Fundamentals of clinical practice 2 Flashcards

1
Q

What are the different sections that can be seen in this panel?

A
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2
Q

What is being assessed in a blood panel?

A

Red cell mass
Evidence for effective and apt erthyropoeisis
Red cells size and variation
Red cell haemoglobinisation
Red cell shapes and inclusions

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3
Q

What are the goals of packed cell volume, red cell count and Hgb?

A

PCV (Hct), RBCC and Hgb
All three are measures of red cell mass and oxygen carrying capacity
Usually interpret them as a block
All equally affected by haemoconcentration
Will usually increase and decrease in line with one another
When they are discordant find out why – “rule of three”

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4
Q

How is PCV calculated?

A

PCV = MCV x RBCC

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5
Q

When may PCV be incorrect?

A

PCV may be wrong if…
RBC’s miscounted
Mistaken for platelets
Aggregated into pairs and triplets
MCV misleading
Cell shrinkage or swelling
Transport, tube filling
Osmotic effects in machine

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6
Q

What does high MCHC suggest?

A

misleading results
Not physiological to cram more Hgb into red cells than they will take
Haemolysis (sample handling or intravascular)
Lipaemia

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7
Q

Polycythaemia

A

Implies increased number of several haemopoetic cell lines in humans

In dogs and cats with polycythaemia vera ususally have normal neutrophil and platelet counts

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8
Q

How can MCV cause misleading PCV result?

A

Swelling of transport
Misidentification
Cell shrinkage or expansion in sample
Will impact PCV/HCT

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9
Q

How can the rule of three be used in haematology?

A
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10
Q

How is anaemia classified?

A

Based on MCV and MCHC
Blunt measure
Microscope visible findings may not be sufficient to push parameter out of the reference range
Machine dot=plots and histograms more sensitive

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11
Q

What are the classifications of anaemia?

A

Normocytic normochromic
Macrocytic hypochromic
Microcytic hypochromic

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12
Q

Properties of normocytic normochromic anaeamia

A

Often anaemia of illness or pre regenerative or occasionally non regenerative

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13
Q

Properties of macrocytic hypochromic anaemia?

A

Classic highly regenerative
Sometimes can be due to swelling of transport

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14
Q

Properties of microcytic hypochromic anaemia?

A

Classic iron deficiency- chronic external blood loss
Without anaemia- portosystemic shunts

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15
Q

How is polycytheamia detected on a panel?

A

Increase in PCV, Hgb concentration and RBCC

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16
Q

What are the properties of relative polycythaemia on a panel?

A

Apparent increase in RBC due to a decrease in fluid in circulation (often inc total protein and albumin)

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17
Q

What are the properties of absolute polycythaemia on a panel?

A

True increase in RBC mass due to increased RBC production and release
(usually polychromasia, anisocytosis and reticulocytes)

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18
Q

What is primary polycythaemia?

A

rare myeloproliferative disorder
Abnormal response of RBC precursors
Normal EPO levels

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19
Q

What is secondary polycythaemia?

A

Chronic tissue hypoxia of renal tissues due to heart lung diseases, high altitude, thrombosis, constriction of renal vessels

Renal tumor or cysts (increased intra capsular pressure)
Increased EPO

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20
Q

What are reticulocytes and how can they be visualised?

A

Young immature erythrocytes prematurely released to blood from the bone marrow in regenerative anaemias

Visualise using New methylene blue precipitation demonstrates RNA protein complexes (ribosomal RNA and mitochondria)

Clinical applications
- evaluation of erythropoeisis in bone marrow
- differentiation of regenerative and non regenerative anaemia

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21
Q

Reticulocyte count?

A
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22
Q

Species variation in reticulocyte response?

A
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23
Q

What red cell variations are there within dog breeds?

A

macrocytosis in some poodles
Akitas have unusually small erythrocytes and high potassium content
Greyhounds have high PCVs

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24
Q

Poikilocytosis

A
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25
Q

What red cell inclusions can be seen?

A
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26
Q

What are the key components of a haematology report in veterinary medicine?

A

Red Blood Cells (RBC), Hemoglobin (Hb), Hematocrit/PCV, Mean Corpuscular Volume (MCV), Mean Corpuscular Hemoglobin Concentration (MCHC), White Blood Cells (WBC) and differential, Platelet count.

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27
Q

How is red cell mass evaluated and what does it indicate about erythropoiesis?

A

Red cell mass is evaluated using PCV/Hct, RBC count, and Hgb levels. It provides evidence for effective and appropriate erythropoiesis based on size, color (MCV, MCHC), and reticulocyte count.

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28
Q

What does MCV and RDW indicate in red cell size and variation assessment?

A

MCV indicates the average volume of red cells, suggesting their size, while RDW measures the variation in red cell size, indicating anisocytosis.

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29
Q

How is anemia classified based on red cell parameters?

A

Anemia is classified based on cellular characteristics such as normocytic, normochromic, hypochromic, and macrocytic, which helps in determining the underlying cause and type of anemia.

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30
Q

Differentiate between relative and absolute polycythemia.

A

Relative polycythemia is due to a decrease in plasma volume without an increase in RBC mass, often from dehydration. Absolute polycythemia is a true increase in RBC mass due to increased production/release of RBCs.

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31
Q

What are reticulocytes and their significance in diagnosing anemias?

A

Reticulocytes are immature, non-nucleated erythrocytes released prematurely from the bone marrow during regenerative anemias. Their count helps evaluate bone marrow response and differentiate between regenerative and non-regenerative anemia.

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32
Q

What does a high RBC count indicate in animals?

A

It may indicate polycythemia, which is an increased number of red blood cells.

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33
Q

Why are reticulocyte counts important in veterinary diagnostics?

A

They indicate the bone marrow’s response to anemia, helping differentiate between regenerative and non-regenerative types.

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34
Q

How does dehydration affect PCV (Packed Cell Volume) readings?

A

Dehydration can artificially raise PCV readings by reducing plasma volume, making it seem like there are more red cells than there actually are.

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35
Q

What are the primary functions of white blood cells in disease diagnosis?

A

To aid in the diagnosis of disease through their characteristics, including type and concentration in the blood.

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36
Q

List the different types of white cells found in the blood.

A

Neutrophils, lymphocytes, monocytes, eosinophils, and basophils.

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37
Q

How do white cell counts vary among different species?

A

There is significant species variation in the relative value and distribution of white cells, with specific reference intervals for dogs, cats, horses, and cows.

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38
Q

What is leukocytosis and what can cause it?

A

Leukocytosis is an increase in the number of white blood cells in the blood, caused by conditions like infections, inflammation, and stress.

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39
Q

Explain the significance of neutrophilia and its causes.

A

Neutrophilia is an increase in neutrophils, often indicating inflammation, infection, or stress. Causes include bacterial infections, tissue necrosis, and reactions to steroids or epinephrine.

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40
Q

Describe the process and significance of cells leaving blood vessels (marginalisation, adhesion, migration).

A

This process allows white blood cells to exit the bloodstream and enter tissues where they can engage pathogens or damaged cells. Factors influencing this include epinephrine, glucocorticoids, and infection.

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41
Q

What are the implications of a left shift in a white blood cell differential?

A

A left shift, where immature neutrophils (bands) outnumber mature ones, indicates an active response to infection, inflammation, or stress.

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42
Q

Define eosinophilia and its causes.

A

Eosinophilia is an increased concentration of eosinophils, typically due to allergic reactions, parasitic infections, or certain diseases.

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43
Q

What does lymphocytosis indicate?

A

An increase in lymphocytes, often seen in viral infections, chronic inflammation, or in young animals as a response to vaccination.

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44
Q

Discuss the significance of monocytes in blood analysis.

A

Monocyte levels can indicate chronic inflammation, with an increase suggesting ongoing immune response to infection or tissue damage.

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45
Q

What does a “left shift” in neutrophils mean, and why is it important?

A

It signals an increase in immature neutrophils, indicating a vigorous bone marrow response to infection or disease.

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46
Q

In what situations might eosinophil levels increase, and what does this tell a veterinarian?

A

Elevated eosinophil levels can indicate allergic reactions, parasitic infections, or certain autoimmune conditions, guiding diagnostic and treatment strategies.

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47
Q

What are the primary goals of routine cytological sample examination?

A

To determine the adequacy of the sample for diagnosis, identify the type of cells present, and assess the presence of inflammation, infection, or neoplasia.

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48
Q

What factors should be evaluated during the low power review of a cytological sample?

A

Sample quality, presence and preservation of cells, background characteristics (e.g., hemorrhage, protein matrix, debris), and predominant cell types.

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49
Q

How do you assess cells at high magnification during cytology review?

A

By examining cell organization, population (single or mixed), cell size and shape variation, and nuclear characteristics including size, shape, and any abnormal mitoses.

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50
Q

What criteria are used to determine if a sample is inflammatory, and how do you identify its type?

A

Based on the presence of specific cell types (e.g., neutrophils) and characteristics such as septic versus non-septic inflammation.

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51
Q

What are the key features to differentiate between benign and malignant neoplasia in cytology?

A

Cellularity, degree of differentiation, presence of mitotic figures, and cellular atypia.

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52
Q

How can cytological examination help differentiate between epithelial, mesenchymal, and round cell tumors?

A

By assessing cell shape, arrangement, and other morphological features specific to each cell type.

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53
Q

Why is it important to match the cytology findings with the known normal cell population of a tissue?

A

To determine if the sample reflects normal tissue architecture or indicates pathology, such as neoplasia or inflammation.

“Known tissue approach”

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54
Q

What steps are involved in writing an in-clinic cytological report?

A

: Assessing sample adequacy, describing findings (cell types, inflammation, neoplasia), and providing a diagnosis or differential diagnoses.

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55
Q

How are reference intervals for biochemical panels determined, and what challenges are associated with their creation?

A

Reference intervals are ideally determined using data from 120 clinically normal animals to account for variability across age and breeds, but this is rare. In practice, they’re often based on smaller samples or extrapolated data. The central 95% of a healthy population defines these intervals, acknowledging that a small percentage of healthy animals will have values outside this range due to biological variability and measurement limitations

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56
Q

Explain the statistical basis for determining what constitutes a “normal” result in a biochemical panel.

A

The “normal” range is defined as the central 95% of a healthy population, calculated as mean ± 2 standard deviations for normally distributed data or the 2.5th to 97.5th percentiles for skewed distributions. This accounts for natural biological variation but also means that approximately 5% of healthy individuals will have results outside this range by chance alone.

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57
Q

Discuss the significance of abnormal results when multiple tests are performed. (biochem panel)

A

With each additional test performed, the likelihood of encountering at least one “abnormal” result in a healthy animal increases due to statistical probability. For example, running 15 tests might result in abnormal results 54% of the time purely by chance. This highlights the importance of interpreting test results within clinical context and considering the possibility of compound statistical anomalies.

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58
Q

How should veterinarians approach the interpretation of borderline biochemical panel results?

A

Borderline results, especially those near the limits of reference intervals, require careful consideration of analytical variation. For instance, a result slightly outside the reference range might fall within it when measurement imprecision is accounted for. Clinicians should consider the entirety of clinical evidence, potentially retesting to confirm findings.

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59
Q

What factors should be considered when evaluating the plausibility of lab results?

A

Assessing result plausibility involves considering pre-analytical and analytical factors such as sample handling (e.g., hemolysis, lipemia), the potential for contamination, and the limits of the testing technique. Unusual values that don’t fit clinical expectations may necessitate reevaluation or additional testing to rule out artifacts.

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60
Q

Why is understanding the distribution of test results critical for interpreting individual values?

A

nderstanding the statistical distribution helps clinicians to interpret how individual results relate to the overall health status of the population. It provides a framework for assessing the likelihood that a result reflects a true physiological deviation versus a statistical outlier or measurement error.

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61
Q

How do leakage enzymes like ALT and AST differ in indicating organ damage compared to function indicators like bile acid for hepatic function?

A

Leakage enzymes (ALT, AST, CK) increase in serum due to cell damage allowing their escape, reflecting organ damage. In contrast, function indicators (bile acid, ammonia for hepatic function; creatinine, USG for renal) assess the organ’s performance in executing its physiological roles. Understanding both provides a comprehensive view of not just the presence of damage but also the affected organ’s functional capacity.

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62
Q

Why is alanine aminotransferase (ALT) considered liver-specific in dogs and cats, and how does its half-life influence monitoring liver health?

A

ALT is liver-specific in dogs and cats, making it a reliable marker for hepatic damage when elevated. Its half-life (40-60 hours in dogs, 3.5 hours in cats) dictates the timing for retesting to evaluate ongoing or resolving hepatic insult. Early and higher level increases post-damage allow precise monitoring of liver health and recovery.

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63
Q

How does enzyme induction by drugs or endogenous compounds like glucocorticoids affect the interpretation of biochemical panels?

A

Enzyme induction refers to increased enzyme activity without direct organ damage, often triggered by drugs (glucocorticoids, barbiturates) or pathological states. This distinction is crucial as elevated enzyme activities may not always signify organ damage but could reflect adaptive responses to external stimuli, complicating the diagnosis and necessitating careful evaluation of potential inducers in the patient’s history.

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64
Q

How do tests for hepatic function, such as bile acid and ammonia levels, differ in their diagnostic utility compared to liver damage enzymes?

A

Hepatic function tests, including measurements of bile acids and ammonia, evaluate the liver’s ability to perform essential metabolic processes, such as detoxification and synthesis. Unlike enzymes that leak from damaged cells, these function tests provide insight into the liver’s capacity to metabolize substances, with abnormalities indicating compromised liver function rather than structural damage. These tests are particularly valuable in diagnosing liver insufficiencies that may not yet have caused significant cellular damage.

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65
Q

What is the difference between organ damage and organ function indicators in veterinary biochemistry panels?

A

Organ damage indicators (e.g., leakage enzymes like ALKP, ALT, AST, CK, troponin I for cardiac damage, and PLI for pancreatic damage) are substances that leak into the bloodstream when cells are damaged. Organ function indicators (e.g., bile acid, ammonia for hepatic function; creatinine, USG for renal function; NT-proBNP for cardiac function) measure the ability of an organ to perform its physiological functions.

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66
Q

How are different biochemical parameters assessed and interpreted in veterinary practice?

A

Biochemical parameters are assessed based on their location (e.g., within the liver, other tissues, or cells), persistence in serum, degree of change, and their relation to disease or dysfunction. For example, enzyme activities (ALT, AST) indicate liver health, while creatinine and USG assess renal function. Parameters must be interpreted in the context of the animal’s overall health and specific condition.

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67
Q

What do elevated levels of ALT and ALKP indicate in dogs and cats, and how are they interpreted?

A

Elevated levels of ALT (alanine aminotransferase) and ALKP (alkaline phosphatase) in dogs and cats can indicate liver damage or dysfunction. ALT is more liver-specific, especially in dogs and cats, and increases earlier and to a higher degree following hepatic damage. ALKP can be induced by impaired biliary flow and medications, and is not liver-specific due to iso-enzymes present in bone and intestinal tissues.

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68
Q

How is renal function evaluated in veterinary medicine, and what does an elevated urea with normal creatinine suggest?

A

Renal function is evaluated using creatinine levels, urine specific gravity (USG), and the presence of proteinuria. Elevated urea with normal creatinine suggests pre-renal effects like dehydration or post-prandial states. A USG less than 1.030 in dogs or 1.035 in cats with azotemia suggests inappropriate dilution, indicating renal dysfunction.

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69
Q

Why are different biochemical indicators used in different veterinary species, and give examples?

A

Different species metabolize and respond to substances differently, necessitating species-specific biochemical indicators. For example, ALT elevations are more concerning in cats than in dogs due to their shorter half-life in cats. Urea is not a reliable renal function indicator in equidae and ruminants due to GI tract and other clearance mechanisms. Acute phase proteins and electrolyte balance also vary significantly among species, influencing test selection and interpretation.

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70
Q

What signifies organ damage in a biochemical panel?

A

Enzymes like ALT and AST leaking into the bloodstream indicate cell damage.

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71
Q

How do you differentiate between liver damage and liver function tests?

A

Liver damage is indicated by enzymes like ALT, while function tests involve bile acids and ammonia levels.

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72
Q

Why is creatinine important in assessing renal health?

A

Creatinine levels reflect the kidney’s ability to filter waste from the bloodstream.

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73
Q

How does species affect the choice of biochemical indicators?

A

Metabolic differences across species dictate which tests are relevant for assessing organ health.

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74
Q

What does an elevated ALKP level indicate in a dog or cat?

A

It can indicate liver damage or dysfunction, but it’s not exclusively liver-specific due to other sources like bone growth.

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75
Q

5-year-old English Springer Spaniel presented with acute onset of weakness. The patient has severe anemia, leukocytosis with neutrophilia, hyperglycemia, prolonged PT/aPTT, and hypoalbuminemia.

A

Immune-Mediated Hemolytic Anemia (IMHA)
Internal bleeding
Coagulopathy, possibly due to rodenticide toxicity

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76
Q

10-year-old cross-breed dog presented with a history of vomiting and anorexia. Bloodwork shows elevated ALP, ALT, GGT, hypercholesterolemia, and bile acids.

A

Hepatic neoplasia
Acute hepatitis
Drug-induced hepatopathy (considering meloxicam use)

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77
Q

A 12.5-year-old Old English Sheepdog presents with anorexia. Significant findings include severe leukocytosis with marked neutrophilia and band neutrophils, hypoalbuminemia, and elevated creatinine levels.

A

Pyometra
Septic peritonitis
Severe systemic infection leading to sepsis

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78
Q

A dog was accidentally exposed to a skin cream. Clinical pathology findings include hypercalcemia, hyperphosphatemia, and azotemia, indicative of potential renal involvement.

A

Toxicological exposure to calcipotriene (a vitamin D analogue) or other topical medication containing steroids, leading to acute renal failure and hypercalcemia.

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79
Q

History: 12-year-old Warmblood cross mare, refusing to move post a 40Km trail ride. Gluteal muscles hard, discomfort signs (lip curling, pawing), heart rate 48 bpm, respiratory rate 20 bpm, rectal temperature 38.2°C, dark brown urine.
Biochemistry Highlights:
Creatinine: 222 µmol/l (↑)
AST & Creatine Kinase: Above max detection limit
Total protein: 85 g/l (↑), Albumin: 40 g/l (↑)

A

Differential Diagnoses: Exertional rhabdomyolysis, dehydration, acute renal failure.
Treatment Options: IV fluids for rehydration, analgesics for pain management, and careful monitoring of renal function and muscle enzymes.

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80
Q

History: 5-year-old Thoroughbred mare, lethargic for 2 days, decreased appetite, not drunk for 12 hours, slightly increased respiratory effort, heart rate 52 bpm, respiratory rate 28 bpm, rectal temperature 38.5°C, mucous membranes pink and moist, capillary refill time <2 seconds.
Biochemistry Highlights:
Urea: 14.9 mmol/l (↑)
Creatinine: 141 µmol/l (↑)
Total protein: 58 g/l (↓), Albumin: 21 g/l (↓)
AST: 4.6 µkat/l (↑), Creatine Kinase: 6.5 µkat/l (↑)

A

Differential Diagnoses: Acute renal failure, dehydration, sepsis, electrolyte imbalances.
Treatment Options: IV fluids to address dehydration and renal function, antibiotics if sepsis is suspected, monitor electrolytes, supportive care.

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81
Q

History: 18-year-old Arabian gelding, off feed for 24 hours, lethargic, mild colic signs, heart rate 44 bpm, respiratory rate 16 bpm, rectal temperature 37.8°C, pale mucous membranes, capillary refill time 3 seconds.
Biochemistry Highlights:
Total Bilirubin: 34 µmol/l (↑)
AST: 12.5 µkat/l (↑)
GGT: 45 U/l (↑)
Albumin: 25 g/l (↓), Globulins: 55 g/l (↑)

A

Differential Diagnoses: Hepatic disease, hemolytic anemia, intestinal parasitism.
Treatment Options: Supportive care including IV fluids, nutritional support, possibly corticosteroids for liver inflammation, anthelmintics if parasitism is suspected.

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82
Q

History: 3-year-old Holstein Friesian cow, decreased milk yield, off feed for 48 hours, isolated, lying down more than usual, heart rate 88 bpm, respiratory rate 32 bpm, rectal temperature 39.4°C, mucous membranes pale.
Biochemistry Highlights:
Total Calcium: 1.75 mmol/l (↓)
Phosphorus: 1.9 mmol/l (normal)
Magnesium: 0.8 mmol/l (↓)

A

Differential Diagnoses: Hypocalcemia (Milk Fever), hypomagnesemia (Grass Staggers).
Treatment Options: IV calcium borogluconate for immediate relief, oral calcium supplements for maintenance, magnesium supplementation if necessary.

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83
Q

History: 4-year-old Aberdeen Angus, recently purchased, coughing, nasal discharge, heart rate 70 bpm, respiratory rate 40 bpm, rectal temperature 39.7°C.
Biochemistry Highlights:
Not specified in detail but indications of respiratory infection and stress.

A

Differential Diagnoses: Bovine Respiratory Disease Complex (Shipping Fever), parasitic lung infections.
Treatment Options: Antibiotics for bacterial infection, anti-inflammatories, supportive care, and stress reduction strategies.

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84
Q

What is haemostasis and its primary objective in vascular injury?

A

Haemostasis is the process by which blood clots form at sites of vascular injury to prevent excessive bleeding. Its primary objective is to seal damaged blood vessels through a series of events involving platelet aggregation and the coagulation cascade, which are divided into primary, secondary, and tertiary stages.

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85
Q

Describe the three traditional stages of haemostasis.

A

The three traditional stages of haemostasis are: 1) Primary haemostasis, where platelets aggregate to form a plug at the site of injury; 2) Secondary haemostasis, where the coagulation cascade stabilizes the platelet plug with fibrin strands; 3) Tertiary haemostasis (fibrinolysis), where the clot is dissolved after it has served its purpose.

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86
Q

What are the key components and inhibitors of primary haemostasis?

A

Primary haemostasis involves the adhesion, activation, and aggregation of platelets, facilitated by endothelial cells and von Willebrand factor (vWF). Key inhibitors include aspirin and NSAIDs, which inhibit thromboxane production, and clopidogrel, an ADP receptor antagonist, affecting platelet function.

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87
Q

What are the clinical signs and tests for evaluating primary haemostasis disorders?

A

Clinical signs include petechiae, ecchymosis, and purpura, indicating ineffective platelet function. Evaluation tests include platelet count, plateletcrit, Buccal Mucosal Bleed Time (BMBT), and assays for vWF antigen and activity for specific breed-related conditions.

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88
Q

What are the causes and types of thrombocytopenia and thrombocytosis in primary haemostasis disorders?

A

Thrombocytopenia can result from decreased production, immune-mediated destruction, consumption (e.g., DIC), sequestration, or loss, while thrombocytosis can be reactive (secondary to inflammation, neoplasia, or GI disease), drug-induced, or due to increased platelet production. Both conditions can be inherited or acquired.

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89
Q

What are the three stages of haemostasis and their basic functions?§

A

The three stages are primary haemostasis (platelet plug formation at a damaged vessel wall), secondary haemostasis (coagulation cascade forming fibrin strands to hold the plug together), and tertiary haemostasis or fibrinolysis (dissolution of the clot after it served its purpose).§

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90
Q

What key components can be measured from a clinical pathology perspective to assess haemostasis, and what do they indicate?

A

Clinically measurable components include platelet count and function, coagulation factors, and fibrin degradation products like D-Dimers. These measurements help evaluate the body’s ability to form and dissolve blood clots.

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91
Q

What are the cellular components and key events of primary haemostasis?

A

Primary haemostasis involves platelets and endothelial cells (producing vWF) in events like adhesion (platelets to exposed matrix proteins), activation (promoting platelet recruitment and shape change), and aggregation (mediated by fibrinogen).

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92
Q

What clinical signs and tests are used to assess primary haemostasis?

