4. Pathology Flashcards
Define pathology
The study of disease OR
The structural, biochemical, and functional changes in cells, tissues and organs that underlie disease
What are the 2 broad categories of pathology
General pathology
Systemic pathology
What is meant by general pathology
Basic responses of cells and tissues to insults and injuries, irrespective of the organs, systems, or species of animal involved
What is meant by systemic pathology
Pathology of organ systems
Alterations in specialized organs and tissues
When examining patients, what are the 2 types of pathology
Anatomic pathology
Clinical pathology
What is meant by anatomic pathology
Examination of tissues taken during life (biopsy) or after death (autopsy, necropsy)
What is meant by clinical pathology
Examination of blood and other body fluids, as well as cells (cytology) during life, laboratory diagnostics and technology
What is meant by inflammation
Vascular and interstitial tissue changes that develop in response to tissue injury and that are designed to sequester, dilute, and destroy the causal agent
What is meant by ‘healing’ and what 4 processes does it involve
Repair of injured tissue
Involves: angiogenesis, fibrosis, regeneration and epithelialisation
What is meant by the term thrombosis
Interaction of the blood coagulation system and platelets to form, within a vascular lumen, an aggregate of fibrin and platelets
How does thrombosis differ from normal clotting (Virchow’s triad)
Involves Virchow’s triad:
Vascular wall damage
Hypercoagulable state
Changes in blood flow
What is meant by the term neoplasia
New cellular growth
Leads to unrestrained mitosis and an expanding mass of uncontrolled cells that affects adjacent normal tissue.
2 mechanisms by which neoplasia affects normal tissue
Compression
Replacing them
What is meant by the word necrosis
Death of cells or tissue in the living animal
What Is meant by the word biopsy
Removal and examination of a tissue sample from a living animal body for diagnostic purposes
What do you need to include in a pathologic description of a lesion (x8)
Location
Number/extent
Demarcation
Distribution
Colour
Size
Shape
Consistency and texture
What are the 4 main aspects of disease
Aetiology
Pathogenesis
Molecular and morphologic changes
Clinical manifestation
What are the 2 aspects of a pathologic exam
Biopsy
Post mortem exam
What is a ‘clinical diagnosis’ based on
Based on data obtained from the case history, clinical signs and physical examination
What is a ‘clinical pathologic diagnosis’ based on
Based on changes observed in the chemistry of fluids and the haematology, structure, and function of cells collected from the living patient
What is a ‘morphologic diagnosis’ based on
Based on what is seen
Can be macroscopic or microscopic
What does a morphologic diagnosis describe
Describes severity, duration , distribution, location (organ or tissue), and nature (degenerative, inflammatory, neoplastic) of the lesion
What does a morphologic diagnosis describe
Describes severity, duration , distribution, location (organ or tissue), and nature (degenerative, inflammatory, neoplastic) of the lesion
What are the common post mortem changes which can be seen in tissues (x7)
Autolysis
Putrefaction
Rigor Mortis
Livor Mortis
Post Mortem clotting
Haemoglobin/bile imbibition
Pseudomelanosis
What is autolysis
Changes to a tissue due to ‘self digestion’
What is putrefaction
Colour and texture changes, gas production, and odours that are caused by post-mortem bacterial metabolism and dissolution of host tissues
What is rigor mortis, when does it start and how long for
Contraction of muscles occurring after death
Due to depletion of ATP and glycogen
Commences 1-6 hours after death
Persists for 1-2 days
What is Livor mortis
Gravitational pooling of blood in the animal
What is post mortem clotting
Evident in the heart and great vessels
Differs from thrombosis as not adhered to vessel wall
What is haemoglobin imbibition
Red staining of tissues by haemoglobin
What is bile imbibition
Bile from the gallbladder staining adjacent tissues yellow/green/brown colour
What is pseudomelanosis
Blue/green discolouration of tissue by iron sulphide
Are post mortem changes the same as a lesion
No
What are the 5 cardinal signs of acute inflammation
Redness
Heat
Swelling
Pain
Loss of function
What is the definition of acute inflammation
A redundant, complex, adaptative and protective response of vessels, resident cells and leucocytes to noxious stimuli.
