shrinkage or expansion in sample

166
Q

What are the classifications of anaemia, and which test tests for them

A

MCV (size of RBC) - can be normocytic, microcytic or microcytic
MCHC (haemoglobin in RBC)- can be normochromic, hyperchromic or hypochromic

167
Q

What is meant by ‘polycythaemia’ and how is it identified

A

Too much red cell mass
Increased PCV, haemoglobin and RBC count

168
Q

What is relative polycythaemia

A

Apparent increase in RBC due to decrease of fluid in circulation (dehydration)

169
Q

What is absolute polycythaemia

A

True increase in RBC mass due to increased RBC production/release

170
Q

What are primary and secondary absolute polycythaemia

A

Primary = normal EPO levels, abnormal response of RBC precursors
Secondary = Increased EPO, chronic tissue hypoxia of renal tissue or renal tumours or cysts

171
Q

What do reticulocytes show

A

Evidence of regeneration

172
Q

Name 2 causes of alteration in red cell shape

A

Abnormal erythropoiesis
Specific organ dysfunction

173
Q

3 causes of inclusions in RBC

A

Active regeneration
Infective agents
Heinz bodies

174
Q

What is a Rouleaux formation and what does it indicate

A

Clustering, sticky piling of RBC
Indicates Inflammation in small animals

175
Q

3 steps for cells to leave blood vessels

A

Marginalisation
Adhesion
Migration

176
Q

Name 4 factors that can cause a shift from marginal to circulating pool in blood

A

Epinephrine
Glucocorticoids
Infection
Stress

177
Q

Name 3 causes of neutrophillia

A

Inflammation
Steroids (stress, steroid therapy, HAC)
Physiological (epinephrine, fight or flight)

178
Q

Signs of neutrophil toxic change

A

Foamy cytoplasm
Diffuse cytoplasmic basophilia
Dohle bodies

179
Q

Causes of neutrophil toxic change

A

Rapid neutropoesis
Usually severe bacterial infection
Other causes - Parvo, IMHA, neoplasia

180
Q

3 causes of neutropenia

A

Inflammation
Decreased production
Rare causes - canine hereditary neutropenia, immune mediated neutropenia

181
Q

What is cytopenia

A

When there is marrow disruption, lineage kinetics result in disappearance of neutrophils first, then platelets then RBC’s

182
Q

Name 5 causes of lymphocytosis (high)

A

Physiological
Chronic inflammation
Young animals
Recently vaccinated animals
Hypoadrenocorticism

183
Q

6 Causes of lymphopenia (low)

A

Stress/steroids
Acute inflammation
Loss of lymph
Cytotoxic drugs/radiation
Immunodeficiency syndrome
Lymphoma

184
Q

Name 3 causes of eosinophilia

A

Hypersensitivity
Parasitism
Hypoadrenocorticism

185
Q

Name 3 causes of eosinopenia

A

Glucocorticoids
Stress
Inflammation

186
Q

What are the three zones of a blood smear

A

Feathered edge
Monolayer
Body

187
Q

What do reference intervals tell us

A

If a lab result is normal or abnormal

188
Q

What percentage of the healthy population does a reference interval contain

A

central 95%

189
Q

Damage vs dysfunction

A

Damage = pathology
Dysfunction = how bad it is

190
Q

What (liver) enzymes on biochemistry tell us

A

Location - where enzymes are coming from
Persistence in serum - how likely we have caught the active disease
Degree of change - severity
Induction - enzymes in circulation due to pathology, drugs or endogenous compounds

191
Q

What presence of ALT tells us

A

Cytosolic enzyme in hepatocytes
Tells us damage to cell walls

192
Q

what the presence of ALKP tells us

A

Located in membrane of caniculi
Induced by impaired biliary flow and medications

193
Q

What does elevated urea and normal creatinine suggest

A

Pre-renal effects

194
Q

What 2 acronyms are used for causes of hypercalcaemia

A

HOGS IN YARD
HARD IONS

195
Q

What does HARD IONS stand for (hypercalcaemia)

A

Hyperparathyroidism
Addisons
Renal
Vitamin D
Idiopathic
Osteolysis
Neoplasia
Spurious

196
Q

What species is urea not a helpful test and why

A

Horses and ruminants
GIT and clearance mechanisms mean it cannot be used to indicate renal function

197
Q

Which species is ALT not helpful

A

Horses and ruminants as not liver specific

198
Q

What 3 things does faecal egg count allow us to do

A

Determining level of parasite burden
Identify animals which require treatment
Allows us to target our therapy => reducing selectrion pressure for anthelmintic resistance

199
Q

Give advantages and disadvantages of a direct smear for faecal egg count

A

Adv - cheap, short processing
Dis - Qualitative, low accuracy, precision and sensitivity

200
Q

Give advantages and disadvantages of the Cornell-Wisconsin method for faecal egg count

A

Adv - cheap, high limit of detection
Dis - time consuming, low accuracy

201
Q

Give advantages and disadvantages of the McMasters method for faecal egg count

A

Adv - cheap, medium processing
Dis - requires specialised slides, sensitivity limit = 50 eggs/gram of faeces

202
Q

what is a faecal egg count reduction test used for and ow is it carried out

A

Detecting anthelmintic resistance
2 faecal egg counts
1 at the time of treatment
2 at defined times after treatment
Calculate % reduction In eggs after treatment

203
Q

what % shows anthelmintic resistance for the FEC reduction test

A

If <95% reduction => resistance

204
Q

Which categories of parasites live above the skin surface

A

Fleas
Lice
Surface mites

205
Q

Which categories of parasites live below the skin surface

A

Deep mites
Demodex

FCP (8 decks)

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