A

Clinical signs include petechiae, ecchymosis, and purpura. Key tests include platelet count, plateletcrit, Buccal Mucosal Bleeding Time (BMBT), and assays for von Willebrand factor (vWF) antigen and activity.

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93
Q

What are the types and causes of thrombocytopenia and thrombocytosis?

A

Thrombocytopenia can be inherited or acquired due to decreased production, destruction (e.g., immune-mediated), consumption (e.g., DIC), sequestration, or loss. Thrombocytosis can be primary or secondary, caused by increased platelet production or decreased clearance.

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94
Q

Describe thrombopathia and von Willebrand Disease (vWD) in terms of occurrence, diagnosis, and clinical signs.

A

Thrombopathia, an abnormal platelet function, is uncommon and difficult to diagnose, with normal or mildly reduced platelet count. vWD is the most common inherited disorder of haemostasis, characterized by deficient or abnormal vWF, diagnosable through vWF antigen concentration tests and BMBT.

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95
Q

What are the intrinsic, extrinsic, and common pathways in secondary haemostasis?

A

The intrinsic pathway is activated by contact with collagen, the extrinsic by tissue factor (TF), and both lead to the common pathway, where factor X is converted to thrombin, which then forms fibrin.

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96
Q

How is secondary haemostasis evaluated clinically and what tests are used?

A

Clinical signs of hypo- and hypercoagulability include haematoma, haemorrhage, and thrombosis. Tests include Prothrombin Time (PT) for extrinsic and common pathways, Activated Partial Thromboplastin Time (aPTT) for intrinsic and common pathways, and Activated Clot Time (ACT) for a quick in-house screening.

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97
Q

Discuss the types of disorders affecting secondary haemostasis.

A

Inherited disorders include haemophilia A (factor VIII deficiency) and haemophilia B (factor IX deficiency), while acquired disorders include anticoagulant rodenticide toxicosis and conditions affecting coagulation factors like liver disease.

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98
Q

How does vitamin K inhibition affect coagulation, and what are the clinical implications?

A

Vitamin K is essential for synthesizing coagulation factors II, VII, IX, and X. Inhibition (e.g., rodenticide toxicosis) leads to prolonged PT and aPTT, mimicking factor deficiencies and indicating significant liver pathology or dysfunction.

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99
Q

What is fibrinolysis, and how does it relate to conditions like Greyhound Delayed Bleeding Syndrome?

A

Fibrinolysis is the process of dissolving blood clots, primarily through the action of plasmin converting fibrin into fibrin degradation products like D-dimers. Greyhounds may experience delayed bleeding post-surgery due to premature or excessive fibrinolysis, suggesting that clots formed are weak or dissolved too quickly. Treatments like tranexamic acid or epsilon aminocaproic acid (EACA) can be effective in preventing or reducing plasmin formation, thus improving the condition.

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100
Q

Discuss the pathology of the mammary gland.

A

Mammary gland pathologies include mastitis in farm animals, caused by various pathogens (bacterial, viral, mycoplasma), and mammary tumors in small animals. Mammary tumors can be benign (often adenomas with a benign histological appearance) or carcinomas (with a wide range of types, grading based on factors like differentiation, tubule formation, and mitotic rate).

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101
Q

What are the key pathological conditions of the uterus and external genitalia?

A

Conditions include congenital lesions (like segmental aplasia), inflammatory disorders (endometritis, metritis, pyometra), and neoplasms (leiomyoma, endometrial carcinoma). External genitalia may also be affected by neoplasms like squamous cell carcinoma and transmissible venereal tumors.

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102
Q

What is a granulosa cell tumor, and what are its characteristics?

A

Granulosa cell tumors are the most common type of sex cord-stromal tumor, typically benign, and can occur in any species. They feature a variety of histopathological patterns, including solid sheets, islands, and Call-Exner bodies, and may present with both solid and cystic areas, sometimes including areas of hemorrhagic necrosis.

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103
Q

Describe the main pathological conditions affecting the ovary.

A

Ovarian pathologies include ovotestis, cysts (follicular, luteinized, cystic rete ovarii, cysts of the subsurface epithelial structures), and neoplasms (sex cord-stromal tumors like granulosa cell tumors, tumors of the surface epithelium, germ cell tumors like teratoma and dysgerminoma, and rare tumors like yolk sac tumors).

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104
Q

What are disorders of sexual development (DSD), and how are they classified?

A

DSDs are conditions involving atypical development of chromosomal, gonadal, or anatomical sex. Classification is based on karyotype (XX, XY, or variations) and includes true hermaphroditism, male and female pseudohermaphroditism, with diagnoses often requiring assessment of sex chromosomes, gonadal type, and genital phenotype.

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105
Q

Disorders of Sexual Development (DSD)

A

Conditions involving abnormal development of chromosomal, gonadal, or anatomical sex. Classified based on karyotype and includes true hermaphroditism and pseudohermaphroditism.

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106
Q

Ovotestis

A

A rare condition where both ovarian and testicular tissue are present in the same individual, often associated with true hermaphroditism.

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107
Q

Granulosa Cell Tumor

A

A type of sex cord-stromal tumor originating from the granulosa cells of the ovary, often hormonally active and potentially malignant.

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108
Q

Pyometra

A

A serious reproductive condition in females characterized by the accumulation of pus within the uterine cavity, often secondary to infection.

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109
Q

Mastitis

A

Inflammation of the mammary gland, typically due to bacterial infection, leading to swelling, pain, and reduced milk production.

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110
Q

Leiomyoma

A

A benign tumor of smooth muscle origin, commonly found in the uterus (uterine fibroids) and sometimes in the external genitalia.

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111
Q

Endometrial Carcinoma

A

A type of cancer that originates from the lining of the uterus (endometrium), more common in older females.

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112
Q

Chimerism

A

A genetic condition where an individual has cells from two different zygotes, leading to mixed genetic profiles within the body.

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113
Q

Mammary Tumors

A

Neoplasms occurring in the mammary glands, ranging from benign (adenomas) to malignant (carcinomas), with varying prognoses based on type and grade.

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114
Q

What are the main categories of disorders affecting the testis and epididymis?

A

: Developmental anomalies, degeneration, inflammation, and neoplasia.

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115
Q

What is cryptorchidism and its implications for testicular health?

A

Cryptorchidism is the incomplete descent of one or both testes, often leading to hypoplasia and an increased risk of tumor formation.

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116
Q

Describe testicular hypoplasia and its common causes.

A

Testicular hypoplasia is characterized by underdeveloped testes, often due to congenital or pre-pubertal factors like nutrition, genetics, or endocrine abnormalities, leading to absent or incomplete spermatogenesis.

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117
Q

What causes testicular atrophy/degeneration and its typical histological appearance?

A

Caused by factors like infections, increased scrotal temperature, and nutritional deficiencies, it’s characterized by a reduction in testicular size with firm consistency and microscopic findings similar to hypoplasia, possibly with fibrosis.

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118
Q

How does epididymitis differ from orchitis in its impact on the male reproductive system?

A

Epididymitis, often caused by ascending infection, primarily affects the tail of the epididymis and can lead to secondary testicular degeneration/atrophy, while orchitis involves direct inflammation of the testes.

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119
Q

What condition describes undescended testes and its risk?

A

Cryptorchidism; increases tumor risk.

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120
Q

What is a key feature of testicular hypoplasia on microscopy?

A

Absent/incomplete spermatogenesis with hypoplastic tubules.

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121
Q

Main cause of testicular atrophy in adult males?

A

Infections and environmental factors leading to decreased size and firmness.

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122
Q

Primary site affected by epididymitis in males?

A

Tail of the epididymis, often leading to secondary testicular issues.

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123
Q

What’s a common histological finding in testicular degeneration?

A

Similar to hypoplasia, potentially with fibrosis.

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124
Q

What are the two main pathways for infectious diseases to affect the kidneys?

A

Haematogenous (descending) and urinary (ascending).

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125
Q

List some viral, bacterial, and parasitic agents causing kidney infections in animals.

A

Viral: Canine herpesvirus, Canine Adenovirus. Bacterial: Leptospira, E. coli. Parasitic: Toxocara canis, Leishmania spp.

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126
Q

Differentiate between non-suppurative and suppurative interstitial nephritis.

A

Non-suppurative involves lympho-histiocytic inflammation, while suppurative involves pus formation and can lead to embolic nephritis or pyelonephritis.

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127
Q

What causes acute and chronic interstitial nephritis, and how do they appear macroscopically?

A

Causes include various infectious agents. Acute shows kidneys swollen and pale tan, chronic shows fibrosis.

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128
Q

What is the primary cause and outcome of non-suppurative tubulointerstitial nephritis in dogs?

A

Primarily caused by acute leptospirosis, leading to lympho-histiocytic inflammation.

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129
Q

Describe the pathogenesis and causative agents of suppurative embolic nephritis.

A

Caused by bacteremia with agents like Actinobacillus equuli, leading to septic emboli and possibly abscesses or infarcts.

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130
Q

How does pyelonephritis typically begin, and what are its microscopic findings?

A

Begins with ascending infection, showing necrotic epithelium, neutrophil infiltration, and in chronic cases, severe fibrosis.

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131
Q

What are the primary pathways for the development of lower urinary tract infections?

A

Descending (leading to nephritis or pyelonephritis) and ascending.

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132
Q

Compare ureteritis, cystitis, and urethritis in terms of occurrence and associated factors.

A

Ureteritis is rare without cystitis, cystitis is the most common lower UTI, and urethritis is often linked to obstructions.

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133
Q

What is the most common cause of kidney infections in animals?

A

Bacterial agents like Leptospira and E. coli.

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134
Q

How does suppurative nephritis differ from non-suppurative nephritis?

A

Suppurative involves pus formation, non-suppurative involves immune cell inflammation.

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135
Q

: What is the hallmark microscopic feature of pyelonephritis?

A

Necrotic epithelium with neutrophil and bacterial infiltration.

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136
Q

What leads to lower urinary tract infections most frequently?

A

Ascending infections from the urethra.

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137
Q

How can urinary tract infections affect the kidneys?

A

Through ascending infection leading to pyelonephritis or descending infection causing nephritis.

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138
Q

Define triage and its primary goal in veterinary emergency settings.

A

Triage is the process used to prioritize patients based on the severity of their condition, aiming to do “the greatest good for the greatest number” by directing therapy where it’s most needed.

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139
Q

What constitutes effective triage in emergency veterinary medicine?

A

Effective triage means timely and appropriate prioritization, influenced by experience, a clear plan, stress management, leadership, and agile decision-making.

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140
Q

What are key methods to optimize triage in veterinary emergencies?

A

Optimization methods include practice, developing and following algorithms, and leveraging experienced triage officers supported by their team.

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141
Q

What are the drawbacks of using mnemonics like ‘ABCDE’ and ‘ACRASHPLAN’ in triage, according to the lecture?

A

: The drawbacks include the challenge of remembering what each letter stands for and the lack of incorporating point-of-care ultrasound (POCUS), which is crucial for immediate assessment.

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142
Q

Describe the algorithm approach to triage for a patient with RTA, haemoabdomen, and pulmonary contusions.

A

The algorithm includes assessing hypovolaemia through symptoms and diagnostics like ultrasound for blood loss, POCUS for pulmonary contusions, and evaluating reduced perfusion with oxygenated blood through blood pressure, lactate, and blood gas analysis.

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143
Q

Importance of POCUS in triage?

A

Allows immediate assessment of trauma or internal bleeding.

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144
Q

Compare the uses and limitations of isotonic crystalloids in fluid therapy.

A

Isotonic crystalloids like Hartmann’s and 0.9% saline are used for fluid resuscitation in hypovolemia and dehydration due to their rapid equilibration across membranes. However, their effect on intravascular volume expansion is short-lived, necessitating repeated administration or alternative therapy for sustained effects.

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145
Q

Explain the clinical applications and risks of using hypertonic saline versus hypotonic saline in veterinary medicine.

A

Hypertonic saline (7.2%) is used for rapid volume expansion and managing raised intracranial pressure with minimal volume, but risks inducing hypernatremia. Hypotonic saline (0.45%) can correct hypernatremia but may cause cerebral edema if hypernatremia is corrected too rapidly, leading to serious neurological complications.

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146
Q

Detail the specific clinical indications for the use of whole blood, packed red blood cells, fresh frozen plasma, and albumin in veterinary fluid therapy.

A

Whole blood is used for significant blood loss when packed red blood cells (pRBCs) aren’t available, targeting anemia. pRBCs are selected for anemia with no donor. Fresh frozen plasma addresses coagulopathies and supports oncotic pressure, while albumin is used in severe hypoalbuminemia to manage anaphylaxis and prevent acute kidney injury.

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147
Q

Discuss the role of colloids in managing hypoalbuminemia and the risks associated with their use in critically ill patients.

A

Colloids, like hetastarch and geloplasma, are used to improve oncotic pressure in hypoalbuminemia and vascular leak conditions. However, their use can exacerbate interstitial edema and minimal volume expansion due to vascular leakage, with potential risks including acute kidney injury and coagulopathy. Their use is cautioned against unless no alternatives are available.

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148
Q

Outline the approach to fluid therapy in hypovolemia, dehydration, and the endpoints for fluid resuscitation.

A

For hypovolemia, initial therapy involves micro boluses followed by larger boluses (10-15ml/kg for larger animals, 5-10mls/kg for cats), potentially including hypertonic saline. Dehydration correction prioritizes hypovolemia first, aiming for weight gain equivalent to the deficit over 24 hours. Endpoints for resuscitation include improved oxygen supply, mentation, blood pressure, lactate levels, and POCUS findings indicating improved volume status.

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149
Q

Why are isotonic crystalloids like Hartmann’s used in fluid therapy?

A

For rapid equilibration in hypovolemia and dehydration, despite short-lived vascular expansion effects.

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150
Q

When is hypertonic saline preferred in fluid therapy?

A

For rapid volume expansion in large animals and managing raised intracranial pressure, with careful monitoring to avoid hypernatremia.

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151
Q

Role of fresh frozen plasma in fluid therapy?

A

Addresses coagulopathies and supports oncotic pressure in hypoalbuminemia.

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152
Q

What complicates colloid use in critically ill patients?

A

Risk of exacerbating vascular leakage and interstitial edema, with potential for acute kidney injury.

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153
Q

Key considerations in monitoring fluid therapy effectiveness?

A

Monitoring involves assessing mentation, blood pressure, lactate levels, and volume status via POCUS, aiming for specific clinical improvement endpoints.

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154
Q

How do you calculate the initial fluid bolus for a 9.1kg dog showing signs of hypovolemia due to vomiting and diarrhea after ingesting mushrooms?

A

Calculate the initial bolus using the formula: patient weight in kg x 10 mL/kg. For a 9.1kg dog, the initial bolus would be approximately 91 mL, adjusted on the drip pump to ensure precise delivery over 15 minutes.

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155
Q

After administering an initial fluid bolus and observing slight improvement but persistent hypovolemia (e.g., elevated heart rate and low blood pressure), how do you adjust the fluid therapy plan?

A

Increase the bolus to 15 mL/kg over 15 minutes based on patient response, with continuous monitoring of vital signs and lactate levels to guide further adjustments.

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156
Q

How do you transition fluid therapy from treating hypovolemia to addressing dehydration in a dog that has stabilized?

A

Calculate the total fluid deficit based on the difference between the current and previous healthy body weight, subtracting the volume already administered. Adjust the ongoing fluid rate to cover the deficit plus maintenance needs over 24 hours.

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157
Q

In a case of AKI with polyuria, how do you adjust fluid therapy to prevent further kidney damage while ensuring adequate hydration?

A

: Increase the fluid rate to account for ongoing losses plus maintenance, continuously reassessing urine output and adjusting the rate accordingly to prevent fluid overload.

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158
Q

How do you adjust fluid therapy to prevent fluid overload in a patient recovering from AKI with evidence of peripheral edema?

A

Gradually reduce the fluid rate based on urine output and clinical signs, aiming to maintain a stable weight without causing hypervolemia. Consider additional diagnostics to assess for complications like hypoalbuminemia or vascular leak syndrome.

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159
Q

Upon noticing peripheral edema in a recovering AKI patient, what steps do you take to identify the cause and adjust treatment?

A

Investigate potential causes of edema, such as hypoalbuminemia or reduced oncotic pressure, through diagnostic tests like biochemistry and urinary protein:creatinine ratio. Adjust the fluid therapy accordingly, possibly incorporating nutritional support and physiotherapy to manage edema.

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160
Q

What is assisted feeding and when is it required in veterinary medicine?

A

Assisted feeding refers to providing nutritional support to animals unable to meet their daily nutritional requirements due to inability to eat normally or absorb nutrients from certain GI tract sections. It’s needed when animals cannot consume enough nutrients on their own.

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161
Q

Compare enteral and parenteral nutrition in terms of administration route and indications.

A

Enteral nutrition involves using the gastrointestinal tract for feeding, preferred for its physiological benefits and lower infection risk. Parenteral nutrition, including TPN (Total Parenteral Nutrition) and PPN (Partial Parenteral Nutrition), is administered directly into the venous circulation, indicated when the GI tract is not functional or cannot be used.

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162
Q

Describe the decision-making process for choosing between enteral and parenteral nutrition.

A

The decision is based on the animal’s ability to use its GI tract, the nutritional status, and the specific health condition. Factors include GI tract functionality, risk of aspiration, and the need for immediate nutrition without GI involvement.

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163
Q

What are the different types of feeding tubes and their placement?

A

Types include naso-oesophageal, naso-gastric, oesophagostomy, gastrostomy (including PEG tubes), and enterostomy tubes, each chosen based on the patient’s condition, required feeding duration, and specific nutritional needs.

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164
Q

How do you calculate the amount of food for enteral feeding?

A

Calculate the Resting Energy Requirement (RER) using the formula RER = 30 x (body weight in kg + 70). Determine the caloric density of the chosen diet (Kcal/ml) and plan the feeding regimen to match the animal’s energy needs within clinic working hours, ensuring not to exceed 50ml/kg/feed.

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165
Q

Identify common issues with feeding tubes and their solutions.

A

Problems include blockages, tube dislodgement, trauma, infection, and over-granulation. Solutions involve regular tube flushing, careful handling to prevent dislodgement, maintaining good surgical site hygiene, and addressing infections promptly with antibiotics.

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166
Q

Discuss the considerations and challenges associated with parenteral feeding.

A

Parenteral feeding is complex, requiring meticulous calculation of nutrient needs and monitoring for complications like infections at the catheter site. It’s chosen when enteral feeding is contraindicated but requires careful balance to avoid metabolic disturbances.

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167
Q

Define hypovolaemic shock and its primary causes.

A

Hypovolaemic shock is a condition of inadequate organ perfusion due to acute loss of intravascular volume, leading to a critical drop in cardiac preload and negative consequences for tissue metabolism. Causes include traumatic blood loss, haemorrhage, and fluid loss from severe vomiting, diarrhoea, or polyuria.

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168
Q

What are the clinical signs associated with hypovolaemic shock?

A

Clinical signs include tachycardia (increased cardiac output), peripheral vasoconstriction (pale mucous membranes, prolonged capillary refill time, poor pulse quality), and reduced mentation due to decreased cerebral oxygen supply.

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169
Q

How is hypovolaemic shock diagnosed?

A

Diagnosis is based on clinical signs, history, low blood pressure, elevated lactate levels, and point-of-care ultrasound findings like a collapsing caudal vena cava and a poorly filling heart.

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170
Q

What is the treatment approach for hypovolaemic shock?

A

Treatment focuses on restoring volume with isotonic fluids and transfusions (blood/plasma) as needed. Speed is crucial to prevent rapid onset of hypoxia and potential brain death.

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171
Q

Define distributive shock and its primary causes.

A

Distributive shock is a state of relative hypovolemia resulting from pathological redistribution of intravascular volume, often due to loss of vascular tone regulation or disordered permeability. Common causes include sepsis/SIRS leading to vasodilation and increased vascular permeability.

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172
Q

What are the clinical signs of distributive shock?

A

Signs include vasodilation (injected mucous membranes, shortened CRT, bounding/hyperdynamic pulse, tachycardia), and increased permeability (peripheral oedema, pulmonary oedema, cavitatory effusions).

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173
Q

How is distributive shock diagnosed?

A

Diagnosis involves clinical signs, history, low blood pressure, elevated lactate, POCUS findings (collapsing caudal vena cava, poorly filling heart, septic focus, evidence of vascular leak).

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174
Q

What is the treatment focus for distributive shock?

A

Treatment targets vascular tone and permeability, requiring volume support (fluid bolus), vasopressor support (e.g., noradrenaline or dopamine), and ensuring adequate oncotic pressure (checking albumin levels, considering plasma transfusion, starting feeding).

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175
Q

Define cardiogenic shock and its causes.

A

Cardiogenic shock is a reduction in cardiac output due to myocardial failure (e.g., dilated cardiomyopathy), arrhythmias, or valvular disease, leading to systemic hypoperfusion.

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176
Q

What are the clinical signs of cardiogenic shock?

A

Signs include poor pulses, pale mucous membranes, prolonged capillary refill time, reduced temperature, with heart rate variations based on the underlying cause.

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177
Q

How is cardiogenic shock diagnosed?

A

Diagnosis is based on clinical signs, history, low blood pressure, elevated lactate, point-of-care ultrasound showing a poorly contracting heart, and ECG findings of arrhythmias.

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178
Q

What is the treatment approach for cardiogenic shock?

A

Treatment depends on the cause and may include managing hyperkalemia, splenic disease, and providing positive inotrope therapy (e.g., pimobendan, dobutamine).

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179
Q

Define obstructive shock and its causes.

A

Obstructive shock results from physical obstruction of the heart or great vessels, such as cardiac tamponade, pulmonary thromboembolism, or severe aortic stenosis, leading to reduced cardiac output.

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180
Q

What are the clinical signs of obstructive shock?

A

Similar to cardiogenic shock, with additional signs depending on obstruction location, including distension or compression of the vena cava and reduced diastolic filling.

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181
Q

How is obstructive shock diagnosed?

A

Diagnosis involves clinical signs, elevated lactate, and point-of-care ultrasound findings indicative of specific obstructions like pericardial effusion or pulmonary hypertension.

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182
Q

What is the treatment approach for obstructive shock?

A

Treatment focuses on relieving the obstruction (e.g., pericardiocentesis for cardiac tamponade, thoracocentesis for tension pneumothorax) and supportive care, including fluid therapy and oxygen.

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183
Q

What is the origin and primary purpose of POCUS in emergency settings?

A

POCUS was initially developed to help ER doctors quickly diagnose severe abdominal trauma by identifying free abdominal fluid, primarily blood, without the delays of traditional imaging. Despite being less sensitive than CT for detecting false negatives, it significantly speeds up the identification of severely bleeding patients.

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184
Q

How has the application of POCUS expanded in clinical settings?

A

POCUS use has expanded beyond its original purpose to include fluid detection in other cavities with Thoracic FAST scans and lung disease assessment with the Bedside Lung Ultrasound Examination (BLUE). Its use now also encompasses basic echocardiography and specific vessel assessments, such as the inferior vena cava.

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185
Q

What is the Global FAST approach in veterinary medicine, and what does it entail?

A

The Global FAST approach, developed by Gregory Lisciandro, involves a comprehensive assessment of both thoracic and abdominal cavities in small animals. It combines VetBLUE for lung examination, TFAST for thoracic assessment, and AFAST for abdominal evaluation, aiming for a holistic view of the patient’s condition.

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186
Q

Describe the FLASH protocol and its significance in equine patients.

A

FLASH (Fast Localised Abdominal Sonography of Horses) is a 7-point scan designed to assess abdominal and thoracic free fluid and small intestinal loops in horses. It has shown high sensitivity and specificity for diagnosing small intestinal obstruction, highlighting its importance in equine emergency care.

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187
Q

Summarize the critical role of POCUS in emergency veterinary medicine.

A

POCUS is crucial for rapidly assessing severe conditions in emergency veterinary patients, aiding in decision-making. It requires familiarity with a specific protocol to ensure consistent, speedy, and accurate examinations. A global assessment approach is recommended for thorough evaluation.