How long does acute inflammation last for
Hours to days
Name 6 causes of acute inflammation
Infections
Foreign bodies
Immune reactions (hypersensitivities)
Tissue necrosis
Trauma
Physical and chemical Injury
What are the 3 morphologic hallmarks of acute inflammation
Dilation of blood vessels
Activation and recruitment of leukocytes
Active oxidation of fluid in the extravascular tissues
What are the 6 steps of inflammation (6 R’s)
Recognition of injurious agent
Reaction of blood vessels
Recruitment of leukocytes
Removal of the agent
Regulation of the response
Repair/Resolution
Name the main 4 mediators in acute inflammation and give examples of each
- Vasoactive amines (histamine, serotonin)
- Inflammatory lipids (prostaglandins leukotrienes)
- Complement (C5a, C3a)
- Cytokines (IL-1, TNF, IL-6)
Which mediators are responsible for vasodilation in acute inflammation
Inflammatory lipids
Which mediators are responsible for increased vascular permeability in acute inflammation
Vasoactive amines
Complement
Inflammatory lipids
Cytokines
Which mediators are responsible for Leukocyte recruitment and activation in acute inflammation
Inflammatory lipids
Complement
Cytokines
Which mediators are responsible for Pain in acute inflammation
Inflammatory lipids
Which mediators are responsible for Tissue damage in acute inflammation
Neutrophil granule content
ROS
What is the sequelae of acute inflammation
- Complete resolution
- Scarring or fibrosis
- Progression to chronic inflammation
What is the acute phase response in acute inflammation
The acute phase response is characterized by different systemic effects of acute inflammation (and other conditions) including pyrexia, leucocytosis, metabolic changes.
How is pyrexia caused by acute inflammation
exogenous pyrogens and endogenous triggers
=> neutrophils and macrophages
=> endogenous pyrogens
=> PGE2
=> pyrexia
what are acute phase proteins
Biomarkers of inflammation
Can be positive or negative
Give 4 examples of positive acute phase proteins (increase during inflammation)
C reactive protein
Serum amyloid A
Fibrinogen
Complement
Give 4 examples of negative acute phase proteins (decrease during inflammation)
Albumin
Transferrin
Transthyretin
Retinol binding protein
Name 2 types of effusions
Transudates
Exudates
What is transudate and when is it present
Extravascular filtrate of protein and cell poor fluid
Due to increased hydrostatic pressure or decreased colloido-osmotic pressure
What is an exudate and when is it present
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
Give 4 types of exudates
Serous
Fibrinous
Purulent
Haemorrhagic
What is serous inflammation
Inflammation with exudation of fluid with a low concentration of plasma protein and no to low numbers of leukocytes.
Give 3 examples of serous inflammation
Serous rhinitis
Acute allergic reactions
Cutaneous blisters
What is fibrinous inflammation
Inflammation with exudation of fibrinogen and fluid, and formation of thick, friable, loosely adherent fibrin.
Give 2 examples of fibrinous inflammation
Fibrinous peritonitis
Fibrinous bronchopneumonia and pleurisy
What is purulent inflammation
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
Give 2 examples of purulent inflammation
Purulent pleurisy (pyothorax)
Purulent lymphadenitis and cellulitis
What is haemorrhagic inflammation
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.
How long after acute inflammation does chronic inflammation start
24-72 hours after acute inflammation
How long can chronic inflammation persist for
Weeks/months/years
What is the main cell type involved in chronic inflammation and what are the different classes
Macrophages - M1 or M2
M1 = turn arginine => nitric acid = highly toxic to phagocytoses organisms
M2 = non inflammatory, turn arginine => orthinine => proline
What do activated macrophages produce in chronic inflammation and give examples
Pro inflammatory cytokines
E.g. IL-1, IL-6
What do pro-inflammatory cytokines cause
Pyrexia
Lethargy
Stimulate acute phase proteins
What causes granulomas to form
Persistent stimulus e.g. inert irritant or a pathogen
What cell types are present in pyogranulomatous lesions
Macrophages and neutrophils
Give 2 disease examples with pyogranulomatous lesions
Feline infectious peritonitis
Johnes disease in cattle
What are the 2 types of chronic inflammation
- With a clear pathogen
- Without a clear pathogen
Define neoplasia
The process of abnormal proliferation of cells
Define neoplasm
An abnormal mass of tissue that occurs as result of abnormal cell proliferation (can also be called cancer or tumour)
What is the difference between benign, pre-malignant, and malignant neoplasms
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
What is ‘oncogenesis’
Process of gradual stepwise tumour development
Cancer develops gradually from normal tissue
Name the 3 steps of oncogenesis
- Initiation (mutagenesis)
- Promotion
- Progression into malignancy
Give the different types of initiation/mutagenesis in the process of oncogenesis (x4)
Chemical or physical
Inherited or spontaneous
Viruses or bacteria
Reactive oxygen species (ROS)
Benign vs malignant differentiation
Benign - Well differentiated, similar to tissue or origin, little to no anaplasia
Malignant - lack of differentiation, atypical structure, variable anaplasia
Benign vs malignant growth rates
Benign - slow, progressive, rare and normal mitotic features
Malignant - slow to rapid, many abnormal mitotic figures
Benign vs malignant local invasion level
Benign - no invasion, cohesive growth, capsule often present
Malignant - local invasion, infiltrative growth usually no capsule
Benign vs malignant metastasis level
Benign - no metastasis
Malignant - frequent metastasis
Benign vs malignant host consequences
Benign - space occupying lesion, effect depends on location
Malignant - Life threatening
Benign vs malignant cellular morphology
Benign - Minimal to mild anisocytosis (variation in cell size and shape)
Malignant - marked anisocytosis
Benign vs malignant nuclear to cytoplasmic ratio
Benign - normal to reduced
Malignant - increased
Benign vs malignant nuclear morphology
Benign - Minimal to mild anisokaryosis (variation in nuclear size and shape)
Malignant - marked anisokaryosis with frequent binculeation and multi nucleation
Benign vs malignant mitotic count
Benign - low
Malignant - high
Benign vs malignant necrosis level
Benign - minimal or absent
Malignant - frequently present
Benign vs malignant individualisation and invasiveness of cells
Benign - absent
Malignant - invasiveness to surrounding tissues
What 4 types of neoplastic lesions are common and give examples
Mesenchymal - lymphoma, haemangioma, lipoma, leiomyosarcoma
Epithelial - melanoma, andeocarcinoma
Nervous - ganglioneuroma, astrocytoma
Other - germ cell tumour e.g. teratoma
How are metastases formed
Formed by cancer cells that have left the primary tumour and travelled through blood and lymphatic vessels
What are the main 2 causes of cancer related morbidity and mortality
Invasion
Metastasis
What are the 8 steps in the metastasis cascade
- Primary tumour formation
- Localised invasion
- Intravasation
- Transport through circulation
- Arrest in microvessels of various organs
- Extravasation
- Formation of micrometastasis
- Colonisation
Name the 3 pathways of metastasis
- Transcoelomic
- Lymphatic
- Haematogenous
Name 4 types of tumours which metastasise to the lungs
Osteosarcoma
Hemangiosarcoma
Melanoma
Mammary tumours
Name 2 types of tumours which metastasise to the liver, spleen and kidney
Mast cell tumours
Hemangiosarcomas
Name 3 types of tumours which metastasise to the bone
Mammary gland tumours
Prostatic carcinomas
Urinary bladder tumours
Name the common sites of metastasis
Lungs
Liver, spleen and kidney
Bone
Brain, adrenal glands
Name the direct effects of neoplasias
Space occupying