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188
Q

What is the key benefit of POCUS in emergency settings?

A

It allows for the rapid identification of critical conditions, such as internal bleeding, without the need for traditional, time-consuming imaging techniques.

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189
Q

: How does the Global FAST approach benefit small animal emergency care?

A

It ensures a comprehensive assessment of both the thoracic and abdominal areas, facilitating a more accurate and quicker diagnosis.

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190
Q

Why is the FLASH protocol important for equine emergency care?

A

It enables the effective detection of abdominal and thoracic fluid and intestinal issues, crucial for diagnosing and managing equine emergencies.

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191
Q

How has the use of POCUS evolved in clinical practice?

A

Initially focused on detecting abdominal trauma, POCUS now includes assessments of thoracic conditions, lung diseases, heart function, and blood vessels, making it a versatile tool in emergency medicine.

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192
Q

What is the significance of learning and using a single POCUS protocol?

A

Consistency in using a specific POCUS protocol enhances the speed, accuracy, and reliability of emergency assessments, improving patient outcomes.

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193
Q

Why is nutrition considered an essential component in managing critically ill veterinary patients?

A

Critical illness induces physiological stress and inflammatory responses, leading to protein catabolism and impaired healing. This results in poorer outcomes and increased complication rates, making nutrition a pivotal part of patient management.

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194
Q

How do you assess the nutritional status of critically ill veterinary patients?

A

Assess nutritional status using body condition score (focusing on fat stores) and muscle condition score (focusing on lean mass, which is probably more useful in critical illness). Repeat assessments daily and consider measuring muscle belly size with a tape measure for a more accurate evaluation.

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195
Q

When should nutritional support be initiated in critically ill veterinary patients?

A

Begin nutritional support at the latest by 3 days of anorexia or 7 days of hyporexia. Early intervention is always better, and immediate nutritional support is crucial for hypoalbuminemic patients, such as those with sepsis.

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196
Q

How can specific nutrients modulate disease processes in critically ill patients?

A

Omega-3 fatty acids have anti-inflammatory properties and may benefit early sepsis, though human studies show mixed results. Antioxidants can address oxidative damage but may cause harm in some cases. Glutamine offers anti-inflammatory and antioxidant effects, but veterinary literature is minimal. Probiotics have weak evidence for benefits in critically ill patients and concerns about antibiotic resistance.

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197
Q

Why is monitoring nutritional status critical in ECC patients?

A

To identify and mitigate the adverse effects of critical illness on the body, such as muscle wasting and impaired healing.

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198
Q

What is the significance of early nutritional intervention in ECC patients?

A

Early intervention can prevent further nutritional decline and support the body’s healing process, potentially improving patient outcomes.

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199
Q

How does nutritional support vary based on the patient’s clinical status?

A

Nutritional plans are tailored based on the patient’s condition, including the urgency for intervention (e.g., hypoalbuminemia) and specific needs (e.g., omega-3 for inflammation).

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200
Q

What role do omega-3 fatty acids and antioxidants play in critically ill patients?

A

They may modulate inflammation and oxidative stress, though their efficacy varies by case and existing literature.

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201
Q

How are body and muscle condition scores used in managing ECC patients?

A

They help assess nutritional status and guide the development of a targeted nutritional intervention plan.

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202
Q

What are common causes of head trauma in animals?

A

Head trauma in animals commonly results from crushing injuries, such as running into a tree, being hit by a vehicle, or experiencing a major fall.

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203
Q

What are the first and second considerations when assessing an animal with head trauma?

A

The first consideration is whether the animal can breathe, assessing for crushed nasal bones or soft tissue damage. The second consideration is the condition of the brain, looking for evidence of traumatic brain injury or skull fractures.

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204
Q

How do you assess and manage breathing in an animal with head trauma?

A

Assess the respiratory rate, effort, signs of cyanosis, and pulse oximetry. For emergency therapy, provide oxygen if the airway is patent, or perform rapid induction and intubation if not. Have suction available to clear the airway and consider emergency tracheostomy if intubation fails.

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205
Q

What are primary and secondary injuries in TBI, and their impacts?

A

Primary injuries include concussion, contusion, hematoma, and laceration, leading to increased intracranial pressure (ICP). Secondary injuries result from the neurological tissues’ excitation, causing ATP depletion, pro-inflammatory state, neuronal damage, and disruption of the blood-brain barrier, making the brain sensitive to peripheral blood pressure changes.

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206
Q

How can TBI be identified in animals?

A

Through neurological assessment of mentation and eyes, including observing the pupillary light reflex (PLR) and checking for signs like bilateral miosis or unilateral mydriasis, which indicate varying prognoses.

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207
Q

What are the main considerations in treating TBI in animals?

A

The main considerations include reducing the intracranial pressure (ICP) and normalizing perfusion. This can involve the use of hypertonic fluids like hypertonic saline or mannitol and managing blood pressure to maintain normal MAP.

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208
Q

What are the two main types of thoracic injuries and their consequences?

A

Thoracic injuries can be blunt (causing bruising, contusions, lung rupture, diaphragm rupture, or orthopedic injuries) or penetrating (causing direct injury to lungs, airways, major vessels, the heart, external contamination, or esophageal injury).

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209
Q

What is the initial step in evaluating an animal with head trauma?

A

Assess if the animal can breathe properly.

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210
Q

What is the significance of the pupillary light reflex (PLR) in head trauma assessment?

A

PLR helps in prognosticating the outcome based on the response.

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211
Q

How is increased intracranial pressure (ICP) managed in animals with TBI?

A

Through the administration of hypertonic saline or mannitol.

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212
Q

What is the importance of maintaining normal MAP in TBI patients?

A

It helps in preventing further neuronal damage by ensuring adequate cerebral perfusion.

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213
Q

What differentiates blunt from penetrating thoracic injuries?

A

Blunt injuries are primarily concussive, while penetrating injuries directly damage internal structures.

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214
Q

What are the two main types of abdominal injuries, and how do they differ?

A

Abdominal injuries can be blunt, causing concussions, contusions, swelling, and possibly organ ruptures, or penetrating, which may directly injure organs or major vessels and lead to external contamination.

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215
Q

What role does POCUS play in diagnosing abdominal trauma?

A

: POCUS (Point-of-Care Ultrasound) is crucial for triaging abdominal trauma, as it helps in identifying free fluid and guiding further diagnostic procedures like abdominocentesis.

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216
Q

How is haemoabdomen managed in the case of blunt trauma?

A

Management usually involves conservative measures such as fluid therapy, potentially using hypertonic saline and blood products if necessary. Surgical intervention is rare unless an organ has ruptured.

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217
Q

What is the role of tranexamic acid in managing trauma, and what are the considerations for its use?

A

: Tranexamic acid is an anti-fibrinolytic that stabilizes clot formation. It has shown a survival benefit when administered within 3 hours post-trauma in humans, with veterinary studies indicating its utility in reducing bleeding during surgeries, though with varying outcomes in non-surgical case

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218
Q

What is pneumoperitoneum, and how is it managed?

A

Pneumoperitoneum, usually resulting from blunt or penetrating trauma, indicates gastrointestinal tract damage. It often requires surgical intervention, with diagnosis challenging via POCUS and management including antibiotic cover and exploratory laparotomy.

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219
Q

What are the primary concerns and management strategies for uroabdomen?

A

The main concern is hyperkalemia, treated with glucose and insulin, alkalinizing fluid therapy, and potentially draining the abdomen and placing a urinary catheter to allow healing before any necessary surgery.

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220
Q

How is spinal trauma diagnosed and managed?

A

Spinal trauma diagnosis requires careful radiographic examination with orthogonal views, and management includes supportive care, pain relief, nutritional support, and physiotherapy, with surgical intervention considered based on the severity and type of injury.

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221
Q

When is tranexamic acid beneficial in trauma cases?

A

Within 3 hours post-trauma to stabilize clot formation.

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222
Q

What indicates pneumoperitoneum, and how is it confirmed?

A

Free gas in the abdomen indicates damage, confirmed by radiography.

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223
Q

What is the primary threat in uroabdomen, and initial treatment?

A

Hyperkalemia is the primary threat, treated with glucose, insulin, and alkalinizing fluids.

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224
Q

When is oxygen therapy indicated based on SpO2, PaO2, and lactate levels?

A

Oxygen therapy is indicated for SpO2 <93%, PaO2 <70mmHg, and lactate >2.0mmol/l, signaling reduced oxygen supply to tissues and the potential need for anaerobic respiration avoidance.

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225
Q

What conditions exemplify the need for oxygen therapy?

A

Conditions include ventilation/perfusion mismatch, pleural space pathology (e.g., pneumothorax), lung pathology (e.g., pneumonia), perfusion abnormalities (e.g., hypovolemic shock), distributive shock (e.g., sepsis/SIRS), anaemia, acid-base disturbances affecting the Hb/Sat curve, and right to left shunts.

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226
Q

What are the pros and cons of using flow-by, mask, tent/cage, nasal prongs, nasal catheter, and intubation for oxygen therapy?

A

Each modality has unique benefits and limitations. For example, flow-by is non-invasive but less efficient, while intubation offers direct oxygen delivery but requires sedation or anesthesia and carries a risk of complications.

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227
Q

Name two conditions that may require oxygen therapy due to impaired oxygenation.

A

Pneumothorax and pneumonia.

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228
Q

: What is the main advantage of using a nasal catheter for oxygen therapy

A

It provides precise oxygen delivery directly to the airways.

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229
Q

Why is monitoring important during oxygen therapy?

A

To ensure adequate oxygenation without causing oxygen toxicity.

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230
Q

How does acidosis affect hemoglobin’s oxygen affinity?

A

Acidosis reduces hemoglobin’s affinity for oxygen, increasing oxygen offloading to tissues.

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231
Q

What are the consequences of fluid overload and deficit in veterinary patients?

A

Fluid overload increases interstitial fluid, impairing oxygen and nutrient diffusion, adversely affecting renal and lung function. Fluid deficit impairs perfusion and promotes catabolism, insulin resistance, and cellular stress.

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232
Q

How does hypoalbuminemia affect fluid distribution, and what are its management strategies?

A

Hypoalbuminemia leads to poor oncotic pressure, causing fluid loss to the interstitial space, hypovolemia, peripheral and pulmonary edema. Management includes increasing protein intake, plasma transfusion, and careful use of synthetic colloids due to the risk of acute kidney injury.

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233
Q

What are common electrolyte disturbances in critically ill patients and their management?

A

Hypokalemia and hyponatremia are common, leading to weakness and mentation disturbances. Management involves fluid supplementation and careful correction, especially for sodium due to the risk of osmotic changes.

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234
Q

: Why is monitoring mentation crucial in inpatient management?

A

Mentation assessment provides clues about perfusion status and potential intracranial issues, utilizing tools like the Modified Glasgow Coma Scale for standardization.

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235
Q

How are cardiac issues identified and managed in inpatient care?

A

Cardiac issues like bradycardia and arrhythmias indicate systemic or myocardial disease. Monitoring includes ECG, and management may involve anti-arrhythmics, positive inotropes, and assessing cardiac output via POCUS.

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236
Q

How does blood pressure assessment guide inpatient management?

A

Blood pressure measurement helps identify hypovolemia, distributive shock, or poor cardiac contractility, informing the management approach.

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237
Q

What are the implications of hypo- and hyperthermia in critically ill patients?

A

Hypo- and hyperthermia result from various causes like anesthesia or inflammation, respectively. Management focuses on gradual temperature correction and addressing the underlying cause.

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238
Q

How is respiratory function monitored and managed in inpatient care?

A

Monitoring includes mucous membrane color, respiratory rate, and pulse oximetry, with advanced tools like blood gas analysis. Management involves oxygen therapy and addressing any identified respiratory issues.

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239
Q

Why is monitoring immune status important in critically ill patients?

A

Critical illness can weaken the immune response, heightening secondary infection risk. Management includes identifying infection sources, sampling for culture, and appropriate antibiotic use.

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240
Q

What is the mechanism of action for local anesthetics (LAs) in veterinary medicine?

A

Local anesthetics work by interacting with receptors within the Na+ channel close to the cytoplasm in their ionized charged form. This blocks nerve conduction by preventing sodium ions from entering the nerve ending, thus inhibiting the initiation and propagation of nerve impulses.

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241
Q

How are local anesthetics classified based on their chemical structure?

A

: Local anesthetics are classified into two main types based on their chemical link: amides and esters. Amides are metabolized by the liver, whereas esters are broken down by plasma cholinesterases.

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242
Q

Compare the speed of onset, duration, and toxicity between procaine and lidocaine.

A

Procaine has a rapid onset with a duration of 40-60 minutes and moderate toxicity. Lidocaine also has a rapid onset, but its duration is longer, lasting 1-2 hours, with similar toxicity levels.

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243
Q

What is the significance of using adrenaline with local anesthetics?

A

Adrenaline (epinephrine) is added to local anesthetics to prolong their duration of action. It causes vasoconstriction, which reduces blood flow in the area, slowing the absorption of the anesthetic and extending its effects.

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244
Q

How is lidocaine used in different local anesthetic techniques?

A

Lidocaine is versatile and used in various applications like spray for cat intubation, cream for skin numbing, eye drops for cornea anesthesia, and as part of infiltration techniques for surgical sites.

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245
Q

Describe the technique and benefits of intratesticular blocks.

A

Intratesticular blocks involve injecting a local anesthetic directly into the testicle, targeting the spermatic cord and associated structures. This method provides intraoperative pain relief and postoperative analgesia, particularly effective during castrations.

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246
Q

What are the indications for using lumbosacral and sacrococcygeal epidurals in veterinary medicine?

A

These epidurals are indicated for surgeries in the tail, perineal, and genital areas, including tail amputations, perineal urethrostomies, and anal sacculectomies. They provide effective analgesia for procedures in these regions.

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247
Q

How does the femoral nerve block compare to epidural anesthesia in terms of benefits?

A

Femoral nerve blocks offer an alternative with a reduced risk of urine retention and lower postoperative opioid consumption. They also tend to have less impact on mean arterial blood pressure, suggesting a potentially lower risk of hypotension during anesthesia.

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248
Q

What are local anesthetics, and how do they work?

A

Local anesthetics are drugs that cause temporary loss of sensation in a specific area. They work by blocking nerve signals in the body.

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249
Q

What’s the difference between amide and ester local anesthetics?

A

Amide local anesthetics are metabolized by the liver, and ester local anesthetics are broken down by plasma cholinesterases.§

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250
Q

Why is adrenaline added to some local anesthetics?

A

Adrenaline is added to prolong the effect of local anesthetics by slowing their absorption through vasoconstriction.

slowsabsorption

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251
Q

What is an intratesticular block, and when is it used?

A

It’s a technique of injecting anesthetic into the testicle for pain relief during and after procedures like castrations.

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252
Q

How do peripheral nerve blocks benefit veterinary patients?

A

They reduce the need for systemic opioids, minimize postoperative pain, and can lower the risk of certain anesthesia-related complications.

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253
Q

What is the primary goal of equine regional anaesthesia?

A

To provide localized pain relief during and after surgical procedures on horses, minimizing systemic medication use.

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254
Q

What is the mechanism of action for local anesthetics (LAs) in veterinary medicine?

A

Local anesthetics work by interacting with receptors within the Na+ channel close to the cytoplasm in their ionized charged form. This blocks nerve conduction by preventing sodium ions from entering the nerve ending, thus inhibiting the initiation and propagation of nerve impulses.

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255
Q

How are local anesthetics classified based on their chemical structure?

A

Local anesthetics are classified into two main types based on their chemical link: amides and esters. Amides are metabolized by the liver, whereas esters are broken down by plasma cholinesterases.

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256
Q

Compare the speed of onset, duration, and toxicity between procaine and lidocaine.

A

Procaine has a rapid onset with a duration of 40-60 minutes and moderate toxicity. Lidocaine also has a rapid onset, but its duration is longer, lasting 1-2 hours, with similar toxicity levels.

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257
Q

What is the significance of using adrenaline with local anesthetics?

A

Adrenaline (epinephrine) is added to local anesthetics to prolong their duration of action. It causes vasoconstriction, which reduces blood flow in the area, slowing the absorption of the anesthetic and extending its effects.

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258
Q

What is the primary purpose of equine regional anesthesia?

A

The primary purpose of equine regional anesthesia is to provide localized pain relief during surgical procedures or diagnostic interventions by blocking sensory nerve signals in specific areas of the horse’s body.

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259
Q

What are the main types of nerve blocks used in equine regional anesthesia?

A

Main types include peripheral nerve blocks (for limbs and tail), paravertebral blocks (for flank and thorax), and epidural anesthesia (for procedures involving the caudal part of the body).

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260
Q

How is a supraorbital nerve block performed, and what area does it desensitize?

A

A supraorbital nerve block is performed by injecting anesthetic near the supraorbital foramen to desensitize the forehead and the area around the eyes.

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261
Q

What are potential complications associated with equine regional anesthesia?

A

Complications can include inadvertent vascular injection, local anesthetic toxicity, and nerve damage, leading to temporary or permanent loss of sensation or motor function.

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262
Q

What factors influence the choice of anesthetic agent for equine regional blocks?

A

Factors include the desired duration of anesthesia, the specific area to be anesthetized, potential side effects, and any pre-existing health conditions of the horse.

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263
Q

Why is regional anesthesia important in equine medicine?

A

It allows for pain-free surgical and diagnostic procedures in a targeted area, improving animal welfare and procedural outcomes.

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264
Q

How do veterinarians decide where to administer a nerve block in horses?

A

Veterinarians choose the injection site based on the anatomical origin of the nerve supplying the area requiring anesthesia.

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265
Q

What is the role of ultrasound in equine regional anesthesia?

A

Ultrasound helps in visualizing the nerve and surrounding structures for more precise and safer administration of the nerve block.

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266
Q

Can equine regional anesthesia be used for chronic pain management?

A

Yes, it can be used for chronic pain management, especially in cases of limb lameness or other persistent pain conditions, by providing targeted relief.

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267
Q

What safety precautions should be taken when performing equine regional anesthesia?

A

Safety precautions include proper patient restraint, choosing the correct anesthetic agent and dose, and monitoring the horse for adverse reactions post-procedure.

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268
Q

Why are local blocks important in farm animal surgery?

A

Local blocks are crucial for performing surgeries on farm animals while they are standing, minimizing the stress and risks associated with general anesthesia. They provide targeted pain relief and allow for a variety of surgical and diagnostic procedures to be performed with the animal conscious but comfortable.

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269
Q

What are the key considerations when choosing local anesthesia techniques for farm animals?

A

Key considerations include the type of surgery or procedure, the specific area requiring anesthesia, the animal’s size and condition, potential side effects of the anesthetic agents, and the ability to manage any complications that may arise.

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270
Q

Describe the three main local anesthesia techniques for flank surgery in farm animals.

A

he three main techniques are the “Line” block, which involves direct injection along the surgical site; the “Inverted L” block, which creates an anesthetic field in the shape of an inverted L around the surgical area; and Paravertebral anesthesia, which targets the spinal nerves supplying the flank area, providing a wider area of anesthesia.

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271
Q

What are the local anesthesia options for foot surgery in farm animals?

A

Options include the “Ring” block, where anesthetic is injected in a ring around the top of the hoof to numb the entire foot, and Intravenous Regional Anesthesia (IVRA), where anesthetic is injected into a vein of the limb after applying a tourniquet, numbing the area distal to the tourniquet.

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272
Q

Which blocks are used for eye surgery in farm animals and what do they target?

A

The Retrobulbar block targets nerves behind the eye for procedures on the eyeball itself, the Peterson block is used for anesthesia of the deeper eye structures, and the Auriculopalpebral block is motor only, used to paralyze the eyelid muscles without affecting sensation.

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273
Q

How is local anesthesia achieved for teat surgery in farm animals?

A

Local anesthesia for teat surgery can be achieved through a “Ring” block at the base of the teat or through Intravenous Regional Anesthesia (IVRA) for more extensive procedures, with or without the use of additional local infiltration techniques.

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274
Q

Why is local anesthesia important in farm animal surgery?

A

It allows for pain management and stress reduction during procedures, improving animal welfare and surgical outcomes.

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275
Q

What is the difference between a “Line” block and an “Inverted L” block?

A

A “Line” block is a straight line of anesthesia at the surgery site, while an “Inverted L” block encircles the area in an inverted L shape for broader coverage.

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276
Q

How does Paravertebral anesthesia work in farm animals?

A

It involves injecting anesthetic near the spinal nerves to numb a large area of the body, such as the flank or abdomen, by blocking nerve signals to and from that region.

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277
Q

When might IVRA be preferred for local anesthesia?

A

IVRA is preferred for surgeries on limbs or teats where it’s necessary to numb the entire area below a tourniquet, providing a bloodless field and extensive numbness.

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278
Q

What are the key steps in managing complications from local anesthesia in farm animals?

A

Key steps include monitoring for signs of toxicity or allergic reactions, being prepared to support respiratory and cardiovascular functions, and knowing how to treat local anesthetic systemic toxicity (LAST).

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279
Q

What analgesic regime would you employ for a dairy cow undergoing a difficult calving due to foetal-maternal disproportion?

A

For analgesia during difficult calving, consider using epidural anesthesia with local anesthetics like lidocaine or bupivacaine to provide pain relief to the pelvic area. Also, systemic analgesics such as NSAIDs (e.g., flunixin meglumine) can be administered to manage pain and inflammation.

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280
Q

How can the cost of an analgesic protocol for difficult calving be justified?

A

The cost can be justified by comparing it to the overall value of the animal’s health, productivity, and welfare benefits from effective pain management. The cost of the protocol is often significantly less than the potential loss from complications arising from inadequate pain management.

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281
Q

What potential complications can arise from analgesic approaches in difficult calving, and how do they alter case management?

A

Potential complications include systemic effects of opioids, risk of infection with invasive procedures, and local anesthetic toxicity. Management alterations might include monitoring for adverse effects, adjusting dosages, and employing multimodal analgesia to minimize risks.

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282
Q

Describe the anaesthesia and analgesia protocol for a left displaced abomasum surgery via standing right flank approach.

A

The protocol includes local infiltration anesthesia or a regional block for the surgical site, systemic analgesics like NSAIDs for pain and inflammation, and potentially sedatives to maintain standing sedation. Specific medicines, doses, and routes should be selected based on the animal’s condition, the expected surgery duration, and legal regulations for drug use in food-producing animals.

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283
Q

What is an effective anesthesia plan for a 12-week old dairy calf undergoing umbilical hernia repair surgery?

A

An effective plan includes premedication with a sedative and an opioid for pain relief, induction with an injectable anesthetic agent suitable for young calves, maintenance of anesthesia with inhalant anesthetics via intubation if needed, and local infiltration at the surgery site. Post-operative analgesia should include NSAIDs and careful monitoring for recovery.

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284
Q

Why is pain management critical in veterinary procedures like difficult calving?

A

Pain management is crucial for animal welfare, reducing stress, and facilitating recovery, leading to better health outcomes and productivity.

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285
Q

What factors influence the choice of analgesia in farm animals?

A

Factors include the type of procedure, the animal’s health status, potential drug side effects, and regulations on drug use in food-producing animals.

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286
Q

How do veterinarians manage the cost of analgesic protocols?

A

By evaluating the benefits of pain management against potential losses from inadequate care and leveraging cost-effective drugs within legal guidelines.

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287
Q

What is multimodal analgesia, and why is it important?

A

Multimodal analgesia involves using multiple drugs and techniques to control pain, minimizing the risk of side effects while maximizing pain relief.

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288
Q

How do potential complications affect analgesic and anesthetic choices?

A

Potential complications necessitate a careful selection of drugs and techniques, balancing effective pain control with the risk of adverse effects.

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289
Q

How would you devise a sedation protocol for a 2-year-old colt undergoing standing castration?

A

A sedation protocol for standing castration in a colt could include the use of an alpha-2 agonist like detomidine or xylazine, combined with butorphanol for additional analgesia. Dosing should be calculated based on the horse’s weight (300kg), considering the specific drug concentrations and manufacturer guidelines. Administration is typically intravenous, using a suitable gauge and length needle for equine IV access.

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290
Q

What anesthetic protocol would you recommend for a mare requiring GA for bilateral stifle arthroscopy?

A

The protocol should include premedication with an alpha-2 agonist and butorphanol, induction with a combination of ketamine and midazolam to ensure a smooth transition to recumbency, and maintenance with an appropriate volatile agent like isoflurane or sevoflurane. Doses should be calculated based on the mare’s weight (480kg). Consideration for local blocks around the stifle may provide additional analgesia and reduce the need for systemic analgesics.

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291
Q

What are the benefits of combining midazolam with ketamine for induction in equine anesthesia?

A

Combining midazolam, a benzodiazepine, with ketamine provides muscle relaxation, reduces the dose of ketamine required for induction, and may result in a smoother induction and recovery phase. This combination can help mitigate some of ketamine’s dissociative effects and enhance patient safety during the transition to recumbency.

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292
Q

Are there any suitable local anesthetic blocks for a dog undergoing bilateral total ear canal ablations (TECA)?

A

For TECA, local anesthetic blocks such as the auriculopalpebral nerve block, which provides analgesia to the ear, can be used to significantly reduce intraoperative and postoperative pain. An appropriate volume of a local anesthetic like bupivacaine or lidocaine can be used, taking care to calculate the dose based on the dog’s weight and the maximum safe dose of the local anesthetic.

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293
Q

How can you provide effective analgesia for notably painful procedures like TECA in a small animal?

A

Effective analgesia can be provided through a multimodal approach, combining systemic analgesics such as NSAIDs and opioids with local anesthetic blocks. This approach targets pain at multiple pathways, offering more comprehensive pain control and potentially reducing the amount of systemic medication required.

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294
Q

Why is premedication important in equine anesthesia?

A

Premedication helps calm the animal, provides initial pain relief, and can make induction smoother and safer by reducing the doses of induction agents needed.

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295
Q

How do local blocks benefit surgical patients?

A

Local blocks provide targeted pain relief, can reduce the need for higher doses of general anesthetics, and help in postoperative pain management.

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296
Q

What is the role of multimodal analgesia in veterinary surgery?

A

Multimodal analgesia involves using different types of pain management strategies together to more effectively control pain, minimize side effects, and improve recovery outcomes.

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297
Q

Why calculate drug doses based on animal weight?

A

Calculating drug doses based on weight ensures the medication is effective while minimizing the risk of overdose and side effects.

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298
Q

How do you ensure safety during the induction of anesthesia?

A

Safety during induction is ensured by careful dosing, monitoring the animal’s vital signs, and preparing for emergency interventions if needed.

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299
Q

What are the main functions of breathing systems in anesthesia?

A

Breathing systems deliver oxygen and anesthetic gases, remove carbon dioxide from exhaled breath, and allow for patient ventilation if needed. They are categorized into non-rebreathing and rebreathing systems, chosen based on patient size and other factors.

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300
Q

Describe the characteristics and appropriate use of non-rebreathing systems in veterinary anesthesia.

A

Non-rebreathing systems are ideal for small patients (less than 10kg) due to their low resistance and reliance on high fresh gas flows. They are commonly used for their simplicity and efficiency in oxygen delivery.

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301
Q

What are the advantages of rebreathing systems, and when are they used?

A

Rebreathing systems are efficient for larger patients (over 10kg) as they recycle exhaled gases (after CO2 removal), reducing the need for high fresh gas flows. They warm and humidify the gas, making them suitable for longer procedures.

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302
Q

How do you calculate the appropriate fresh gas flow for a given patient using a non-rebreathing system?

A

Calculate the fresh gas flow (FGF) by multiplying the patient’s minute volume (MV) by the system factor (SF). For a non-rebreathing system like the T-piece, with an SF of 2.5, FGF = MV x SF.

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303
Q

Compare the T-piece, Bain, and Circle systems regarding their suitability for different patient sizes.

A

The T-piece is suited for very small patients (<10kg), the Bain system works for medium-sized patients (10-30kg) with its tube-within-a-tube design, and the Circle system is versatile for patients ranging from 2-150kg, featuring CO2 absorption capabilities.

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304
Q

Why is patient size important in choosing a breathing system?

A

Patient size determines the breathing system’s efficiency in delivering and removing gases, with smaller patients requiring systems that provide minimal resistance and larger patients benefiting from CO2 absorption capabilities.

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305
Q

How does a rebreathing system conserve gases?

A

By recycling exhaled gases (after removing CO2), reducing the need for continuous high fresh gas flow, making it more efficient and cost-effective for larger patients or longer surgeries.

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306
Q

What role does the system factor (SF) play in calculating fresh gas flow?

A

SF adjusts the calculation of fresh gas flow needed to ensure the patient receives enough oxygen and anesthetic gas while minimizing waste, tailored to the specific breathing system used.

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307
Q

How do you calculate and administer IM premedication of buprenorphine and acepromazine in a 42kg dog?

A

For buprenorphine at 0.02mg/kg and acepromazine at 0.03mg/kg, calculate the doses in milligrams, then convert to the volume based on the concentration of the drugs available. Ensure to adjust for micrograms if necessary.

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308
Q

What management strategy would you use for a pet goat with chronic degenerative arthritis?

A

Consider a multimodal approach, including NSAIDs for pain relief, physical therapy, and environmental modifications to reduce joint stress. Adjust the treatment based on effectiveness and the goat’s tolerance.

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309
Q

Describe the local anesthetic technique for examining a painful equine eye.

A

Use a topical anesthetic like proparacaine for initial examination. For more invasive procedures, consider a retrobulbar block to desensitize the deeper structures of the eye and an auriculopalpebral block to immobilize the eyelid.

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310
Q

What additional analgesia is appropriate for a horse with ongoing laminitis?

A

In the yard, consider NSAIDs, standing support wraps, and soft footing. In the hospital, more advanced pain management like regional limb perfusion with antibiotics or analgesics and systemic opioids may be appropriate.

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311
Q

Calculate the doses for premedication and GA induction for a 450kg horse.

A

For acepromazine (0.03mg/kg) IM, romifidine (0.08mg/kg), and morphine (0.1mg/kg) IV, calculate the total milligrams required. Then, for ketamine (3mg/kg) and midazolam (0.06mg/kg) induction, determine the volume to draw up based on the concentrations available.

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312
Q

Why is accurate drug dose calculation important in veterinary anesthesia?

A

Accurate calculation ensures the animal receives the optimal effect of the medication, minimising risks of underdosing or overdosing, which can impact the safety and effectiveness of anesthesia.

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313
Q

What considerations are important for managing chronic pain in animals?

A

Consider the type of pain, the animal’s overall health, potential side effects of medications, and the need for a multimodal approach to provide effective and sustainable pain relief.

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314
Q

How do local blocks aid in equine eye procedures?

A

Local blocks provide targeted anesthesia, reducing stress and pain for the animal, and allow for a thorough examination or procedure without the need for general anesthesia.

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315
Q

Why choose multimodal analgesia for conditions like laminitis?

A

It targets different pain pathways, offering more comprehensive pain control, improving patient comfort, and potentially reducing the need for high doses of any single medication.

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316
Q

What is the benefit of calculating drug doses based on animal weight?

A

This ensures that each animal receives a dose tailored to its specific needs, maximizing the efficacy of the medication while minimizing the risk of adverse effects.

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317
Q

How does environmental modification aid in managing chronic conditions like arthritis in animals?

A

Adjusting the animal’s living conditions to reduce strain on affected joints can significantly improve comfort and mobility, complementing medical treatments.

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318
Q

Why is patient monitoring crucial during and after anesthesia?

A

Continuous monitoring allows for immediate detection of and response to any physiological changes, ensuring the animal’s safety and facilitating a smooth recovery.

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319
Q

What role does client communication play in veterinary pain management?

A

Effective communication helps ensure that pet owners understand their animal’s condition, the rationale behind treatment plans, and their role in managing their pet’s pain at home, leading to better outcomes.

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320
Q

What initial fluid therapy is recommended for a young wild rabbit in shock due to cat-induced injuries?

A

Administer fluid therapy considering the rabbit’s weight, assessing for shock, and deciding between subcutaneous or intravenous routes based on the severity of dehydration or shock.

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321
Q

How should gut motility issues be addressed in a traumatized wild rabbit?

A

: Prescribe gut motility drugs to prevent gastrointestinal stasis, a common complication in stressed rabbits, ensuring the drugs are safe for rabbits.

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322
Q

: What analgesia strategy is appropriate for a young rabbit with traumatic wounds?

A

Provide analgesia suitable for rabbits, considering NSAIDs or opioids depending on pain severity and ensuring dosages are rabbit-specific.

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323
Q

Describe the dietary considerations for a young wild rabbit under emergency care.

A

Initiate feeding with easily digestible, high-fiber foods to support gut health, and consider critical care formulas if the rabbit is not eating voluntarily.

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324
Q

What antibiotic choices and monitoring strategies should be employed for cat-induced wounds in rabbits?

A

Choose antibiotics carefully to avoid those harmful to rabbits’ gut flora and monitor for signs of infection or adverse reactions to medication.

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325
Q

What fluid therapy is indicated for a wild buzzard after a collision trauma?

A

Calculate fluid needs based on bird’s weight and condition, choosing the route (subcutaneous, intravenous) based on severity of dehydration or shock.

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326
Q

How should analgesia be managed for a buzzard with a leg fracture?

A

Administer bird-appropriate analgesics, carefully dosed to manage pain without impairing recovery or causing toxicity.

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327
Q

What feeding strategy should be adopted for a recovering buzzard?

A

Provide a diet that meets the nutritional needs of a carnivorous bird, initially through assisted feeding if necessary, and ensuring the food is easily digestible.

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328
Q

Describe the initial monitoring and fracture management for a buzzard with a mid-shaft leg fracture.

A

Monitor the bird’s vitals, pain level, and response to treatment; stabilize the fracture minimally until further definitive treatment can be planned.

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329
Q

What environmental and further triage considerations are important for a buzzard in critical care?

A

Ensure a quiet, stress-free environment to promote recovery, with appropriate enclosure sizing and perch adjustments to accommodate the injury, alongside planning for further diagnostic tests or specialist referral for the fracture.

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330
Q

2-day-old foal presented with signs of weakness, lethargy, and failure to nurse effectively.

A

Differential Diagnoses: Neonatal sepsis, hypoxic-ischemic encephalopathy, prematurity.
Diagnostic Plan: Complete blood count, blood culture, IgG levels, ultrasound of the thorax, arterial blood gas analysis.
Treatment Plan: IV fluids for dehydration, broad-spectrum antibiotics for suspected sepsis, supportive care including warming and nutritional support.
Outcome and Prognosis Considerations: Prognosis depends on timely identification and treatment of underlying causes; monitoring for improvements or complications is critical.

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331
Q

“Adult cat with acute onset of vomiting and lethargy

A

Differential Diagnoses: Foreign body obstruction, pancreatitis, toxic ingestion.
Diagnostic Plan: Physical examination, radiography, complete blood count, serum biochemistry, abdominal ultrasound.
Treatment Plan: Fluid therapy, antiemetics, analgesics, and, depending on diagnosis, surgical intervention or specific antidotes for toxins.
Outcome and Prognosis Considerations: Early intervention can significantly improve outcomes; prognosis varies with the underlying cause and response to initial treatment.

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332
Q

Neonate presenting with signs of neurological distress, including seizures, lethargy, and poor feeding, following a difficult birth or oxygen deprivation event.”

A

Definition: Hypoxic-ischemic encephalopathy (HIE) is a condition resulting from inadequate oxygen and blood flow to the brain near the time of birth, leading to neurological dysfunction.
Differential Diagnoses: Sepsis, intracranial hemorrhage, metabolic disorders.
Diagnostic Plan: Clinical observation, MRI or CT scan to assess brain injury, EEG for seizure activity, blood tests to rule out metabolic causes.
Treatment Plan: Supportive care (maintaining normal blood glucose, temperature, and blood pressure), therapeutic hypothermia (cooling therapy) for eligible neonates to reduce neurological damage, seizure management with anticonvulsants.
Outcome and Prognosis Considerations: Prognosis varies; early intervention with therapeutic hypothermia has been shown to improve outcomes in some cases. Long-term follow-up for developmental and neurological assessment is essential.

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333
Q

Acute Respiratory Distress Syndrome (ARDS) in dogs is a serious respiratory condition. This syndrome is the failure of the respiratory system to perform properly because of the accumulation of fluid in the lungs. This leads to inflammation and is a life-threatening syndrome. This condition is also known as “shock lung”, as it is known to occur after a shock to the dog’s system, such as a traumatic injury. Plotting a graph of lung volume against trans-lung pressure can show hysteresis in patients with ARDS. In ARDS, there is collapse of the alveoli, such that higher pressures are required to inflate the lungs. What is meant by hysteresis in this case?

A

Hysteresis is the phenomenon whereby the individual curves for inflation and deflation are not the same

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334
Q

What are the two main objectives when learning to optimize ultrasonographic images?

A

The main objectives are to understand how to optimize ultrasonographic images by manipulating various machine settings and to be able to label and store images for future review.

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335
Q

Why is selecting the appropriate preset important before performing an ultrasound scan?

A

Selecting the appropriate preset (e.g., cardiac, abdomen, superficial structures) is crucial because using a mismatched preset, like a cardiac preset for an abdominal scan, will make it difficult to obtain a good image.

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336
Q

What steps should be taken before placing the transducer on the animal for an ultrasound scan?

A

Enter patient details, reduce ambient light if possible, prepare the animal appropriately, select the correct transducer type, and select the suitable transducer frequency.

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337
Q

What initial settings should be adjusted on the ultrasound machine before scanning?

A

Set an approximate depth of penetration (labeled as ‘magnification’ or with in/out arrows), and adjust overall gain and power settings (if available) to mid/low values.

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338
Q

How should the depth of penetration and focal zone be adjusted once the transducer is on the animal?

A

Adjust the depth of penetration so the organ fills the screen and adjust the focal zone to the middle of the organ.

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339
Q

What is Time Gain Compensation (TGC) and why is it important in ultrasound imaging?

A

TGC adjusts the gain at different depths to compensate for sound attenuation in deeper tissues, ensuring even echotexture and visibility throughout the image.

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340
Q

How does adjusting TGC affect tissue consistency in ultrasound images?

A

Adjusting TGC ensures that tissues have an even consistency across different depths, improving the diagnostic quality of the ultrasound image.

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341
Q

What are the different ways to move the transducer for optimal ultrasound imaging?

A

The transducer can be moved in standard and non-standard planes, slid in various directions, angled, or rotated to capture the best possible image.

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342
Q

What is knobology in the context of ultrasound imaging, and what does it involve?

A

Knobology refers to the skill of adjusting machine controls like frequency, depth, focal depth, and TGC to optimize imaging for different organs.

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343
Q

How can you ensure you capture and correctly label ultrasound images?

A

Use the machine’s freeze function to capture images, label them appropriately (e.g., orientation), and then store or print. For dynamic imaging, pressing ‘store’ during scanning saves a video clip.

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344
Q

How do ultrasound machines assist in making measurements on images?

A

Ultrasound machines provide cursors for measuring linear lengths, areas, or peripheries, and selecting a body system allows for specific measurements like ‘renal length.’

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345
Q

What functionality does calculation software in ultrasound machines offer?

A

It transforms measurements into biological values, such as estimating gestational age or predicting the date of parturition, enhancing diagnostic accuracy and planning.

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346
Q

What are the essential safety and preparation steps before an ultrasound exam?

A

Use appropriate personal protective equipment (PPE), ensure proper restraint of the animal, consider the need for analgesia or sedation, and adjust the examination setting based on the animal’s size and the area being examined.

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347
Q

How do you prepare an animal’s skin for ultrasound imaging?

A

Clip hair, clean the skin with alcohol, apply ultrasound gel, and ensure good contact between the transducer and skin to allow sound penetration.

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348
Q

What are the differences between linear and curved transducers?

A

Linear transducers emit parallel sound lines creating a rectangular beam for full cross-sectional images, requiring full contact. Curved transducers emit diverging sound lines for a larger cross-sectional image with a smaller contact area, useful for areas like between ribs.

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349
Q

Why and how are stand-offs used in ultrasound imaging?

A

Stand-offs, such as gel pads or extra gel, move superficial structures further from the transducer to reduce near-field noise, essential for imaging superficial structures like equine tendons.

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350
Q

How does frequency selection affect ultrasound imaging?

A

Higher frequencies provide better resolution but less depth penetration, suitable for shallow structures like the eye, while lower frequencies offer deeper penetration but lower resolution, used for deeper structures like sheep pregnancy detection.

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351
Q

Why use a stand-off in ultrasound imaging?

A

To improve imaging of superficial structures by reducing near-field noise and enhancing image clarity.

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352
Q

When should radiographs be taken, and what is crucial to obtain?

A

Radiographs should only be taken when there is definite clinical justification. It’s imperative to obtain a standard view for accurate interpretation.

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353
Q

What defines a Controlled Area in radiography?

A

Once x-ray equipment is switched on, the radiography room becomes a Controlled Area, permitting only authorized personnel to enter while radiography is being performed.

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354
Q

Describe the key components of radiography equipment and their purposes.

A

Key components include the tube head for generating x-rays, lead shutters for beam area control, a light beam diaphragm for positioning, cassettes for image capture, and a grid for improved image quality in deeper tissues.

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355
Q

What are key safety measures for operators during radiography?

A

Safety measures include staying at least 2 meters away from the primary beam, wearing PPE, using a personal dosimeter, recording all exposures, ensuring equipment is in good order, and avoiding radiography if pregnant.

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356
Q

What are the practical difficulties encountered in large animal radiography?

A

Radiographs are often taken with the animal conscious and standing, requiring multiple people (machine operator, plate holder, animal handler), and usually done at the client’s premises, demanding careful safety planning and technique due to the horizontal beam and large patient size.

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357
Q

What are the risks associated with horizontal beam radiography in large animals?

A

The risks include the potential for the beam to travel further, creating more scatter and requiring higher exposures than in small animals. This necessitates the use of protective clothing and adherence to the inverse square law for safety.

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358
Q

How can you ensure safety during large animal radiography?

A

Ensure correct machine settings, patient positioning, labeling, focal distance, beam centering, and collimation. Perform a final safety check to ensure everyone is correctly positioned.

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359
Q

What are the conventions for orienting radiographic images in large animals?

A

The cranial aspect of the animal should be on the left of the image, and the proximal aspect on the upper part of the image. Lateromedial views of specific areas like the tarsus are standard.

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360
Q

Why are oblique views used in large animal radiography, and what do they highlight?

A

Oblique views are used to provide additional perspectives on joints, highlighting medial and lateral aspects that may not be visible in standard projections, such as the dorsolateral-palmaromedial oblique view.

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361
Q

What is the basic structure of an imaging report?

A

An imaging report should detail the findings (‘What have you got?’), describe the observable details (‘What can you see?’), and conclude with the clinical significance (‘What does it mean?’).

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362
Q

How should abnormalities in radiographs be described in a report?

A

Abnormalities should be described using specific radiographic and ultrasonographic descriptors, such as “fluffy new bone on the distal patellar groove,” indicating mild osteoarthritic changes.

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363
Q

What are common pitfalls in interpreting imaging series?

A

Common pitfalls include overinterpretation, using wrong terminology, concluding without adequate observations and interpretations, and failing to provide or consider adequate context for the findings.

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364
Q

Why is sticking to the basic structure important when submitting reports for imaging series?

A

Adhering to a basic structure ensures clarity, comprehensiveness, and relevance, facilitating accurate diagnosis and appropriate clinical decision-making.

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365
Q

: Why is terminology important in imaging reports?

A

Precise terminology prevents misunderstandings and ensures clear communication among veterinary professionals.

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366
Q

How can overinterpretation be a pitfall in imaging analysis?

A

It may lead to incorrect diagnoses or unnecessary treatments, emphasizing the need for a balanced and evidence-based approach.

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367
Q

What role does the imaging report template play in veterinary diagnostics?

A

It standardizes reporting, ensuring all necessary information is conveyed and interpreted correctly for optimal patient care.

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368
Q

What are the two common views taken when radiographing a dog’s stifle?

A

Lateral (medio-lateral) view and caudo-cranial view.

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369
Q

How should the dog be positioned for a lateral stifle radiograph?

A

In lateral recumbency with the leg to be imaged against the table.

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370
Q

: How is the dog positioned for a caudo-cranial view of the stifle?

A

In ventral recumbency with the limb extended caudally.

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371
Q

How should the limb be positioned for a medio-lateral projection of the dog’s stifle?

A

The limb to be radiographed is flexed 90 degrees, with the upper limb moved cranially or laterally out of the way using a rope tie or sandbag.

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372
Q

What is a common error to avoid when positioning the limb for a medio-lateral projection?

A

Avoid pulling the leg too far cranially or laterally as it can rotate the pelvis and thus the lower leg and stifle.

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373
Q

What additional positioning aids are used for a lateral view of the stifle to ensure optimal radiographic quality?

A

A foam pad under the hock to keep the tibia parallel to the table and a sandbag to hold the hock in position.

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374
Q

What areas should be included in the exposed area for a lateral view of the stifle?

A

Include 50% of the femur and 50% of the tibia-fibula, with collimation centered at the stifle joint or slightly more distal.

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375
Q

What indicates a well-positioned stifle radiograph in the lateral view?

A

The femoral condyles should be superimposed and not rotated.

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376
Q

For a caudo-cranial view, how should the limb be rotated and where should the center of collimation be?

A

Rotate the limb so the patella is in the midline, with the center of collimation at the middle of the stifle joint.

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377
Q

What are key features of a well-positioned caudo-cranial radiograph of the stifle?

A

The femoral condyles are of equal size with the patella in the midline, ensuring no limb rotation and good visualization of the joint space.

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378
Q

What are the two primary radiographic views for examining a dog’s shoulder?

A

Lateral (medio-lateral) and caudo-cranial views.

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379
Q

What positioning is required for the lateral view of a dog’s shoulder?

A

The dog is placed in lateral recumbency with the leg to be imaged against the table.

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380
Q

Describe the positioning for a caudo-cranial view of the dog’s shoulder.

A

The dog is placed in dorsal recumbency, and the limb is extended cranially.

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381
Q

How is the limb positioned for a medio-lateral projection of the shoulder?

A

The limb is pulled into extension, the upper limb is moved caudally, and the neck is flexed dorsally to avoid superimposition over the shoulder joint.

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382
Q

What are the positioning details for a lateral view of the dog’s shoulder?

A

Use a foam pad under the chest for alignment, include the distal 50% of the scapula and proximal 50% of the humerus, and collimate around the shoulder joint.

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383
Q

What indicates a well-positioned shoulder radiograph?

A

Clear visualization of the joint space without overlying tissue from the neck, other limbs, or the cervical spine.

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384
Q

How should the limb be positioned for a caudo-cranial view of the shoulder?

A

The dog is in dorsal recumbency, limb extended and slightly away from the midline, with the head and neck slightly pushed away if needed for clarity.

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385
Q

What is the recommended restraint for a horse during an ultrasound of the distal limb?

A

The horse should be well-restrained, preferably held rather than tied, using a headcollar or bridle/chifney as needed, with the examination ideally conducted in stocks or a stable.

386
Q

When might sedation be considered necessary for equine ultrasound?

A

Sedation may be required for horses that are spooky or dislike the ultrasound machine to ensure they remain quiet and not fidgety during the exam.

387
Q

What are the key settings and equipment for an equine tendon ultrasound?

A

Use a linear probe with a high frequency (8.5-10 MHz), a standoff pad if available, and obtain both transverse and longitudinal views.

388
Q

How should you conduct a systematic ultrasound examination of the equine distal limb?