Displaces and puts pressure on surrounding tissues
=> atrophy, necrosis or death of surrounding tissues
Name the indirect effects of neoplasias
Normally caused by tumour cell products
Haematological, endocrinological and metabolic complications
Such complications may be the main presenting sign
Define cachexia
Weakness and wasting of the body due to severe chronic illness
How does cancer cause cachexia
Results from altered carbohydrate, protein and lipid metabolism
Complex pathogenesis due to TNF-a, IL-1, IL-6 and prostaglandins
How is a fever caused by tumour/cancer
Caused by tumour-induced production of cytokines (IL-1)
What is an endocrine neoplasm, give an example and what can they cause
Functioning endocrine tumour
Hypoglycaemia - caused by insulinoma
What is a non-endocrine neoplasm, give examples and what they can cause
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
What is hypertrophic pulmonary osteopathy, and what tumours are they commonly associated with
Rapid periosteal new bone growth affecting distal limbs
Lung tumours
What is myelofibrosis
Overgrowth of nonneoplastic fibroblasts in the bone marrow, which impairs normal haematopoiesis
Name some common paraneoplastic syndromes
Alopecia
Epidermal necrosis
Vascular and haematological disorders
Name the intrinsic and extrinsic causes of neoplastic transformation
Intrinsic - DNA damaging metabolites e.g. ROS and organic acids
Extrinsic - Chemical environmental agents, physical environmental agents, oncogenic viruses
What is the difference between a mutagen and a carcinogen
Mutagens = agents that create the DNA damage and gives rise to mutation
Carcinogens = agents that can cause cancer
(Many mutagens are carcinogens)
What are the two types of chemical environmental agents (extrinsic factors for neoplasms)
Direct acting chemical carcinogens - effective in the form the enter the body
Indirect acting chemical carcinogens - procarcinogens
Give 3 categories of physical environmental extrinsic factors for neoplasms and how they act
Complete carcinogens - initiation and promotion
Ionising radiation - DNA damage and ROS generation
UV radiation - formation of hallmark pyrimidine dimers and ROS generation
What is a proto-oncogene
Unmutated gene which are involved in growth factor pathways
When they are mutated, they will lead to uncontrolled cell proliferation
What is an oncogene
Mutated proto-oncogene
Promote autonomous growth
Can encode for specific proteins (oncoprotein)
What is an oncoprotein
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
Name 3 direct mechanisms the oncogenic viruses have and explain them
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
Name 2 indirect mechanisms of oncogenic viruses
Suppression of animals immune system
Stimulation of target cell proliferation
2 methods of diagnosing neoplasms
Cytopathological examination
Histopathological examination
What method of extraction do we use for cytopathology of a neoplasm
Fine needle aspiration
Why do we need to do histopathology on a neoplasm as well as cytopathology
Give additional info needed which can direct the therapeutic plan
Helps to provide microscopic description
Gives tumour grade
Importance of surgical margins tissue biopsies
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
Define cytology
The study of cell number and type in a tissue mass or fluid accumulation, to investigate its cause
Name 4 common cytological specimens
FNA
Touch imprints
Body fluids
Lavages
What does cytological examination allow (4 things)
Differentiation of inflammation from tissue growth
Differentiation of types of inflammation
Detect neoplasia
Differentiation of different fluid
Give the main advantages of cytology
Quick, safe and inexpensive
Demands little equipment
Quickly available results
Give the main limitations of cytology
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
Name 3 lesion types which are identifiable by cytology and give examples
Inflammation - Neutrophillic, eosinophilic, granulomatous
Cystic lesions - epidermal, serum, haematoma
Neoplastic - epithelial, round, mesenchymal, benign vs malignant
Cell types identifiable by cytology
Epithelial
Spindle/mesenchymal
Round
What can cytology tell us about cells
Inflammatory - sterile vs septic
Non inflammatory - Cystic, hyperplastic, neoplastic
Name 4 types of inflammation (based on cell type)
Neutrophillic inflammation
Pyogranulomatous inflammation
Granulomatous inflammation
Eosinophillic inflammation
Give specific examples of epithelial skin tumours (6)