A

Start at the proximal metacarpus/metatarsus, image in transverse and then longitudinal sections from proximal to distal, and identify any abnormalities based on their location and appearance.

389
Q

What are the key preparation steps for equine limb ultrasound?

A

Proper limb preparation includes clipping, applying spirit gel, and using appropriate pressure to ensure good image quality, remembering that ultrasound waves do not travel well through air.

390
Q

What are the primary health and safety concerns with CT and MRI imaging?

A

: For CT, ionizing radiation; for MRI, magnetic fields, implanted medical devices, metallic implants, missile risk, and magnetic media.

391
Q

How is significant pathology identified on spinal CT and MRI?

A

By understanding applied anatomy, recognizing deviations from normal structure, and identifying specific signs of diseases like spinal fractures, calcified disc extrusion, neoplasia, discospondylitis, spinal tumors, and fibrocartilaginous embolisation.

392
Q

What anatomical landmarks are crucial for evaluating spinal health in MRI and CT images?

A

Vertebrae, intervertebral discs, spinal cord, and surrounding soft tissues.

393
Q

How are spinal fractures identified on MRI and CT?

A

By looking for discontinuities in the vertebral bodies, misalignment, or abnormal spacing between vertebrae.

394
Q

What role does software reconstruction play in spinal imaging?

A

It enhances the visualization of spinal structures, allowing for detailed analysis of complex anatomies and pathologies.

395
Q

What imaging characteristics distinguish calcified disc extrusion and discospondylitis?

A

Calcified disc extrusion shows as hyperdense areas on CT, whereas discospondylitis may show disc space narrowing, endplate irregularities, and possible abscess formation.

396
Q

What are the key components of an imaging report for spinal CT and MRI?

A

The report should detail the findings (“What have you got?”), describe the observed abnormalities (“What can you see?”), and interpret the clinical significance (“What does it mean?”).

397
Q

What factors influence the choice between MRI and CT in medical imaging?

A

Factors include the type of tissue being examined, the presence of metal implants, patient condition, and the specific clinical question being addressed.

398
Q

When is CT preferred over MRI?

A

CT is preferred for imaging bone structures, detecting acute bleeding, and situations requiring rapid imaging, such as emergencies.

399
Q

When is MRI preferred over CT?

A

MRI is preferred for detailed soft tissue contrast, imaging of the brain and spinal cord, and situations where radiation exposure is a concern.

400
Q

Why might MRI be chosen over CT in certain cases?

A

MRI does not use ionizing radiation, making it a safer option for pregnant patients and repeated imaging scenarios.

401
Q

What imaging modality provides better soft tissue contrast?

A

MRI provides superior soft tissue contrast compared to CT, making it ideal for imaging ligaments, tendons, and the brain.

402
Q

Which imaging modality provides better visualization of bone structures?

A

CT provides superior detail of bone structures, including fractures and bony pathology.

403
Q

How do metal implants affect the choice between MRI and CT?

A

MRI is often contraindicated or limited by the presence of metal implants due to artifact creation, whereas CT may be less affected.

404
Q

What are the common pathologies to look for in stifle radiographs?

A

Look for signs of joint effusion, cranial movement of the tibia indicating cranial cruciate ligament rupture, chronic stifle arthrosis, and osteochondrosis.

405
Q

: How is joint effusion identified on a stifle radiograph?

A

Joint effusion is indicated by an increased soft tissue density around the joint capsule, often accompanied by displacement of the fat pad.

406
Q

What radiographic sign indicates a cranial cruciate ligament rupture?

A

Progressive cranial displacement of the tibia relative to the femur, assessed through different stages from mild to severe.

407
Q

What are the radiographic features of chronic stifle arthrosis?

A

Features include the presence of osteophytes, joint effusion, and, although the underlying cause may not be evident, it could be secondary to trauma.

408
Q

How is osteochondrosis identified in stifle radiographs?

A

Look for radiolucent defects with surrounding sclerosis, which could evolve into chronic arthrosis over time.

409
Q

What are common pathologies identifiable on shoulder radiographs?

A

Medial shoulder luxation, osteochondrosis, and chronic shoulder arthrosis.

410
Q

How is medial shoulder luxation typically identified on radiographs?

A

By the displacement of the humeral head medially compared to the glenoid cavity, often due to trauma.

411
Q

What radiographic signs suggest osteochondrosis in the shoulder?

A

Loss of the rounded contour of the caudal surface of the humeral head, radiolucent defects, possibly with surrounding sclerosis or calcified free bodies in the joint.

412
Q

What features on a radiograph indicate chronic shoulder arthrosis?

A

Presence of new bone formation (osteophytes) around the joint, with the underlying cause often not evident.

413
Q

Describe the sensitization phase of Type 1 Hypersensitivity and the role of cytokines in B cell class switching.

A

In the sensitization phase of Type 1 Hypersensitivity, exposure to an allergen via respiratory or skin routes leads antigen-presenting cells to capture antigens, causing naïve T cells to differentiate into T helper 2 cells, which favor a humoral response. These Th2 cells release cytokines (IL-4, IL-10, IL-5, IL-9, IL-13) that induce B cell proliferation and class switching from IgM to IgE. IgE then binds to mast cells, which relocate to the area of initial allergen encounter, without causing clinical signs initially.

414
Q

What are the immediate and late phase responses in Phase 2 of Type 1 Hypersensitivity?

A

Upon re-exposure to the same allergen, primed IgE-coated mast cells bind the allergen, leading to the release of cytoplasmic granules containing histamine, heparin, and serotonin. This causes symptoms like pruritis, bronchoconstriction, and edema within 15 minutes (immediate hypersensitivity). The late phase reaction occurs 4-24 hours later, characterized by eosinophil infiltration, as seen in cytological examinations, indicating a sustained inflammatory response.

415
Q

Explain how Type 2 Hypersensitivity differs from Type 1 in terms of the immune response and provide an example.

A

Type 2 Hypersensitivity is mediated by antibodies (IgG subtype) that recognize cell surface or extracellular matrix antigens, activating the classical complement pathway and leading to cell destruction or dysfunction. This differs from Type 1, where IgE binds to mast cells. An example of Type 2 reaction is autoimmune hemolytic anemia, where antibodies target cell surface antigens, leading to cell lysis and anemia.

416
Q

Describe the mechanism of Type 3 Hypersensitivity and the clinical implications of immune complex deposition.

A

Type 3 Hypersensitivity involves the formation of antigen-antibody (immune) complexes, which deposit in tissues, activating the complement system and attracting neutrophils. However, neutrophils cannot ingest these complexes, leading to tissue damage through the release of toxic granules. This mechanism can result in conditions like vasculitis, where small complexes deposit in capillaries, indicating the severity of tissue damage due to immune complex deposition.

417
Q

Explain the cell-mediated mechanism of Type 4 Hypersensitivity and its pathophysiological effects.

A

Type 4 Hypersensitivity, also known as delayed-type hypersensitivity, is mediated by T cells rather than antibodies. Upon re-exposure to an antigen, sensitized T cells (Th1) are reactivated and release cytokines like interferon-gamma, which recruit macrophages and lead to inflammation. This response can cause granulomatous lesions and tissue damage, seen in conditions like tuberculosis, where mycobacterium tuberculosis triggers a prolonged immune response.

418
Q

Which hypersensitivity leads to anaphylaxis?

A

Type 1 hypersensitivity

Causes acute systemci manifestation
Breakdown of mast cells
Broncho or pulmonary oedema

419
Q

Where does anaphylaxis occur in dogs

A

Liver due to hepatic vein issues

420
Q
A

Atopic dermatitis
Prurititc skin disease

421
Q

Type 2 hypersensitivity

A

Antibody mediated cytotoxicity
Mediated by antibodies that recognise antigens on a cell surface or in the space between cells
Intrinsic or extrinsic antigens

This uses the classical complement pathway

422
Q

Describe how Type 2 hypersensitivity can occur with penecillin

A

Binds to extrinsic antigens
igG binds and causes activation of the complement system
This destructs red blood cells and leads to anaemia

Autoimmune anaemia
Impacts cellular adhesion, nutrition and waste disposal

423
Q

What hypersensitivity uses IgG

A

type 2

424
Q

What hypersensitivity uses IgE

A

Type 1

425
Q

Myasthenia gravis

A
426
Q

Which hypersensitivy is immune complec hypersensitivity?

A

Type 3

427
Q

Type 3 hypersensitivity

A
428
Q

WHat are the 2 subtypes of type 3 hypersensitivity

A

Antibody excess- lots of IgG
Antigen excess - less circulating igG- capillary depostion = vasculitis and thrombosis

429
Q

Equine recurrent airway obstruction

A

type 3 hypersensitivity

430
Q

Canine blue eye

A

type 3 hypersensitivity

431
Q

Type 4 hypersensitivity

A

Cell mediated not antibody mediated
Prolonged onset

432
Q

Tuberculosis hypersensitivity

A

Type 4
Sensitised T helper cells
Lateral skin on neck in cattle for testing

433
Q

What are the goals for treatment of type 4 hypersensitivity

A
434
Q

What is a primary immune deficiency?

A

Inherited or congential
Occurs when there is a mutation in a gene that is associated with the immune response

435
Q

What is a secondary immune deficiency?

A
436
Q

What are primary immune deficiencies?

A

Clinical apparent in early life
Increase mortalitiy
Breed associated
Very rare
Lack of research here

Depends on the impact of the mutation

437
Q

SCID

A

Severe combined immunodeficiency is primary immune def

438
Q

CLAD

A

Canine leukocyte adhesion deficiency
Primary immunodeficiency

439
Q

How to respond to primary immune deficiency in practice

A

Blood work
Low lymphocyte levels - low in some cases due to stress response so not always helpful
Breed susceptibilities
Many markers

440
Q

Secondary immune def

A

Age related decline decline in CD4+
Specific infections such as FIV (greater 4% incidence)
Chronic stress - glucocorticoids suppress immune response increases infection susceptibility)
Malnutrition causes decrease in leptin and T lymphocytes

441
Q

What is immune deficiency and its implications for susceptibility to infectious diseases?

A

Immune deficiency is an impairment in parts or functions of the immune system, rendering an animal more susceptible to infectious diseases. This condition can be due to inherent genetic defects (primary) or acquired factors (secondary) such as age, chronic disease, infection, or therapeutics.

442
Q

Compare and contrast primary and secondary immune-mediated deficiencies.

A

Primary immune deficiencies are inherited or congenital, often presenting early in life with increased susceptibility to infection and possibly increased mortality. Secondary immune deficiencies are acquired, common, and can arise from physiological or pathological changes within the immune system, like age, chronic diseases, or specific treatments, leading to diminished immune responses.

443
Q

Describe Canine Leukocyte Adhesion Deficiency (CLAD) and Severe Combined Immunodeficiency (SCID) and their genetic bases.

A

CLAD, common in Irish Setters, is an autosomal recessive disorder due to a mutation in the beta-2 integrin gene, leading to impaired immune response and abnormal blood clotting. SCID affects dogs, horses, and is characterized by mutations affecting cytokines (IL-2, 4, 7, 9, 15) or lymphocyte formation, resulting in a complete failure of the immune system.

444
Q

: How should immune deficiencies be approached and diagnosed in veterinary practice?

A

Diagnosis involves assessing blood work for signs like neutrophilia or lymphopenia, considering breed susceptibilities, evaluating response to vaccination, and monitoring for recurrent infections. Distinguishing between chronic stress effects and genuine immunodeficiency markers is crucial for accurate diagnosis.

445
Q

What factors contribute to secondary immune deficiencies, and how do they affect animals?

A

Secondary immune deficiencies result from age-related decline in CD4+ memory cells, chronic stress leading to suppressed immune response via glucocorticoids, malnutrition affecting T lymphocyte function, and specific infections like FIV that directly compromise the immune system.

446
Q

How can diagnosis of infection occur?

A

Clinical signs - may not be pathognomic
Detect pathogen
Detect host response to pathogen = antibodies
Narrow window for detection of pathogen

447
Q

How can genetic material be tested for virus diagnosis?

A

DNA via PCR
RNA via reverse transcription and PCR/ qPCR

448
Q

What is a lateral flow device

A

Based on latex agglutination test these are an animal side test
Depends on the availability of pathogens

449
Q

How can antibodies be tested?

A

Indirect ELISA
Antibody on the plate is much more accurate than indirect
Capture may work better than indirect

450
Q

Why is competitive ELISA good?

A

Dont need a specific antibody
Multispecies test

451
Q

What are some specialised lab test for ELISA?

A

Agglutination/haemagglutination inhibition
Singla radial haemolysis
Complement fixation

452
Q

Describe the principle of ELISA in antigen detection and its application in veterinary diagnostics.

A

ELISA (Enzyme-Linked Immunosorbent Assay) is a plate-based assay technique designed for detecting and quantifying soluble substances such as peptides, proteins, antibodies, and hormones. In veterinary diagnostics, ELISA is utilized for antigen detection by capturing the target antigen from the sample with a specific antibody coated on the plate, followed by detection using a secondary antibody conjugated with an enzyme. This method is widely used due to its sensitivity and specificity for various pathogens.

453
Q

Compare laboratory tests and animal-side tests for pathogen detection in terms of applicability and specificity.

A

Laboratory tests, such as PCR, qPCR, and ELISA, offer high specificity and sensitivity, allowing detailed analysis and quantification of pathogens’ genetic material or proteins. Animal-side tests, including lateral flow devices and latex agglutination tests, provide rapid results and are useful for on-site screening. However, they may have lower specificity and sensitivity compared to laboratory tests, making them more suited for preliminary diagnosis rather than definitive identification.

454
Q

Explain the IMAC ELISA technique and its significance in diagnosing active infections.

A

IgM antibody capture (IMAC) ELISA is a diagnostic method used to measure active infection by specifically detecting IgM antibodies, which are typically produced early in the body’s immune response to infection. This technique involves capturing IgM antibodies from the sample onto the plate, followed by detection of specific antigens. It is particularly significant for diagnosing acute infections and for screening diseases like toxoplasmosis in cats.

455
Q

Discuss the diagnostic approach for tuberculosis in cattle, including the use of the SICCT test and the interferon gamma (IFNγ) test.

A

Tuberculosis in cattle is diagnosed using the Single Intradermal Comparative Cervical Tuberculin (SICCT) test, a type IV hypersensitivity reaction that measures the skin’s response to tuberculin antigens. The Interferon Gamma (IFNγ) test is another method that measures the release of IFNγ from blood cells in response to tuberculosis antigens. Both tests have high sensitivity and specificity, with the IFNγ test providing a rapid and early diagnosis compared to the SICCT test.

456
Q

Why is effective sampling critical in veterinary diagnostics, and how does it influence the accuracy of test results?

A

Effective sampling is vital because it directly impacts the accuracy and reliability of diagnostic tests. The right type of sample, collected correctly from the appropriate location and animal at the optimal time, ensures that the sample accurately represents the disease state or pathogen presence, minimizing false negatives or positives.

457
Q

What considerations should be made when choosing sample types for veterinary diagnostics?

A

Considerations include the suspected disease (bacterial, parasitic, viral), the most likely site of infection, and the stage of the disease. Blood, mucosal swabs, respiratory tract samples, and less invasive options like milk or saliva can all be appropriate, depending on the pathogen and the diagnostic goal.

458
Q

Explain the importance of timing in sample collection and the consequences of improper handling.

A

Timing affects the detection of pathogens, especially in relation to the disease’s progression and the immune response, like seroconversion. Improper handling or timing can lead to degradation of the sample or its components, leading to inaccurate diagnostic outcomes.

459
Q

What are the inflammatory markers?

A

Fibrinogen
C reactive protein
Serum amuyloid A in th cat horse cow and dog
Haptaglobin in cows
Pigs also have p-MAP

460
Q

What are the main types of vaccines used in veterinary medicine, and how do they differ?

A

Vaccines in veterinary medicine are categorized as inactivated (killed), attenuated (live), subunit, vectored, DNA, and mRNA vaccines. Inactivated vaccines contain killed pathogens and are safe but often require adjuvants. Attenuated vaccines contain live, weakened microbes, offering robust immunity but with a risk of reverting to virulence. Subunit, vectored, DNA, and mRNA vaccines target specific parts of the pathogen to stimulate an immune response, with variations in their effectiveness and safety profiles.

461
Q

Describe the role of adjuvants in vaccines and list common types.

A

Adjuvants enhance the immune response to the antigen present in the vaccine. Common types include aluminium salts, oil emulsions, saponins, immune-stimulating complexes (ISCOMs), liposomes, microparticles, non-ionic block copolymers, derivatised polysaccharides, cytokines, and bacterial derivatives. They work by forming a depot of antigen, stimulating cytokine and chemokine secretion, enhancing immune cell recruitment, and promoting antigen uptake, processing, and presentation.

462
Q

What are the different types of adverse vaccine reactions, and how can they be mitigated?

A

Adverse vaccine reactions can be categorized as vaccine-induced, vaccine-potentiated, programmatic errors, or coincident effects. Strategies to mitigate these include using non-adjuvanted or recombinant vaccines when possible, adhering to vaccine site recommendations, varying the injection site annually, and avoiding unnecessary vaccinations. Feline Injection Site Sarcoma (FISS) is a specific concern, with recommendations to avoid adjuvanted vaccines and use specific sites for injections.

463
Q

Summarize the four types of hypersensitivity reactions to vaccines and provide examples.

A

Type I hypersensitivity involves an immediate allergic reaction (e.g., anaphylaxis), mediated by IgE. Type II involves cytotoxic reactions, such as bovine neonatal pancytopenia. Type III hypersensitivity, mediated by immune complexes, can lead to reactions like cutaneous vasculitis. Type IV, or delayed hypersensitivity, is T-cell mediated, leading to granuloma formation. Each type has different timeframes from exposure to reaction, ranging from within an hour to weeks.

464
Q

What are the main immunological pathways activated by vaccines, and how do they contribute to protective immunity?

A

Vaccines primarily activate the adaptive immune system through two pathways: the humoral immune response, mediated by B cells that produce specific antibodies against pathogens, and the cell-mediated immune response, involving T cells that eliminate infected host cells or help B cells. Live attenuated vaccines often stimulate both responses, while inactivated and subunit vaccines mainly provoke a humoral response unless combined with adjuvants to enhance cell-mediated immunity.

465
Q

List some common vaccines used in veterinary medicine for dogs and cats and the diseases they protect against.

A

Dogs Core vaccines- Rabies, Canine distemper virus, Canine parvovirus, Canine adenovirus
Dogs non core – leptospirosis, bordatell bronchiseptica, canine influenze

Cats core vaccines- Rabies, feline herpes virus, feline calcivirus, feline panleukopenia
Cats non core- Feline leukemia virus, bordetella bronchiseptica

466
Q

Describe the stages of vaccine development and testing in veterinary medicine.

A

Vaccine development involves several stages, starting with research to identify antigens that can induce immunity. Pre-clinical trials in cell cultures or animal models assess safety and efficacy. Clinical trials in the target species follow, with Phase I focusing on safety, Phase II on immunogenicity and dosing, and Phase III on efficacy against disease. Regulatory review and approval are required before a vaccine can be marketed, and post-marketing surveillance monitors adverse effects in the wider population.

467
Q

Discuss the importance of vaccine scheduling and how vaccine protocols may be adapted for individual animals.

A

Vaccine scheduling ensures that animals are immunized at the appropriate age and intervals to establish and maintain protective immunity throughout their lives. Protocols may be adapted based on an animal’s health status, breed, exposure risk, and lifestyle. Tailoring vaccine schedules helps optimize protection while minimizing the risk of adverse reactions.

468
Q

Describe how vaccines contribute to disease eradication and control efforts in animal populations.

A

Vaccines play a crucial role in disease eradication and control by reducing the incidence of infectious diseases, cutting down the pathogen’s spread, and building herd immunity. Successful vaccination campaigns can lead to the complete eradication of diseases, as seen with rinderpest in cattle.

469
Q

Explain the role of laws and regulations in the development, approval, and administration of veterinary vaccines.

A

Laws and regulations ensure the safety, efficacy, and quality of vaccines before their market approval. They govern clinical trials, manufacturing processes, distribution, and post-market surveillance. Compliance with regulatory standards protects animal health and supports public confidence in vaccine programs.

470
Q

Highlight recent advances in vaccine technology and their potential impact on veterinary medicine.

A

Recent advances include mRNA vaccines, vectored vaccines, and nanotechnology-based delivery systems. These technologies offer the potential for more rapid development, improved efficacy, and better safety profiles. They may enable more targeted and effective immunization strategies against emerging and zoonotic diseases, enhancing animal and public health.

471
Q

Types of bacterial vaccine

A

Inactivated
Attenuated
Subunit-
Recombinant- purified OspA encoded by a gene from borrelia burgdorferi protects dogs against Lyme disease

472
Q

What are the pros and cons for infectious and non infectious vaccines?

A
473
Q

Pros and cons of different vaccines

A
474
Q

Type 2 hypersensitivity reactions to vaccines in COws

A

Bovine neonatal pancytopenia

475
Q

Type 2 hypersensitivities to vaccines in cats

A
476
Q

What type 3 hypersensitivities can occur with vaccines

A
477
Q

What are vaccine-induced hypersensitivity reactions, and how can they be identified and managed in veterinary practice?

A

Vaccine-induced hypersensitivity reactions are adverse immune responses that occur in some animals following vaccination, manifesting as allergic reactions that can range from mild (e.g., skin rash, itching) to severe (e.g., anaphylaxis). Identification involves monitoring for symptoms post-vaccination, and management includes pre-vaccination assessment of hypersensitivity history, judicious use of vaccines (especially those known to have higher risks), and having emergency treatments available for immediate intervention.

478
Q

How are hypersensitivity considerations integrated into the development of veterinary vaccines?

A

In developing veterinary vaccines, researchers consider potential hypersensitivity by selecting antigens and adjuvants that minimize the risk of adverse immune reactions. This involves rigorous preclinical testing for immunogenicity and safety, including assessments for hypersensitivity potential. Modern vaccine technologies, such as recombinant vaccines, are designed to reduce unnecessary immunostimulatory components, thereby lowering the risk of hypersensitivity reactions.

479
Q

: Describe strategies for vaccinating animals with known hypersensitivity disorders.

A

For animals with known hypersensitivity disorders, vaccination strategies include careful selection of essential vaccines only, to minimize exposure to potential allergens. Timing of vaccinations may be adjusted to ensure the animal is in optimal health, and split dosing or titer testing may be employed to reduce the immune system’s burden. Close monitoring and readiness to manage allergic reactions are critical components of these strategies.

480
Q

ASIT

A

Allergen specific immunotherapy

481
Q

How should veterinarians evaluate the most appropriate vaccine for differing clinical scenarios in veterinary medicine?

A

Veterinarians consider factors like animal species, age, health status, exposure risk, and geographical location to select the most appropriate vaccine. Tailoring vaccine choice to individual needs optimizes efficacy and safety.

482
Q

: What are the differences between prophylactic, therapeutic, and immunocontraceptive vaccines, and in what scenarios are each utilized?

A

Prophylactic vaccines prevent diseases, therapeutic vaccines treat existing diseases, and immunocontraceptive vaccines control population by inducing infertility. Each is used based on specific goals, whether preventing infection, treating an ongoing disease, or managing wildlife populations.

483
Q

How does the concept of herd immunity apply to veterinary practice, and what factors influence its achievement?

A

Herd immunity involves vaccinating a significant portion of the population to reduce disease spread, protecting unvaccinated individuals. It’s influenced by vaccine efficacy, population density, and vaccination coverage.

484
Q

: Discuss the role of ring vaccination and the challenges posed by imperfect viral vaccines in containing outbreaks among animal populations.

A

Ring vaccination involves vaccinating all susceptible individuals in the vicinity of an outbreak to contain the disease. Imperfect vaccines may not prevent infection but can reduce disease severity and transmission.

485
Q

What distinguishes core from non-core vaccines in dogs and cats, and how do veterinarians decide which vaccines are necessary for individual animals?