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
Where do mesenchymal skin tumours arise from
Connective tissue, muscle, bone, cartilage, nerve and endothelial cells
Give examples of mesenchymal skin tumours
Lipoma and liposarcoma
Melanoma
Haemangioma/haemangiosarcoma
Give characteristics of a lipoma
Adipocytes with small nucleus and abundant cytoplasm
free fatty droplets
Appears identical to subcutaneous fat cytologically
Give examples of round cell tumours
Mast cell tumour
Lymphoma
Plasmacytoma
Histiocytic tumours
what is clinical pathology (tests involved)
combination of haematology, clinical biochemisrty, cytology
What anticoagulants are used for: haematology, clinical chemistry, glucose and haemostasis
Haematology - EDTA
Clinical chemistry - Lithium heparin, EDTA
Glucose - Fluoride-oxalate
Haemostasis - citrate
If a sample is contaminated with EDTA, what electrolyte levels will be affected
Calcium - will be very low
Potassium - will be very high
How to to avoid haemolysis of a blood sample
Choose appropriate gauge needle
Don’t dispense blood back through the needle
What are the effects of haemolysis on a blood sample
Increases in plasma/serum values of some compounds due to higher conc. in RBC
Interferes if using colorimetry and chemical interactions
What are the effects of lipaemia on a blood sample
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
3 sources of variation and errors in lab results and give examples
Pre-analytical - patient and sample prep, shipping
Analytical - Appropriate equipment, quality control
Post analytical - appropriate interpretation, diagnostic sensitivity and specificity
When looking at validation of an analytical techniques, what does PASS stand for
Precision
Accuracy
Specificity
Sensitivity
What is an internal quality control
Done with patient samples
What is an external quality control
Non contemporaneous - at a different time
3 aspects of urinalysis
Physical analysis
Chemical analysis
Microscopy/ sediment examination
What do you look at in a physical exam of urine
Colour, turbidity, odour
USG
What do you look at in a chemical exam of urine
pH
Protein, glucose, ketones, bilirubin
Blood
What do you look at in a microscopy/sediment exam of urine
RBC, Leukocytes
Epithelial cells
Bacteria
Casts
Crystals
What is measuring USG actually measuring
Urine osmolality
If urine is isosthenuric in a dehydrated/azotaemic patient what does this suggest
Shows the tubules are not secreting or absorbing
Suggests a problem with the kidney
Concentrating ability is impaired around 60-70% of nephron loss
What do you have to do to determine if there is a problem with concentrating ability alongside USG
Needs correlation with hydration status and/or azotaemia
3 mechanisms causing proteinuria and describe
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
Which type of proteinuria causes blood albumin to fall and cause “nephrotic syndrome”
Glomerular proteinuria
Causes of glomerular proteinuria
Inflammation in the glomeruli (glomerulonephritis)
Damage to glomeruli - diabetes, hypertension, kidney diseases
Which 3 chemical readings on urinalysis are not reliable/applicable in dogs and cats
Leukocytes
Urobilinogen
Nitrites
What do casts in urine suggest
Tubular damage/disease
Name 4 types of casts in urine
Hyaline - protein
Cellular
Granular
Waxy
Name 4 types of crystals that can be seen in urine
Calcium carbonate
Struvite - magnesium ammonium phosphate
Calcium oxalate monohydrate and dihydrate
Urates (ammonium and amphorus)
Two approaches to cytology of tissue
Unknown mass
Known tissues
How to classify cavity effusions with cytology
Protein content, cell count and classification
Protein poor transudate vs protein rich transudate vs exudate (inflammatory)
Name 3 cytological criteria of malignancy
Cellular
Nuclear
Cytoplasmic
Give 4 reasons why lymph nodes may be enlarged
- Reactive hyperplasia
- Lymphadenitis
- Metastatic neoplasia
- Lymphoma
What are we looking for when looking at red cell parameters
Red cell mass
Evidence of erythropoiesis
Red cell size and variation
Red cell colour (haemoglobinisation)
Red cell shapes and inclusions
How to assess red cell mass (3 methods)
PCV
RBC count
Hgb levels
Causes of high haemoglobin
Haemolysis of the blood sample
Lipaemia
Causes of misleading mean cell value results
Swelling in transport
Misidentification
Cell shrinkage or expansion in sample
What are the classifications of anaemia, and which test tests for them