A

Core vaccines are essential for all animals, providing protection against diseases with widespread risk. Non-core vaccines are recommended based on individual risk assessments, including lifestyle and geographical exposure.

486
Q

What are the advantages of different vaccine administration routes, such as intramuscular, subcutaneous, intradermal, and intranasal, in veterinary practice?

A

Different routes (intramuscular, subcutaneous, intradermal, intranasal) offer advantages in terms of immune response, ease of administration, and vaccine type suitability. The choice depends on the vaccine’s formulation and targeted immune response.

487
Q

Discuss the critical factors veterinarians must consider regarding the timing and sequence of vaccinations in animals, including age, pregnancy status, and disease risk.

A

The timing of vaccinations is critical and must consider the animal’s age, pregnancy status, and specific disease risks. Proper scheduling ensures effective immunity development without interfering with maternal antibodies or compromising animal health.

488
Q

What best practices should be followed for the storage and handling of veterinary vaccines to ensure their efficacy?

A

Best practices include storing vaccines at recommended temperatures, avoiding exposure to light, and rotating stock to use older vaccines first. For example, live vaccines are particularly sensitive and must be kept refrigerated and used promptly once reconstituted.

489
Q

Discuss the importance of species-specific considerations in vaccine protocol development and give examples of how vaccine recommendations may differ between species.

A

Vaccine protocols must consider the unique physiology and disease risks of each species. For instance, rabies vaccine is core for dogs, cats, and ferrets due to public health implications, but vaccination strategies for livestock focus on diseases affecting food safety and herd health, such as foot-and-mouth disease.

490
Q

How can veterinarians identify, manage, and report adverse vaccine reactions in animals?

A

Veterinarians should monitor for immediate and delayed reactions post-vaccination, manage reactions according to severity (from antihistamines for mild reactions to epinephrine for anaphylaxis), and report incidents to vaccine manufacturers and regulatory bodies. Maintaining detailed vaccination records helps in identifying patterns that might indicate a problem with a particular vaccine batch or type.

491
Q

What ethical considerations must veterinarians keep in mind when making vaccination decisions, especially regarding the use of non-core vaccines?

A

Ethical considerations include weighing the benefits of vaccination against potential risks, especially for non-core vaccines. Veterinarians must consider the individual animal’s health status, exposure risk, and the potential impact on public health while respecting owner’s preferences and informed consent. Decisions should be guided by evidence-based medicine and the principle of doing no harm.

492
Q

What is the immediate response to a vaccine

A

IgM
Followed by IgG which is longer lasting and more effective with a higher affinity

493
Q

Viruses

A
494
Q

Dogs core viruses and vaccination schedules

A
495
Q

Why do we not start vaccines before 8 weeks?

A

Maternally derived antibodies

496
Q

Feline vaccination schedules

A
497
Q

What are the common vaccines for rabbits and ferrets?

A
498
Q

What are the common vaccines for horses?

A
499
Q

Core vaccines for livestock animals

A

Split into cat 1 and cat 2 which are core and non core

500
Q

What are the non core vaccines for livestock vaccines

A
501
Q

What are the Cat 1 vaccines for sheep

A
502
Q

How can vaccines be combined?

A

Multiplex vaccines such as canine vaccines can be reconstituted with dilent or lepto2 for DHPPI-L2

Cant combine vaccines from different manufacturers

503
Q

How is equine strangles vaccine administered?

A

submucosal

504
Q

What are the less common routes for vaccines?

A
505
Q

What are the general considerations for who to vaccinate and when?

A
506
Q

What are the considerations for vaccinating farm animals

A
507
Q

What are the british horse racing authority rules for vaccinations?

A
508
Q

What considerations should there be when vaccinating older cats?

A
509
Q

What factors should be considered when planning vaccinations for a flock of sheep, particularly to prevent enzootic abortion and toxoplasmosis, considering the breeding and lambing schedule? the shepard is pregnant.

A

No pregnant people should be involved in vaccination
Both are Cat 1 vaccines by NOAH
2 separate vaccines but can be given at the same time. Cannot be mixed
One off vaccination so not annual etc
Should be given 3 weeks prior to mating/tupping

510
Q

How should a veterinarian approach booster vaccinations for a dog that has moved to a new area, especially considering boarding kennel requirements and previous vaccination history?

A

Course needs restarting as the time passed
Needs DHPPi as eurican
This practice only stocks canigen and therefore needs to restart
Adult restart means 2 doses of lepto 4 weeks apart ( animal is in kennels in 3 weeks)
DHPPI needs 1 injection as an adult
Kennel cough can also be given
Going to kennels in 3 weeks so potentially may not be able to go to the kennels
Vaccine lapse may affect insurance
Onset of immunity for kennel cough is 3 weeks so this may affect kennels

DHPPI and Lepto can be mixed in a syringe and given subcut

Immunocompromised people should stay away for 3 weeks as they are attenuated vaccines

511
Q

In the context of a high disease status closed herd that is BVD free but neighboring a herd with confirmed BVD, what considerations should be made for BVD vaccination and minimizing stress during vaccination procedures?

A

Beef cows are not handled as often so multiple vaccinations can cause stress
BVD should be vaccinated for due to shared boundaries
Cows should be vaccinated with leptavoid H and bravoxin 10
Handling system potentially needs updating
Vaccinate when TB is being read
TB vaccine and lepto can be given on the same day and mixed

Other options include double fencing to avoid mix with neighboring cows

512
Q

How should a veterinarian determine a vaccination plan for a new equine import with unknown vaccination status intended for international competition, and a companion animal not previously considered for vaccination?

A

They should vaccinate both against Equine influenza, strangles (if mixing with other horses water etc), Tetanus vaccine

Equine influenza can be mixed with tetanus. Immunity is longer with tetanus so first use a mix and then less commonly. Just equine influenza following

Herpes vaccine can be administered- can cause abortions and the vaccine isnt always effective. Owner choice and assess repro health.

513
Q

What issues arose with RHD2 vaccine for rabbits?

A

The backbone meant that rabbits that had been vaccinated once with RHD 1 may have an averse reaction to RHD2

Vax with inactivated type 2 and then vaccinated with type 2 followign

514
Q

What is the incidence of FIV?

A
515
Q

What is the virus entry for FIV?

A

Pathogens enter host cell
Viral genes and enzumes are released into the host cell
Host cell internally replicated viral components
Viral particulates are then further released into the body
Makes development of antivirals challenging
To increase efficacy antiviral should target common viral proteins

516
Q

Describe FIV exposure

A

Feline Immunodeficiency Virus (FIV) affects cats by targeting their immune system, specifically CD4+ T lymphocytes. FIV binds to the CD134 (OX40) receptor on activated T cells during the initial stages of infection and subsequently uses the CXCR4 chemokine receptor to gain entry into the cells. This viral entry leads to the depletion of CD4+ T lymphocytes, which are crucial for mounting an effective immune response. The progressive depletion of these cells compromises the cat’s immune system, making it susceptible to secondary infections, chronic diseases, and a decrease in overall health.

517
Q

What are the clinical signs for FIV and what is the treatment?

A
518
Q

How does Feline Immunodeficiency Virus affect a cat’s immune system, specifically concerning T lymphocytes?

A

: FIV targets and depletes CD4+ T lymphocytes, leading to an imbalanced immune response. This depletion compromises the cat’s ability to fight off infections, making them susceptible to secondary infections and diseases.

519
Q

What are the acute, sub-clinical, and terminal stages of FIV, and how do they present clinically in infected cats?

A

In the acute stage, cats may experience mild illness with a decrease in CD4+ cells. The sub-clinical stage is often asymptomatic but characterized by a continual reduction in CD4+ cells and an increase in CD8+ cells, leading to a higher CD8+ to CD4+ ratio. The terminal stage involves severe immunodeficiency, resulting in secondary infections, weight loss, and potentially neurological disease.

520
Q

What factors influence the incidence and transmission of FIV among cats?

A

The incidence of FIV varies by geographic location and cat population, being higher in feral cats (average 4%) compared to domestic cats (average 1%). Sexually intact males have an increased risk due to their propensity for fighting and bite-wound transmission.

521
Q

What are the recommended clinical management and treatment options for a cat diagnosed with FIV?

A

Management focuses on supportive care and treatment of secondary infections, with no specific antiviral treatment for FIV itself. PCR diagnostics are used for confirmation. While a vaccine exists, it is not licensed in all countries, including the UK.

522
Q

What are the different ways pathogens evade immune response?

A

Secreted modulators or toxins
Modulators on the pathogen surface
Hide from immune surveillance
Antigenic hypervariability
Subvert or kill immune cells
Block acquired immunity
Inhibit complement
Inhibit cytokines/chemokines or interferons
Modulate apoptosis
Interfere with TLRs
Block antimicrobial small molecules
Block intrinsic cellular pathways

523
Q

How do pathogens use secreted modulators or toxins to evade the immune system?

A

Pathogens secrete substances like virokines and toxins that mimic host molecules to disrupt immune responses, including interfering with cytokine function or directly damaging immune cells.

524
Q

What role do surface modulators on pathogens play in immune evasion?

A

Surface modulators, including complement inhibitors and molecular mimics like viroceptors, help pathogens avoid detection or neutralization by the immune system.

525
Q

Describe how pathogens hide from immune surveillance.

A

Pathogens evade the immune system by hiding in immunoprivileged sites, entering latency, or altering surface antigens to avoid recognition by immune cells.

526
Q

How does antigenic variation contribute to immune evasion?

A

Through mechanisms like error-prone replication or gene reassortment, pathogens frequently change their surface antigens, evading antibody recognition and T cell responses.

527
Q

In what ways do pathogens subvert or kill immune cells?

A

Pathogens can infect and kill immune cells, produce superantigens that overstimulate the immune response, or block the killing pathways of cytotoxic cells, thereby impairing the immune defense.

528
Q

How do pathogens inhibit the complement system to evade immune responses?

A

They produce soluble inhibitors, degrade complement components, or alter their surface to prevent complement activation and membrane attack complex formation.

529
Q

Discuss how pathogens interfere with cytokines and immune signaling pathways.

A

Pathogens can block cytokine production, inhibit receptor-ligand interactions, and divert or disrupt signaling pathways essential for effective immune responses.

Cytokine production, Ligand receptor reactions, disrupt signal pathways

530
Q

What strategies do pathogens use to modulate apoptosis and autophagy in their favor?

A

They may inhibit apoptosis to prolong cell survival, activate apoptosis in immune cells, or alter autophagy processes to facilitate their replication or survival within host cells.

531
Q

: Explain how pathogens interfere with TLRs to evade detection.

A

Pathogens block or alter TLR signaling, modify TLR ligands, or mimic host molecules to reduce their recognition and dampen inflammatory responses.

532
Q

How do pathogens block the action of antimicrobial small molecules?

A

They may inactivate enzymes like iNOS, degrade antimicrobial peptides, or alter their surface to resist peptide insertion, among other mechanisms.

533
Q

What role do commensal organisms play in the reproductive system, and where are they commonly found?

A

Commensal organisms, which do not invade tissues under normal circumstances, play a crucial role in controlling pathogens by competing for living spaces and priming the immune system. In females, they are found in areas from the perineum to the uterus, with greater numbers towards the outside. In males, they are located on the preputial skin, lining, and less commonly, within accessory sex glands.

534
Q

How does the innate immunity function in the reproductive system of males and females?

A

Innate immunity maintains the balance of commensal bacteria and pathogens in both males and females. In females, it also addresses introduced bacteria, allogenic sperm, and the immunologically distinct fetus.

535
Q

What constitutes a reproductive pathogen, and how can they be transmitted?

A

A reproductive pathogen affects the reproductive tract, and transmission can occur via semen or vaginal secretion (venereal pathogens) or through other routes such as the respiratory tract (non-venereal).

536
Q

How do herpes viruses affect the reproductive system?

A

Herpes viruses can cause respiratory tract disease and, in the context of reproduction, may lead to pregnancy loss due to placental invasion. They may also cause reproductive tract disease by transmitting venereally and causing local vesicular disease.

537
Q

What routine screenings are performed for reproductive pathogens in different species?

A

Routine screenings vary by species. For horses, stallions and mares are screened for bacterial venereal pathogens and EHV. Dogs and cats have no routine reproductive screening but have vaccination regimes. Cows undergo brucella surveillance and serology for diseases affecting reproduction, while sheep, pigs, and other animals have specific screenings for diseases like PRRS, Brucella, and more.

538
Q

What are the common terms for inflammation of the female repro system

A
539
Q

Venereal pathogen

A

Via semen or vaginal secretion

540
Q

Non venereal

A

Repro pathogens that can be transmitted via other routes (eg respiratory)

541
Q

When is infection most likely to occur in the female reproductive tract?

A
542
Q

How does uterine contamination occur post partum

A
543
Q

How does uterine contamination occur at mating?

A
544
Q

Incomplete ossification of cuboidal bones

A

Congenital disease

545
Q

What can be seen in the image

A

Incomplete ossification of cuboidal bones

546
Q

What can be seen?

A

a developmental joint disease
Osteochondrosis dissecans

The bone doesnt mineralise and instead turns into soft necrotic tissue

547
Q

What are the three main aetiologies of joint sepsis?

A

1) Traumatic wounds, 2) Iatrogenic causes, 3) Haematogenous spread.

548
Q

Which species are most commonly affected by joint sepsis?

A

Horses and farm animals are commonly affected, mainly through wounds, haematogenous spread, and iatrogenic causes. It’s rare in small animals and exotics.

549
Q

Why are neonates particularly at risk for joint sepsis?

A

Neonates are at high risk due to their lack of natural immunity and the potential failure of passive transfer, leading to bacteraemia and the sequestration of pathogens in the synovial membrane.

550
Q

What are the key components in diagnosing joint sepsis?

A

History, clinical examination, synovial fluid analysis (appearance, nucleated cell count % neutrophils, total protein, and culture & sensitivity).

551
Q

What are the fundamental approaches to treating joint sepsis?

A

Early treatment for better outcomes, involving lavage (‘the solution to pollution is dilution’), antibiotics (local and systemic based on C&S), and addressing the underlying cause.

552
Q

What is the purpose of lavage in treating joint sepsis?

A

Lavage is used to dilute and remove inflammatory agents, debris, and bacteria from the joint, following the principle that “the solution to pollution is dilution.”

553
Q

How are antibiotics used in the treatment of joint sepsis?

A

Antibiotics are selected based on culture and sensitivity results and are administered both locally and systemically to combat the infection.

554
Q

: Why is it important to resolve the underlying cause in joint sepsis treatment?

A

Successfully treating joint sepsis requires identifying and resolving the primary source of the infection to prevent recurrence and ensure complete recovery.

555
Q

What is arthritis and what components of the joint does it affect?

A

Arthritis is the inflammation of the joint affecting the cartilage, synovial fluid, sub-chondral bone, synovial membrane, and joint capsule.

556
Q

Give an example of a congenital joint disease.

A

Incomplete ossification of cuboidal bones.

557
Q

What are examples of developmental joint diseases?

A

Osteochondritis Dissecans (OCD) and subchondral bone cyst.

558
Q

Provide examples of degenerative joint diseases.

A

Osteoarthritis and osteochondral fragmentation (OCF).

559
Q

What is an example of an immune-mediated joint disease?

A

Canine immune mediated polyarthritis (IMP), especially in sight hound dogs like Whippets.

560
Q

Give an example of an infectious joint disease.

A

Septic arthritis.

561
Q

What are the key methods for investigating joint disease?What are the key methods for investigating joint disease?

A

History, clinical exam, radiography (bones), ultrasonography (soft tissues), advanced imaging (MRI, CT, Nuclear Scintigraphy), and synovial fluid analysis.

562
Q

What are the principles of treating joint disease?

A

Treatment is disease-specific and multifaceted, including medical and surgical approaches, systemic and local treatments, short or long-term management, anti-inflammatory and analgesic medications, disease-modifying agents, and lifestyle changes.

563
Q

Describe the pathway leading to the formation of osteoarthritis.

A

Osteoarthritis begins with cartilage damage, leading to an inflammatory response. This inflammation causes further damage to the cartilage and underlying bone, resulting in joint pain, stiffness, and decreased mobility.

564
Q

How does Osteochondritis Dissecans (OCD) form?

A

OCD forms when a piece of cartilage, along with a thin layer of the bone beneath, separates from the end of a bone due to insufficient blood supply, causing joint pain and instability.

565
Q

What leads to the development of subchondral bone cysts?

A

Subchondral bone cysts develop due to an imbalance in bone formation and resorption, often following joint stress or injury. The cysts form in the subchondral bone, causing pain and affecting joint function.

566
Q

Describe the pathway of immune-mediated polyarthritis development.

A

In immune-mediated polyarthritis, the body’s immune system mistakenly attacks its own joint tissues, leading to inflammation without the presence of an infection. This results in joint swelling, pain, and reduced mobility.

567
Q

: How does septic arthritis develop?

A

Septic arthritis occurs when bacteria or other pathogens infect a joint, either through direct contamination (injury, surgery) or by spreading from another part of the body, leading to severe joint inflammation and damage.

568
Q

What are the systemic and intra-articular management options for osteoarthritis?

A

Systemic options include NSAIDs (for all species) and bisphosphonates (equine), with intra-articular options like corticosteroids, glycosaminoglycan derivatives (including hyaluronic acid), synthetic hydrogels, and biological products (stem cells, IRAP, PRP).

569
Q

What are the treatment options for managing joint sepsis?

A

Systemic antibiotics and NSAIDs, intra-articular antibiotics, and regional options like intravenous regional perfusion (IVRP) with antibiotics.

570
Q

What are the therapeutic options for immune-mediated joint diseases?

A

Systemic corticosteroids and immunomodulators.

571
Q

What are specific considerations for treating osteoarthritis in equines and small animals?

A

Consider the cascade and competition withdrawal times for equines, and evaluate efficacy and evidence of treatment options.

572
Q

How is sepsis managed in equine and farm animals?

A

Treatment involves systemic and intra-articular antibiotics, NSAIDs for systemic management, and may include regional options like IVRP with antibiotics.

573
Q

What approach is taken for treating autoimmune diseases in small animals?

A

Treatment typically involves systemic corticosteroids and immunomodulators to control the immune response.

574
Q
A

Osteoarthritis

575
Q
A

Osteochrondral fragmentation

576
Q
A

Canine immune mediated polyarthritis

577
Q

what would be the aetiology of joint sepsis here

A

Traumatic wounds

578
Q

What are the systemic treatment options for osteoarthritis?

A

systemic arent always the best options

579
Q

What are the intra-articular treatment options for osteoarthritis?

A

anogenic or autogenic stem ells

PRP - platelet rich plasma

580
Q

What are the different options for joint sepsis treatment?

A

Systemic
Intraarticular
Regional options

581
Q
A

withdrawal times for races
: The horse was diagnosed with osteoarthritis in small tarsal joints bilaterally, with a racing event in 16 days, necessitating careful selection of treatment to comply with competition withdrawal times.

corticosteroid administered with shorter withdrawal time.

582
Q
A

Arthrocentesis of the tibiotarsal joint revealed a nucleated cell count of 5x10^9 cells/l with 30% neutrophils and a total protein of 20g/l, indicating joint disease that requires a comprehensive diagnostic and therapeutic approach.

multiple joints affected. Intraarticular wouldnt work so corticosteroids would be the best option

583
Q

What key elements are involved in the development of specific immunity?

A

Generation of diverse T-cell (TCR) and antibody (FAB region) receptors, understanding of tolerance, and the roles of innate and specific (adaptive) immune responses.

584
Q

What happens when there is a failure of the mechanisms underpinning self-tolerance in immune-mediated diseases?

A

: An immune response may be wrongly targeted against the body’s own healthy cells and organs, leading to conditions like pemphigus foliaceus and immune-mediated kidney disease.

585
Q

How is self-harm prevented by tolerance mechanisms in the immune system?

A

Through central tolerance (deletion of reactive T-cells in the thymus) and peripheral tolerance (anergy, activation-induced cell death, and suppression by regulatory T-cells).

586
Q

What are some examples of immune-mediated diseases in dogs?

A

Auto-immune or immune-mediated haemolytic anaemia (IMHA), immune-mediated thrombocytopenia (IMT), and immune-mediated polyarthritis (IMPA).

587
Q

What is the focus when managing immune-mediated diseases?

A

Understanding immunopathological mechanisms like antibody-mediated cytotoxicity, immune complex hypersensitivity, and cell-mediated immunity.

588
Q

What are the trigger factors categorized for immune-mediated polyarthritis (IMPA)?

A

Idiopathic (Type I), associated with infection (Type II), inflammatory GI disease (Type III), and neoplastic disease (Type IV).

589
Q

What is multisystemic immune-mediated disease?

A

It occurs when the immune response targets more than one organ, as seen in SLE-like syndromes in dogs, which may involve concurrent diseases affecting multiple systems.

590
Q

Autoimmune disease

A
591
Q

Auto-immune or Immune-mediated Hemolytic Anemia (IMHA)

A

IMHA is caused by the body’s immune system mistakenly identifying its own red blood cells (RBCs) as foreign and producing antibodies against them. This results in the destruction of RBCs by the immune system, a process known as hemolysis. The destruction can occur within the blood vessels (intravascular hemolysis) or in the liver and spleen (extravascular hemolysis). The antibodies involved are typically of the IgG or IgM class, which bind to the surface of RBCs, marking them for destruction. The exact trigger for this autoimmune response is often unknown, but it can sometimes be linked to underlying conditions, infections, or exposure to certain drugs.

592
Q

Immune-mediated Thrombocytopenia (IMT)

A

IMT involves the immune system producing antibodies against the body’s own platelets, leading to their premature destruction and resulting in a significantly reduced platelet count (thrombocytopenia). Platelets are crucial for blood clotting, and their reduction increases the risk of bleeding. Similar to IMHA, the triggers for IMT can include infections, drugs, or other underlying diseases, but often, the exact cause remains idiopathic. The destruction of platelets primarily takes place in the spleen, mediated by macrophages that recognize and ingest platelets coated with antibodies.

593
Q

Immune-mediated Polyarthritis (IMPA)

A

IMPA is a condition where the immune system attacks the synovial joints, leading to inflammation and arthritis. Unlike osteoarthritis, which is primarily due to wear and tear of the joints, IMPA is an autoimmune response where the immune system mistakenly targets the joint’s synovium, leading to pain, swelling, and stiffness. There are several types of IMPA, categorized based on the underlying cause or associated conditions, ranging from idiopathic (where no cause is identified) to those linked with infections, cancer, or gastrointestinal diseases. The immune response in IMPA often involves a combination of cell-mediated immunity (T cells) and humoral immunity (antibodies) targeting the joints.

594
Q

What is immune-mediated pancreatitis, and what are its causes?

A

Immune-mediated pancreatitis is when the body’s immune system mistakenly attacks the pancreas, causing inflammation.
This damage can disrupt the production of digestive enzymes and hormones like insulin, leading to digestive problems and possibly diabetes.

The exact causes are unclear, but genetics, environmental factors, and past infections may play roles.
This condition is a type of autoimmune disease affecting the gastrointestinal system.

595
Q

How does genetic predisposition act as a trigger for immune-mediated diseases?

A

Genetic predisposition involves inherited genetic factors that increase the susceptibility of an individual to develop immune-mediated diseases. Specific genes can influence the immune system’s regulation, making it more likely to misidentify self cells as foreign, leading to conditions such as IMHA, IMT, or IMPA.

596
Q

How do infections trigger immune-mediated diseases?

A

Infections can trigger immune-mediated diseases by activating the immune system in a way that leads to cross-reactivity with self-tissues (molecular mimicry), or by causing persistent inflammation that disrupts immune tolerance. Bacterial, viral, and parasitic infections are known triggers for diseases like IMPA and IMHA.

597
Q

What role do drugs and medications play in triggering immune-mediated diseases?

A

Certain drugs and medications can act as haptens, triggering immune responses against modified self-cells or directly inducing autoimmunity through mechanisms that are not fully understood. Examples include antibiotics and anticonvulsants that can lead to conditions like drug-induced lupus or IMHA.

598
Q

How do environmental factors trigger immune-mediated diseases?

A

Environmental factors, including exposure to chemicals, pollutants, and dietary components, can influence the development of immune-mediated diseases by altering the immune system’s function or by triggering inflammatory responses that disrupt immune tolerance.

599
Q

How do stress and hormonal changes act as triggers for immune-mediated diseases?

A

Stress and hormonal changes can modulate the immune system’s responsiveness, potentially leading to an increased risk of autoimmunity. Stress-induced hormones and changes in the endocrine system can alter immune regulation, potentially triggering or exacerbating immune-mediated diseases.

600
Q

How do neoplastic diseases trigger immune-mediated conditions?

A

Neoplastic diseases can trigger immune-mediated responses through the production of tumor antigens that the immune system targets, leading to collateral damage to healthy tissues or by inducing systemic inflammation that disrupts immune tolerance, contributing to conditions like paraneoplastic syndromes.

601
Q
A
602
Q

What is Evans Syndrome, and how is it characterized in veterinary medicine?

A

Evans Syndrome in veterinary medicine is an autoimmune condition characterized by the concurrent occurrence of immune-mediated hemolytic anemia (IMHA) and immune-mediated thrombocytopenia (IMT), where the body’s immune system mistakenly attacks and destroys its own red blood cells and platelets. This leads to a combination of symptoms related to both anemia (such as lethargy, weakness, and pale mucous membranes) and thrombocytopenia (such as increased bleeding and bruising). The syndrome can be triggered by a variety of factors, including infections, certain medications, cancer, and possibly genetic predisposition, though in many cases, the exact cause remains unknown. Treatment typically involves immunosuppressive therapies aimed at reducing the immune system’s attack on blood cells, along with supportive care to manage symptoms.

603
Q

What is the rationale for managing overactive immune responses in primary and secondary immune-mediated diseases?

A

Many immune-mediated diseases lack identifiable causes (primary disease) and require management to reduce pain, loss of function, and tissue damage. For secondary diseases, controlling both the immune response and the primary cause (e.g., infection) is necessary.

604
Q

What are immunomodulatory drugs and their types?

A

Immunomodulatory drugs can stimulate, suppress, or modify the immune system. Types include interferons for severe infections (immune stimulation), allergy immunotherapy for increasing T-regulatory cells (immune modification), and broad treatments like steroids or targeted treatments like Lokivetmab for IL-31 (immune suppression).

605
Q

What are the effects and mode of action of steroids as immunosuppressive agents?

A

Steroids are the most commonly used immunosuppressive agents, affecting many parts of the immune system. They bind to glucocorticoid receptors, causing activation or inhibition of gene transcription, and have a wide range of effects, including anti-inflammatory and immunomodulatory actions.

606
Q

How does azathioprine work and what are its side effects?

A

Azathioprine works by damaging DNA, affecting rapidly growing bone marrow and immune cells. Side effects include myelosuppression, pancreatitis, and hepatotoxicity. It’s metabolized into 6-mercaptopurine and further processed by enzyme systems (TPMT) , with variations in metabolism affecting side effect likelihood.

607
Q

Describe chlorambucil and its uses.

A

Chlorambucil is an orally administered alkylating agent with cytotoxic effects, used for immunosuppression in small dogs and cats. It’s less toxic than azathioprine but still can cause myelosuppression, anorexia, vomiting, and diarrhea.

608
Q

What is mycophenolate mofetil and its effects?

A

Mycophenolate mofetil inhibits de novo purine synthesis, suppressing T and B cells. It’s fast-acting, with limited evidence for use in dogs or cats with immune-mediated diseases. Adverse effects include gastrointestinal toxicity and potential for hepatitis.

609
Q

Explain the use and mode of action of ciclosporin.

A

Ciclosporin is a potent T-cell suppressor, used for atopic dermatitis in dogs and cats. It binds to cyclophilin, inhibiting calcineurin and reducing the activation of IL-2 and related cytokines, leading to reduced effector T-cell function.

610
Q

Describe leflunomide and its applications.

A

Leflunomide inhibits DHODH, preventing the expansion of activated and autoimmune lymphocytes. It’s used for conditions like immune-mediated polyarthritis and has potential adverse events like diarrhea, lethargy, and increased liver enzymes.

611
Q

What is oclacitinib and its mechanism?

A

Oclacitinib inhibits JAK-1, blocking cytokine signaling and is licensed for canine atopic dermatitis. It’s used for a range of immune-mediated diseases, with side effects including diarrhea and haematological abnormalities.

612
Q

How do naturally occurring supplements like omega 3 fatty acids and vitamin E help in immune-mediated diseases?

A

Omega 3 fatty acids reduce production of inflammatory mediators and may play a role in early sepsis and inflammatory diseases. Vitamin E acts as an adjunct antioxidative treatment, potentially useful in specific conditions like sterile pyogranulomatous panniculitis.

613
Q

What are the principle effects of steroids?

A
614
Q

What are the metabolic effects of steroids?

A
615
Q

How can glutamine be used for treating IMD?

A
616
Q

How can arginine be used in treating IMD?

A
617
Q

What are the mechanisms of IMD immunological damage?

A
618
Q
A
619
Q

What are the primary therapeutic considerations in pregnancy?

A

Consider the effects on pregnancy and the fetus, including teratogenesis and effects at birth, alongside the balance between treating the dam and potential harm to the fetus.

620
Q

: Why is it difficult to predict plasma drug levels in pregnancy?

A

Changes in absorption, distribution, metabolism, and excretion due to pregnancy can significantly alter drug plasma levels. This includes reduced abdominal space, increased gastric pH, and altered metabolism and excretion.

621
Q

Why is checking datasheets for contraindications important in treating pregnant animals?

A

Datasheets provide crucial information on the safety and contraindications of medications during pregnancy, aiding in the selection of safe treatment options.

622
Q

How should otitis externa be treated in a pregnant bitch?

A

Treatment options must consider the absorption of corticosteroids and the teratogenic potential of gentamicin. Datasheets or pharmaceutical companies should be consulted, weighing the risk-benefit of treatment and potential for off-label use.

623
Q

What are the therapeutic considerations during lactation?

A

Consider the effects on the neonate, impact on lactation, the drug’s licensing, metabolic status of the dam, new routes of elimination, and milk withdrawal times.

624
Q

How do pharmacokinetics change during lactation?

A

Lactation introduces a new route of drug elimination, especially affecting drugs that are lipid-soluble, basic non-ionised, and have low plasma protein binding. Mastitis can also influence drug excretion by altering milk pH and blood flow.

625
Q

What considerations should be made when using Meloxicam in a lactating bitch post-caesarean section?

A

Meloxicam is contraindicated during lactation; thus, any use requires careful risk-benefit analysis, informed written consent, and close monitoring of the offspring. Alternatives, such as opiates or paracetamol, may be considered.

626
Q

How does pregnancy affect ADME of drugs?

A
627
Q

What is meant by transplacental transfer of drugs?

A

If a drug can be absorbed orally it is likely to cross the placenta.

628
Q

What drugs can be used for a pregnant dog with otitis externa?

A

Aurixon
Canaural
Easotic
Otomax ear drops
Surolan ear drops

Always review the data sheet

629
Q

What are common clinical signs of bacterial infections?

A

Pyrexia, depressed demeanor, purulent discharge, changes to white blood cell/neutrophil count, and acute phase proteins.

630
Q

What antibiotic susceptibility is important for treating Greasy Pig Disease?

A

Antibiotics susceptible to Staphylococcus hyicus should be selected based on susceptibility test results, considering what is licensed in the pig.

631
Q

What is the typical approach to treating strangles (Strep equi equi)?

A

Usually, antimicrobials are not treated; biosecurity considerations are crucial.

632
Q

What is the gold standard for confirming bacterial presence?

A

Culture and sensitivity testing, requiring 48h for culture and 72h+ for sensitivity.

633
Q

How should samples for bacterial culture and sensitivity be collected?

A

The method depends on the infection’s location, including peritoneal tap, cytology, and material for culture and sensitivity, like corneal swabs or scrapes.

634
Q

What does the color of peritoneal fluid indicate in empirical decision making?

A

Straw-colored fluid is good, while red indicates infection is present.

635
Q

What are key findings in cytology for bacterial infections?

A

Presence of PMN, MAC, LYM, RBC, and phagocytosed bacteria in a PMN.

636
Q

How do Gram stain results differentiate between bacteria types?

A

Gram-positive bacteria stain purple, and gram-negative bacteria stain pink, based on cell wall properties.

637
Q

When is prophylaxis not required, and what is the rational choice for contaminated or high-risk surgery?

A

Not required for clean surgery, such as neutering. Rational choices for contaminated or high-risk surgery include protective measures.

638
Q

What considerations are important when assessing an equine wound?

A

Age of the wound, whether it’s clean/contaminated/dirty, exposure of bone/tendon/joint, signs of infection, and culture.

639
Q

What differentiates commensal organisms from pathogens in bacterial infections?

A

Commensal organisms form stable communities on body surfaces without causing disease. Pathogens must find a niche within a host, overcome host defenses, and express virulence factors to cause disease.

640
Q

What leads to the clinical consequences of bacterial infections?

A

Pathogenicity exceeding defenses, leading to tissue damage through bacterial toxins (local/systemic), inflammatory response, immune response, and invasion (organism-dependent).

641
Q

What are the pathognomonic clinical presentations in bacterial infections?

A

k: Systemic presentations like pyrexia, and local responses such as pain, heat, swelling, erythema, pus formation (acute), and granulomas (chronic).

642
Q

How is inflammation clinically and pathologically characterized in bacterial infections?

A

Through blood neutrophil numbers, left-shift (younger neutrophils), toxic change, acute phase proteins (Fibrinogen, CRP, SAA, Haptoglobin), cardiovascular effects (acid-base, metabolic acidosis, lactate), tissue responses, coagulopathy, and neutrophil degeneration.

643
Q

How does the neutrophil response to acute inflammation vary by species?

A

Dogs and cats typically show severe lesions with neutropenia, while cows show neutropenia in inflammation regardless of severity. Species differ in marrow reserve, regenerative capacity, and typical inflammation response.

644
Q

What are the steps for cells to leave blood vessels during an infection?

A

: Marginalisation, adhesion, and migration, influenced by various factors like epinephrine, glucocorticoids, infection, and stress.

645
Q

What does a left shift in neutrophils indicate?

A

A left shift indicates a regenerative response with increased segmented over immature neutrophils, pointing towards a severe bacterial infection or rapid neutropoiesis.

646
Q

What characterizes neutrophil toxic change in bacterial infections?

A

Features like foamy cytoplasm, dispersed organelles, diffuse cytoplasmic basophilia, presence of Döhle bodies, and asynchronus nuclear maturation indicate toxic change.

647
Q

Clinical pathology of inflammation

A
648
Q

What is bacterial endocarditis, and which bacteria are commonly involved?

A

Bacterial endocarditis is the inflammation of the inner layer of the heart, including the heart valves, typically caused by bacteria such as Streptococcus spp., Staphylococcus spp., and Enterococcus spp. It often results from bacteria entering the bloodstream and adhering to previously damaged heart valves or endothelium.

649
Q

What are common clinical signs of bacterial endocarditis?

A

Clinical signs include fever, heart murmur, lethargy, weakness, weight loss, and possibly signs of congestive heart failure due to valve dysfunction. Peripheral signs like petechiae, splinter hemorrhages, and Osler’s nodes may also be present.

650
Q

How is bacterial endocarditis diagnosed?

A

Diagnosis is based on clinical signs, echocardiographic evidence of vegetative lesions on heart valves or endocardium, positive blood cultures, and indicative changes in blood tests, such as elevated white blood cell count and inflammatory markers.

651
Q

How do bacterial infections lead to pericarditis, and what are the symptoms?

A

Bacterial pericarditis is caused by the infection of the pericardium, often secondary to spread from lung infections, trauma, or surgery. Symptoms include chest pain, pericardial friction rub, and signs of cardiac tamponade (distended jugular veins, hypotension, muffled heart sounds).

652
Q
A
653
Q

Left shift

A

Moving towards immature cells

654
Q

The lactate story

A
655
Q

Coagulopathy of sepsis

A
656
Q
A

Degenerate vs non degenerate neutrophils

non degenerate on the left

657
Q

What factors contribute to disease outbreaks?

A

Outbreaks can occur due to a susceptible population, changes in the virus, short-lived immunity, and inadequate vaccines.

658
Q

What are the clinical and pathological changes seen in viral infections?

A

Changes reflect the body systems affected, ranging from acute to chronic responses, and may include host responses that help clear the disease or contribute to its pathogenesis.

659
Q

How are viral infections diagnosed?

A

Diagnosis can be based on clinical examination, detection of virus antigen or nucleic acid, detection of antiviral antibody, and specific diagnostic tests like PCR.

660
Q

What measures are important for the control and prevention of viral diseases?

A

Biosecurity, husbandry improvements, vaccination, and understanding the role of colostrum and all-in-all-out policies on farms are crucial for disease control.

661
Q

How does biosecurity contribute to disease control?

A

Biosecurity measures like closed herds, “stamping out” strategies, and adherence to biosecurity principles on farms are vital in preventing the spread of viral diseases.

662
Q

What is an example of a sporadic disease in cats?

A

FIP

663
Q

Common viral zoonoses

A
664
Q

What are the key features of Avian Influenza outbreaks in the veterinary context?

A

Avian Influenza, notably H5N1, has seen continued outbreaks affecting poultry. It’s characterized by high mortality in birds, zoonotic potential, and significant economic impact. Control measures include biosecurity, surveillance, and vaccination where available.

665
Q

What are the clinical signs and economic impact of Calf Respiratory Disease?

A

CRD is a multifactorial disease with mixed viral and bacterial infections. Clinical signs include coughing, nasal and ocular discharge, pyrexia, and depression. It poses significant economic losses due to treatment costs and reduced productivity.

666
Q

What is Feline Infectious Peritonitis, and why is it challenging to diagnose?

A

FIP is a viral disease caused by a mutation of feline enteric coronavirus. It leads to an immune-mediated response, with “wet” (effusive) and “dry” (noneffusive) forms. Diagnosis is challenging due to variable clinical presentations and requires a combination of clinical signs, serology, and specific tests like the Rivalta test.

667
Q

Describe the clinical presentation and diagnosis of Canine Parvovirus.

A

Canine Parvovirus causes severe gastrointestinal illness, with symptoms including vomiting, bloody diarrhea, pyrexia, and neutropenia. Diagnosis can be confirmed with a cage-side antigen SNAP test, PCR, and supportive clinical signs.

668
Q

What is the significance of diagnosing persistently infected (PI) calves in BVD control?

A

PI calves play a crucial role in the spread of BVD on farms. Identifying and managing PI calves through testing (virus positive, antibody negative) is essential for controlling the virus, improving herd health, and reducing economic losses.

669
Q

How is Avian Influenza diagnosed in affected birds?

A

Diagnosis involves collecting tracheal, oropharyngeal, and cloacal swabs or fresh tissue samples, with virus detection performed via RT-qPCR. Confirmatory typing identifies the virus subtype, essential for control measures and epidemiological tracking.

670
Q

What are the major categories of tissue mycoses?

A

Tissue mycoses include superficial, subcutaneous (deep), and systemic infections, each varying in severity and depth of tissue involvement.

671
Q

What are the major tissue reactions seen with fungal infections?

A

Acute suppurative inflammation with micro-abscess formation, chronic inflammation (pyogranulomatous or granulomatous), and necrosis, especially if fungi invade blood vessels.

672
Q

What are examples of superficial mycoses and their clinical changes?

A

Dermatophytosis (e.g., alopecia, claw disease), Malassezia infection (e.g., erythema, hair loss, lichenification), and Candida infection (e.g., ulcers/erosions with tenacious exudate).

673
Q

What characterizes subcutaneous mycoses and their clinical presentation?

A

They present as cutaneous papules or nodules with possible ulceration and discharge, commonly due to traumatic implantation. Regional lymphadenopathy is common.

674
Q

How do systemic mycoses present and affect the body?

A

Systemic mycoses can affect any organ system, leading to granulomas, pyogranulomas, necrosis, and systemic illness due to widespread fungal infection.

675
Q

What are the main diagnostic techniques for fungal diseases?

A

Techniques include direct microscopic examination, fungal culture, histopathology, PCR, and Wood’s lamp for dermatophytosis.

676
Q

What is mycotoxicosis, and what are its clinical effects?

A

Mycotoxicosis results from fungal toxin production, leading to a range of clinical presentations depending on the toxin, such as hepatotoxicity, immunosuppression, and neurotoxicity.

677
Q

What does fungal hypersensitivity involve, and how is it diagnosed?

A

It involves hypersensitivity reactions, mainly type 1, to fungi or molds, presenting as chronic cough, nasal discharge, or pruritus. Diagnosis is based on history, physical examination, and potentially IgE serology or intradermal testing.

678
Q

Fungal diseases can present as superficial, subcutaneous, or systemic mycoses, with major reactions including inflammation and necrosis. Diagnosis requires a combination of clinical signs and specific tests.

A
679
Q
A
680
Q
A
681
Q

What are the basic characteristics of fungi?

A

Fungi are eukaryotic organisms that may grow as yeast (unicellular), mold (multicellular with filamentous hyphae), or both (dimorphic). They digest food externally and absorb nutrients through their cell wall, which consists of chitin and other polysaccharides. Reproduction is via spore formation, both asexual and sexual.

682
Q

How many species of fungi are known, and how many are reported as animal pathogens?

A

Over 100,000 species of fungi are known, with more than 300 reported as animal pathogens. Most fungi are saprophytic, with some causing opportunistic infections.

683
Q

How can fungi be classified based on their normal habitat?

A

Fungi can be classified as geophilic (found in soil/environment), zoophilic (found on animals), and anthropophilic (found on humans).

684
Q

What are the mechanisms by which fungi produce disease?

A

: Fungi can produce disease through tissue invasion (mycosis), toxin production (mycotoxicosis), and the induction of hypersensitivity.

685
Q

What are the categories of mycosis?

A

Mycosis can be categorized into superficial, subcutaneous (deep), and systemic mycoses, each affecting different parts of the body.

686
Q

What is a common example of superficial mycosis?

A

: Dermatophytosis, caused by dermatophytes like Microsporum spp. and Trichophyton spp., is a common superficial mycosis affecting keratinized structures. It is highly contagious with zoonotic potential.

687
Q

How does subcutaneous mycosis typically occur?

A

Subcutaneous mycosis often follows the penetration of foreign bodies, introducing environmental saprophytes, leading to chronic, usually localized lesions.

688
Q

What is an example of systemic mycosis and its common route of infection?

A

Cryptococcosis, caused by Cryptococcus spp., is an example of systemic mycosis. The organism is usually inhaled and can spread to internal organs, causing a range of infections.

689
Q

What causes mycotoxicosis, and what are its effects?

A

Mycotoxicosis is caused by toxins produced by certain fungi on crops, pasture, or stored feed, such as Penicillium, Aspergillus, and Claviceps. The effects vary but can include acute or chronic ingestion symptoms, with potential for accumulation in tissues of food-producing animals.

690
Q

How can fungal infections induce hypersensitivity reactions?

A

Hypersensitivity reactions to fungal infections are rare but can be associated with chronic pulmonary disease in cattle and horses or as allergens in recurrent airway obstruction (RAO) and atopic dermatitis in dogs and cats.

691
Q

What is Dermatophytosis and its common presentations in animals?

A

Dermatophytosis, also known as ringworm, is caused by dermatophytes such as Microsporum spp. and Trichophyton spp. It affects keratinized structures like skin, hair, and nails. Common presentations include circular areas of hair loss (alopecia), scaling, and crusting. Highly contagious and has zoonotic potential, affecting cats, cattle, horses, and less commonly dogs.

692
Q

Describe Malassezia dermatitis and its clinical signs in dogs.

A

Malassezia dermatitis is caused by the overgrowth of Malassezia yeasts, part of the normal skin flora, leading to skin and ear infections. Clinical signs include erythema, scaling, hair loss, and intense itching (pruritus), often secondary to other skin diseases. Commonly affects dogs, sometimes cats.

693
Q

What is Cryptococcosis, and how does it present in animals?

A

Cryptococcosis is a systemic fungal infection caused by Cryptococcus neoformans or C. gattii, usually inhaled from contaminated soil or bird droppings. It can cause respiratory, cutaneous, neural, and ocular infections in cats; disseminated disease with neural and ocular signs in dogs; and nasal granulomas, mastitis, and other systemic infections in cattle and horses. It has zoonotic potential but is not usually contracted from animals.

694
Q

How do subcutaneous mycoses typically occur and present?

A

Subcutaneous mycoses typically occur due to traumatic implantation of fungi from the environment, leading to localized infections. Presentations include cutaneous papules, subcutaneous nodules, and occasionally ulceration with discharging sinuses. Chronic granulomatous inflammation is common, and regional lymphadenopathy may occur.

695
Q

: What is Aspergillosis, and what are its common forms in animals?

A

Aspergillosis is caused by Aspergillus spp., commonly A. fumigatus, and can result in local respiratory infections like guttural pouch mycosis in horses and nasal aspergillosis in dogs. It can also cause keratitis in horses and mastitis in cattle via direct inoculation. Haematogenous spread from the GI tract can lead to mycotic placentitis and abortion in cattle.

696
Q

What is Mycotoxicosis, and what are common clinical findings?

A

Mycotoxicosis results from the ingestion of mycotoxins produced by fungi on crops, pasture, or stored feed, involving fungi like Penicillium, Aspergillus (aflatoxicosis), Fusarium, and Claviceps (ergotism). Clinical findings vary but can include hepatotoxicity, immunosuppression, mutagenesis, teratogenesis, ill-thrift in animals, and acute/chronic ingestion symptoms.

697
Q

What conditions are associated with fungal hypersensitivity in animals?

A

Fungal hypersensitivity is rare but can be linked to chronic pulmonary diseases in cattle and horses, such as recurrent airway obstruction (RAO) caused by fungal spores. In dogs and cats, it can manifest as skin conditions due to hypersensitivity to saprophytic fungi or Malassezia.

698
Q

What is direct microscopic examination, and when is it used in diagnosing fungal infections?

A

Direct microscopic examination involves inspecting hair plucks, skin scales, or other samples under a microscope after staining (e.g., with KOH) to visually identify fungal elements. It’s particularly used for diagnosing dermatophytosis and can be the first step in identifying superficial fungal infections.

699
Q

What is the significance of fungal culture in diagnosing fungal diseases?

A

Fungal culture involves growing fungi from samples (e.g., hair, skin scrapings) on specific media like Sabouraud dextrose agar. It’s crucial for identifying the fungal species causing the infection and for testing fungal sensitivity to antifungal drugs. Incubation times and conditions vary between fungi, and it’s used for both superficial and deep mycoses.

700
Q

How does histopathology contribute to diagnosing fungal infections?

A

Histopathology involves examining tissue samples under a microscope after staining with special fungal stains (e.g., Periodic acid-Schiff (PAS), Grocott-Gomori methenamine silver (GMS)). It’s essential for confirming fungal infections by demonstrating fungi within tissues, used primarily for subcutaneous and systemic infections.

701
Q

What role does PCR play in fungal diagnostics?

A

PCR is a molecular technique that amplifies fungal DNA from clinical samples, allowing for the rapid and specific identification of fungal species. It’s highly sensitive and can be used when traditional culture methods are slow or when fungal species are difficult to grow.

702
Q

When is Wood’s lamp examination used in fungal diagnosis?

A

Wood’s lamp examination emits ultraviolet light to inspect skin and hair for fluorescence, which can indicate a fungal infection (e.g., some strains of Microsporum canis). It’s a quick, non-invasive method used primarily for screening dermatophytosis.

703
Q

How is cytology utilized in diagnosing fungal infections?