MCV (size of RBC) - can be normocytic, microcytic or microcytic
MCHC (haemoglobin in RBC)- can be normochromic, hyperchromic or hypochromic
What is meant by ‘polycythaemia’ and how is it identified
Too much red cell mass
Increased PCV, haemoglobin and RBC count
What is relative polycythaemia
Apparent increase in RBC due to decrease of fluid in circulation (dehydration)
What is absolute polycythaemia
True increase in RBC mass due to increased RBC production/release
What are primary and secondary absolute polycythaemia
Primary = normal EPO levels, abnormal response of RBC precursors
Secondary = Increased EPO, chronic tissue hypoxia of renal tissue or renal tumours or cysts
What do reticulocytes show
Evidence of regeneration
Name 2 causes of alteration in red cell shape
Abnormal erythropoiesis
Specific organ dysfunction
3 causes of inclusions in RBC
Active regeneration
Infective agents
Heinz bodies
What is a Rouleaux formation and what does it indicate
Clustering, sticky piling of RBC
Indicates Inflammation in small animals
3 steps for cells to leave blood vessels
Marginalisation
Adhesion
Migration
Name 4 factors that can cause a shift from marginal to circulating pool in blood
Epinephrine
Glucocorticoids
Infection
Stress
Name 3 causes of neutrophillia
Inflammation
Steroids (stress, steroid therapy, HAC)
Physiological (epinephrine, fight or flight)
Signs of neutrophil toxic change
Foamy cytoplasm
Diffuse cytoplasmic basophilia
Dohle bodies
Causes of neutrophil toxic change
Rapid neutropoesis
Usually severe bacterial infection
Other causes - Parvo, IMHA, neoplasia
3 causes of neutropenia
Inflammation
Decreased production
Rare causes - canine hereditary neutropenia, immune mediated neutropenia
What is cytopenia
When there is marrow disruption, lineage kinetics result in disappearance of neutrophils first, then platelets then RBC’s
Name 5 causes of lymphocytosis (high)
Physiological
Chronic inflammation
Young animals
Recently vaccinated animals
Hypoadrenocorticism
6 Causes of lymphopenia (low)
Stress/steroids
Acute inflammation
Loss of lymph
Cytotoxic drugs/radiation
Immunodeficiency syndrome
Lymphoma
Name 3 causes of eosinophilia
Hypersensitivity
Parasitism
Hypoadrenocorticism
Name 3 causes of eosinopenia
Glucocorticoids
Stress
Inflammation
What are the three zones of a blood smear
Feathered edge
Monolayer
Body
What do reference intervals tell us
If a lab result is normal or abnormal
What percentage of the healthy population does a reference interval contain
central 95%
Damage vs dysfunction
Damage = pathology
Dysfunction = how bad it is
What (liver) enzymes on biochemistry tell us
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
What presence of ALT tells us
Cytosolic enzyme in hepatocytes
Tells us damage to cell walls
what the presence of ALKP tells us
Located in membrane of caniculi
Induced by impaired biliary flow and medications
What does elevated urea and normal creatinine suggest
Pre-renal effects
What 2 acronyms are used for causes of hypercalcaemia
HOGS IN YARD
HARD IONS
What does HARD IONS stand for (hypercalcaemia)
Hyperparathyroidism
Addisons
Renal
Vitamin D
Idiopathic
Osteolysis
Neoplasia
Spurious
What species is urea not a helpful test and why
Horses and ruminants
GIT and clearance mechanisms mean it cannot be used to indicate renal function
Which species is ALT not helpful
Horses and ruminants as not liver specific
What 3 things does faecal egg count allow us to do
Determining level of parasite burden
Identify animals which require treatment
Allows us to target our therapy => reducing selectrion pressure for anthelmintic resistance
Give advantages and disadvantages of a direct smear for faecal egg count
Adv - cheap, short processing
Dis - Qualitative, low accuracy, precision and sensitivity
Give advantages and disadvantages of the Cornell-Wisconsin method for faecal egg count
Adv - cheap, high limit of detection
Dis - time consuming, low accuracy
Give advantages and disadvantages of the McMasters method for faecal egg count
Adv - cheap, medium processing
Dis - requires specialised slides, sensitivity limit = 50 eggs/gram of faeces
what is a faecal egg count reduction test used for and ow is it carried out
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
what % shows anthelmintic resistance for the FEC reduction test
If <95% reduction => resistance
Which categories of parasites live above the skin surface
Fleas
Lice
Surface mites
Which categories of parasites live below the skin surface
Deep mites
Demodex