A

Cytology involves examining cells from impression smears, swabs, or fine-needle aspirates stained with dyes (e.g., Diff-Quick) under a microscope. It’s useful for identifying yeast infections, such as Malassezia dermatitis, by visualizing the yeast cells on the skin or in ear secretions.

704
Q

What is the role of serological tests in diagnosing fungal diseases?

A

Serological tests detect antibodies against fungi in the blood, indicating exposure to or infection by the fungus. Tests like ELISA and latex agglutination for cryptococcal antigen are used for specific fungal infections, helping in diagnosing systemic mycoses.

705
Q

Why is sensitivity testing important in fungal diagnosis?

A

After identifying the fungal species via culture, sensitivity testing determines the effectiveness of various antifungal drugs against the isolated fungus, guiding appropriate and effective treatment.

706
Q

Define an anti-viral agent and name the only one licensed for veterinary use.

A

An anti-viral agent helps the body fight off viruses. Interferon is the only anti-viral licensed in veterinary species, often associated with large costs.

707
Q

How do anti-viral drugs work?

A

Anti-viral drugs work by stopping the replication of the virus within cells, blocking the virus’s ability to attach to or enter host cells, or enhancing the immune response.

708
Q

How do azoles work as anti-fungal agents?

A

Azoles, such as itraconazole and ketoconazole, inhibit the cytochrome P450-dependent synthesis of ergosterol in fungal cell membranes, disrupting cell integrity.

709
Q

What is the mechanism of action for allylamines?

A

Allylamines, such as terbinafine, inhibit the synthesis of ergosterol in fungal cells by inhibiting the enzyme squalene epoxidase.

710
Q

: How do polyenes work against fungal infections?

A

Polyenes, like Amphotericin B and Nystatin, bind to ergosterol in fungal cell membranes, creating pores that lead to cell lysis.

711
Q

What is the action mechanism of pyrimidine analogues in fungal treatment?

A

Pyrimidine analogues, such as 5-fluorocytosine, are converted by fungal cells into 5-fluorouracil, disrupting fungal RNA and protein synthesis.

712
Q

How do cellular toxins exhibit anti-fungal activity?

A

Cellular toxins, like silver sulfadiazine and chlorhexidine, release concentrations toxic to bacteria and yeasts or bind to the skin forming a protective layer, respectively.

713
Q

What anti-fungal agents are used for treating Otitis Externa in cats and dogs?

A

Nystatin, Miconazole, Clotrimazole, Terbinafine, and Posaconazole are used, often combined with steroids and antibiotics. Terbinafine should not be used in cats.

714
Q

What are the treatment options for Malassezia skin infections in cats and dogs?

A

Options include Miconazole (shampoo), Climbazole (wipes), Itraconazole (oral, systemic), Ketoconazole (oral, shampoo), and Chlorhexidine (various forms).

715
Q

What anti-fungals are used for treating ringworm in cats, dogs, and other animals?

A

Itraconazole, Ketoconazole, Enilconazole (rinse), Miconazole (shampoo), Chlorhexidine, Clotrimazole, Terbinafine, and Fluconazole are options, with varying licenses and applications across species.

716
Q

What treatments are available for systemic/deep mycoses like cryptococcosis?

A

Amphotericin B, Fluconazole, and Flucytosine are used, though these diseases are rare in the UK and treatments are often off-license.

717
Q

Where can information about anti-fungal products be found?

A

Information can be found in the VMD Product Information Database, NOAH Compendium, and BSAVA formulary/app, covering licensed and unlicensed products.

718
Q

What is bovine tuberculosis, and what are the main challenges in controlling it in the UK?

A

Bovine tuberculosis (bTB) is a chronic bacterial infection caused by Mycobacterium bovis, affecting cattle and other species, including humans. Major challenges include its persistence in wildlife reservoirs, the economic impact of control measures, and the need for effective vaccination and testing strategies.

719
Q

When did the prevalence of bTB start to increase significantly, and what are the economic implications?

A

The prevalence of bTB started to increase in the mid-1980s. Around 30,000 cattle were culled due to bTB last year, with an average cost of £34,000 per herd TB breakdown, costing the taxpayer approximately £500 million over the last ten years.

720
Q

What are the key components of the 25-year bTB eradication strategy?

A

The strategy includes creating three management zones (High risk, Edge, and Low risk areas), increasing testing frequency, implementing badger culling and vaccination, biosecurity advice, risk-based trading, and financial penalties for overdue tests.

721
Q

What focus areas were highlighted in the 2018 review and 2020 response to the bTB strategy?

A

Focus areas include biosecurity, increased industry ownership, enhancing test sensitivity, research into cattle vaccines and tests (DIVA/bulk milk tests), genetic resistance in cattle, and a shift towards vaccination over badger culling.

722
Q

: Describe the main tests used for diagnosing bTB.

A

The Skin Test (SICCT) with avian and bovine tuberculin, IFN gamma testing for blood, occasionally supplemented by antibody tests, and detailed post-mortem inspections. Sensitivity and specificity vary, highlighting challenges in accurate diagnosis.

723
Q

What are the current efforts towards vaccinating against bTB?

A

Vaccination efforts include developing a BCG vaccine for cattle, despite causing TB test reactions, requiring a DIVA test. Badgers are also vaccinated to reduce disease spread, with oral vaccines in development.

724
Q

What biosecurity measures are recommended to prevent bTB spread?

A

Measures include risk-based trading, pre- and post-movement testing, wildlife proofing (e.g., badger-proof feed stores), environmental management, and using ibTB to assess TB risk.

725
Q

What are the current challenges and future work directions for bTB management?

A

Challenges include improving test frequency and sensitivity, managing cattle movements, enhancing biosecurity, developing effective vaccines, and addressing wildlife reservoirs of the disease.

726
Q

Define a prion.

A

A prion is a misfolded protein that can cause disease by inducing other normal proteins in the brain to also misfold, leading to transmissible spongiform encephalopathies (TSEs).

727
Q

What are prion diseases, also known as Transmissible Spongiform Encephalopathies (TSEs)?

A

TSEs are a group of progressive, invariably fatal, conditions that affect the brain and nervous system of many animals, including humans. Examples include BSE in cattle, scrapie in sheep, and CWD in deer.

728
Q

Name some veterinary prion diseases.

A

Key veterinary prion diseases include Bovine Spongiform Encephalopathy (BSE) in cattle, scrapie in sheep and goats, and Chronic Wasting Disease (CWD) in deer and elk.

729
Q

What are the common clinical signs of prion diseases in animals?

A

Clinical signs include weight loss, behavioral changes, pruritus (in scrapie), ataxia, tremors, licking lips, grinding teeth, and changes in posture and gait. Some animals may be found dead without prior observed illness.

730
Q

Describe the BSE epidemic and its current status.

A

The BSE epidemic reached its peak in the late 20th century, with a significant number of cattle affected. Efforts to control the disease have reduced incidence, but isolated cases still emerge, such as one found in 2021.

731
Q

How is classical scrapie being controlled?

A

Classical scrapie is controlled by the National Scrapie Plan, which includes genetic selection against susceptible genotypes and culling of affected animals.

732
Q

What is the status of Chronic Wasting Disease (CWD) in European cervids?

A

CWD has been identified in European cervids, posing a significant threat to wildlife populations and potentially impacting other species through environmental reservoirs.

733
Q

What are current surveillance and awareness measures for prion diseases?

A

Surveillance includes monitoring for rare clinical disease cases, managing isolated cases of BSE, controlling farm outbreaks of scrapie, and maintaining vigilance for CWD threats to UK deer.

734
Q

What diseases are important to prevent in rabbits, and how?

A

Myxomatosis and Rabbit Haemorrhagic Disease (RHD) strains 1 and 2. Prevention includes vaccination with an initial vaccine at 7 weeks old and yearly boosters.

735
Q

What are the clinical signs of myxomatosis in rabbits?

A

Swelling, redness, ulcers, nasal and eye discharge, blindness, respiratory signs (e.g., dyspnoea), lethargy, and anorexia.

736
Q

Where did myxomatosis originate, and what has happened since?

A

Originally released in France to control wild rabbit populations, it’s now worldwide with new strains developing resistance.

737
Q

What are the clinical signs of RHD in rabbits?

A

Sudden death, anorexia, lethargy, neurological signs, internal bleeding, and jaundice.

738
Q

What should a rabbit vaccination appointment involve?

A

History and husbandry review, full clinical exam, vaccination at 7 weeks old with yearly boosters, offer neutering, and consider social needs. Also, assess the necessity for guinea pig vaccinations.

739
Q

How to manage recurrent respiratory infections in breeding guinea pigs caused by Bordetella?

A

Treat individuals and recommend management options to prevent disease spread, focusing on hygiene, isolation, and possibly vaccination.

740
Q

What antiparasitic medications are available for rabbits, and which are licensed?

A

Panacur (fenbendazole), Baycox (toltrazuril) for coccidia, anthelmintics, Advantage (imidacloprid), Stronghold (selamectin), Advocate (imidacloprid/moxidectin), and Xeno (Ivermectin). Frontline (Fipronil) is toxic to rabbits.

741
Q

What is the best practice for using antiparasitic medication in small mammals?

A

Avoid routine preventive worming; use faecal egg counts to determine treatment necessity. Treat ectoparasites only when clinically necessary, following proper diagnostic workup.

742
Q

What considerations should be made when choosing antibiotics for small mammals?

A

Assess the need for antibiotics, likely bacteria involved, safety, efficacy, licensing in rabbits, and if they are first-line options.

743
Q

What antibiotics are considered for a rabbit with mild lethargy and respiratory signs?

A

Trimethoprim/sulfamethoxazole (oral Sulfatrim), Penicillin G (Injectable Norocillin), Enrofloxacin (oral Baytril), Co-amoxyclav (Synulox oral drops), and Metronidazole (oral suspension).

744
Q

What is the approach to treating gut stasis in anorexic rabbits and guinea pigs?

A

: Treatment includes identifying and addressing the underlying cause, providing analgesia, syringe feeding with probiotics, and using prokinetics like Metoclopramide, Ranitidine, and Cisapride.

745
Q

Why are certain ectoparasites considered ‘important’ in veterinary medicine?

A

Ectoparasites are considered important due to their direct impact on the welfare of the host, potential to cause or predispose the host to other diseases, act as vectors for disease transmission, and their zoonotic and economic significance.

746
Q

List common ectoparasites in large and small animals.

A

Common ectoparasites include fleas, ticks, lice, and mites (e.g., Sarcoptes, Cheyletiella). These parasites may cause pruritus, alopecia, and secondary infections, and can be vectors for diseases like babesiosis and myxomatosis.

747
Q

Describe the diagnostic plan for an animal suspected of suffering from ectoparasitic disease.

A

The diagnostic plan should include history taking, clinical examination, identification of parasites on the host or in the environment, and specific diagnostic tests like skin scrapings, coat brushings, and serological tests.

748
Q

What is the zoonotic and economic importance of ectoparasites?

A

Ectoparasites like fleas and mites can transmit diseases to humans (zoonotic importance) and cause significant economic losses in livestock due to diseases like sheep scab (Psoroptes ovis), which is notifiable in some regions.

749
Q

What clinical signs are commonly associated with ectoparasitic infestations?

A

Clinical signs include pruritus, alopecia, erosions, crusts, scale, secondary bacterial infections, and in severe cases, anemia or neurological signs due to toxins or blood loss.

750
Q

Which parasites are likely to be found on their host and cause visible signs?

A

Parasites like fleas, lice, and surface mites are often found on their host and cause visible signs such as pruritus, alopecia, and secondary skin infections.

751
Q

Name parasites that are unlikely to be detected on their host.

A

Some ectoparasites, such as certain mites and ticks, spend only short periods on the host or have a significant part of their lifecycle in the environment, making them harder to detect directly on the animal.

752
Q

What are the key diagnostic procedures for identifying ectoparasitic diseases?

A

Diagnostic procedures include direct observation of parasites or their effects on the host, use of diagnostic tests such as skin scrapings or tape strips, and environmental examination for parasites like the poultry red mite (Dermanyssus gallinae).

753
Q

How are ectoparasitic diseases managed and treated?

A

Management includes the use of appropriate antiparasitic medications, environmental control measures to reduce parasite populations, and supportive care for affected animals.

754
Q

What are the take-home messages regarding ectoparasitic causes of skin disease?

A

Veterinarians should consider the clinical presentation, species, age, and husbandry conditions when diagnosing ectoparasitic diseases, select appropriate diagnostic tests, and implement effective treatment and control strategies.

755
Q

What factors contribute to the pathogenesis of bacterial skin diseases?

A

Disease occurs when the skin’s protective mechanisms are compromised due to mechanical damage, immunocompromise, defects in skin barrier function, and changes to the skin microclimate.

756
Q

Which organisms are commonly involved in bacterial skin diseases?

A

Coagulase-positive Staphylococci, Dermatophilus congolensis, Mycobacteria from soil, and less commonly, Gram-negative bacteria.

757
Q

What are the clinical manifestations of bacterial skin diseases?

A

Manifestations can range from surface and superficial pyoderma to deep pyoderma, bacterial granulomatous dermatitis, and systemic infections.

758
Q

Give examples of surface pyoderma in dogs.

A

Canine intertrigo (skin fold pyoderma), acute moist dermatitis (hotspots), and bacterial overgrowth syndrome.

759
Q

What is superficial pyoderma, and how does it manifest?

A

Superficial pyoderma involves infection within the epidermis and/or hair follicle, presenting as papules, pustules, crusts, and sometimes alopecia.

760
Q

: Describe deep pyoderma and its causes.

A

Deep pyoderma involves infection beyond the epidermis or hair follicle epithelium, often due to follicle rupture, penetrating wounds, or haematogenous spread, leading to thickening of skin, nodules, and draining sinuses.

761
Q

What diagnostic tests are commonly used for bacterial skin diseases?

A

Diagnostic tests include cytology, culture, and histopathology, with the choice depending on the depth of the lesion.

762
Q

What are the broad principles of treating bacterial skin disease?

A

Treatment involves killing the organism (minimizing antibiotic use and focusing on topical antibacterials), addressing underlying causes, and enhancing the body’s defenses.

763
Q

Why is understanding the underlying cause of bacterial skin disease important?

A

Identifying and addressing the underlying cause is crucial for effective treatment and to prevent recurrence of the infection.

764
Q

Describe the clinical presentation of flea infestations in dogs and cats.

A

Clinical presentations vary. Dogs may show pruritus especially on the caudal/dorsal body. Cats may exhibit four cutaneous reaction patterns: head and neck pruritus, symmetrical alopecia, eosinophilic granuloma complex (EGC), and miliary dermatitis. Fleas can also be vectors of diseases and are zoonotic.

765
Q

What are the signs and zoonotic potential of Sarcoptic mange?

A

Sarcoptic mange causes intense pruritus, crusts on the pinnal margins/hocks/elbows, and positive pinnal-pedal reflex. It is zoonotic, capable of causing temporary skin lesions in humans.

766
Q

Describe the clinical signs and transmission potential of Cheyletiella mites in rabbits and dogs.

A

Cheyletiella mites cause truncal scale, and in rabbits, can lead to significant scaling with little to no pruritus. They are zoonotic, causing dermatitis in humans.

767
Q

What pathogen causes Greasy Pig Disease and what are the clinical signs?

A

Caused by Staphylococcus hyicus, Greasy Pig Disease presents with exudative dermatitis, erythema, and greasy skin in pigs. It requires prompt antibiotic treatment.

768
Q

Identify the causative agent of Dermatophilosis and its predisposing factors.

A

Dermatophilosis, also known as rain scald or mud fever, is caused by Dermatophilus congolensis. It is predisposed by wet skin conditions and presents as crusted scabs that peel off with tufts of hair.

769
Q

What are the classifications of canine pyoderma, and how is it generally treated?

A

Canine pyoderma is classified into surface, superficial, and deep. Treatment includes topical antibacterials for mild cases and systemic antibiotics for deep infections, always based on culture and susceptibility tests.

770
Q

Case 1 Presentation:
A 3-year-old female neutered Labrador presents with lesions on the ventrum, observed for the past week. The dog has experienced low-grade pruritus of the ventrum, face, and feet for 12 months, with an increase in ventral pruritus over the last 1-2 weeks.

A

Differential Diagnosis for Case 1:

Superficial bacterial pyoderma.
Malassezia dermatitis.
Environmental/dietary atopic dermatitis.
Dermatophytosis.
Sarcoptic mange.
Demodicosis.
Flea infestation/FAD.
Cheyletiellosis.
Pediculosis.
Additional Information:
Cytology was consistent with bacterial pyoderma. Further investigations revealed environmental atopy as the underlying cause.

771
Q

A 2-year-old Scottish Blackface ewe presents in December with concerns about skin problems, part of a group of 30 housed sheep. Similar lesions have been observed in a few others, and the farmer noticed a red patch on her hand, suggesting possible zoonosis. The sheep appear otherwise healthy.

A

Differential Diagnosis for Case 2:

Dermatophytosis.
Dermatophilosis (“lumpy wool”).
Ectoparasites (e.g., psoroptic mange, chorioptic mange, lice).
Staphylococcal folliculitis.
Additional Information:
The diagnosis was dermatophytosis (Trichophyton verrucosum), suggested by the evidence of contagion and zoonosis.

772
Q

What are the roles of fungi on the skin, and how can they lead to skin disease?

A

Skin commensals (e.g., Malassezia) can cause colonization.
Transient contaminants, such as environmental saprophytes and occasionally dermatophytes, can carry fungi.
Active pathogens (e.g., dermatophytes) can cause clinical disease. Fungi are a part of the normal skin microbiome but can also lead to skin disease through tissue mycosis, which can be superficial, subcutaneous, deep, or lead to hypersensitization, especially in atopic dogs.

773
Q

How are dermatophytes classified, and what is their pathogenesis?

A

Dermatophytes are classified as geophilic (environment-adapted), zoophilic (mammal-adapted, most common source of animal disease), and anthropophilic (human-adapted).
Infection stages include inoculation and germination of infective arthrospores due to skin microtrauma & moisture, leading to penetration of the stratum corneum and growth of fungal hyphae, resulting in lesions within 5-7 days. They are contagious through direct or indirect contact.

774
Q

Describe uncommon presentations of fungal infections in animals.

A

Furunculosis resembles deep pyoderma with nodular swelling.
Fungal kerion is a nodular inflammatory mass in hunting/working dogs.
Pseudomycetoma, especially in Persian cats and Yorkshire Terriers, features subcutaneous/deep mycosis with nodular granulomas.
Onychomycosis involves claw disease.

775
Q

What methods are used for the diagnosis of dermatophytosis?

A

Direct examination of hair/scales with gentle skin scrape or plucking hair from lesion margins, placed in liquid paraffin on a microscope slide. Infected hairs appear distorted, paler, and wider than normal under a microscope.

776
Q

How is fungal culture performed, and what does fungal PCR entail in the diagnosis of fungal skin diseases?

A

Fungal culture involves sampling with a new toothbrush (McKenzie toothbrush technique) and can be performed in-house using dermatophyte test-medium (DTM) or at an external lab. Fungal PCR is a very sensitive test providing faster results but cannot distinguish between carriage and disease.

777
Q

What is the pathogenesis of Malassezia infections in animals?

A

Malassezia infections are usually secondary, occurring due to anatomical features, other skin diseases, systemic disease, or an imbalance in the normal microbiome (dysbiosis), leading to increased numbers and a shift towards more pathogenic strains.

778
Q

How are Malassezia infections diagnosed in dogs and cats?

A

Diagnosis involves identifying appropriate lesions, identifying Malassezia at these sites with cytology (stained acetate tape strip or impression smear), and assessing the response to antifungal therapy. The presence of organisms such as “peanuts,” “snowmen,” or “Russian dolls” is noted under a microscope.

779
Q

What are the key take-home messages regarding fungal skin infections in animals?

A

Dermatophytes are contagious pathogens causing alopecia, scale, and crust, diagnosed through microscopy, fungal culture, or possibly PCR.
Malassezia is usually a commensal organism leading to disease through dysbiosis, causing pruritic dermatitis/otitis in dogs and occasionally cats, diagnosed through cytology and response to therapy.

780
Q

Why are viral skin diseases particularly important in large animal practice?

A

Viral skin diseases are more common in large animals and equines than in small animals, often leading to serious economic losses due to their notifiable status. Many of these diseases require no treatment but lead to the slaughter and disposal of infected animals, movement restrictions, and initiation of quarantine, disinfection, vaccination, eradication, and surveillance programs.

781
Q

What are the general clinical signs of vesicular diseases in animals?

A

Vesicular diseases cause vesicles and erosions/ulcers that progress to crusts, affecting the muzzle, oral mucosa, tongue, udder teats, and coronary band. These diseases can lead to the shedding of hooves and horns and affect a wide range of species, especially cloven-hooved ones, and occasionally humans.

782
Q

What makes vesicular diseases significant in veterinary practice?

A

Many vesicular diseases are notifiable due to the severe economic losses they can cause, with the UK’s 2001 Foot and Mouth Disease (FMD) outbreak costing over £6 billion. Some vesicular diseases are also zoonotic.

783
Q

What are the general characteristics of papilloma viruses in animals?

A

Papilloma viruses are epitheliotropic, causing proliferative lesions or warts. They are typically host-specific, enter through microabrasions, and affect mostly young animals, which usually recover spontaneously. However, there is a rare risk of malignant transformation to squamous cell carcinomas.

784
Q

Describe the general features and impacts of pox viruses in animals.

A

Pox viruses cause diseases like cowpox in cats (transmitted by rodent bites and zoonotic), horsepox, swinepox, sheep pox, goat pox, lumpy skin disease in cattle, and myxomatosis in rabbits, leading to edematous thickening of various body parts and potentially death.

785
Q

What are some other notable viral skin diseases in animals?

A

Other viral skin diseases include Post-weaning Multisystemic Wasting Disease (PMWD)/Porcine Dermatitis Nephropathy Syndrome (PDNS), Psittacine beak and feather disease, and Border disease in sheep, which can lead to a variety of skin and systemic symptoms.

786
Q

What methods are used for the diagnosis of viral diseases in animals?

A

Diagnostic methods include detecting virus/viral antigens or nucleic acids, diagnostic serology for antibodies, virus isolation, ELISA, PCR/RT-PCR, serum neutralization tests, electron microscopy, histopathology, immunofluorescence/immunohistochemistry, and more, depending on the virus and test availability.

787
Q

Describe the characteristics and diagnostic approach for Leishmaniasis in animals.

A

Leishmaniasis, caused by Leishmania spp. and transmitted by sandflies, is more common in dogs than cats and is also zoonotic. It causes a range of skin and systemic signs with a long incubation period. Diagnosis can be challenging and involves aspirates (e.g., lymph node, bone marrow), serology/PCR, and skin biopsies. The disease can be controlled but not cured.

788
Q

What are the key take-home messages regarding viral and protozoal skin diseases in animals?

A

Viral skin diseases are more prevalent in large animals and equines, representing a significant potential economic loss. Many large animal viral infections are notifiable, and some are zoonotic. Protozoal skin diseases, such as Leishmaniasis, are serious vector-borne diseases increasingly common in the UK, especially

789
Q

What are immune-mediated skin diseases and how are they categorized?

A

Immune-mediated skin diseases involve hypersensitivity reactions, with all four classes of hypersensitivity represented. These can include allergies to external antigens (e.g., flea saliva, dust mites, pollens, molds) and immune-mediated reactions against self-antigens (e.g., desmosomal proteins in pemphigus foliaceus, epidermal cells in discoid lupus, sebaceous glands in sebaceous adenitis).

790
Q

How is allergic skin disease divided and what are its major clinical signs?

A

Allergic skin disease is categorized into food and environmental induced-atopic dermatitis, flea allergy, and contact allergy. The major clinical sign across these categories is pruritus, leading to secondary infections, lesions, and behavioral changes.

791
Q

What are the components of feline atopic skin syndrome?

A

Feline atopic skin syndrome includes reactions to house dust mites, pollens, molds, flea saliva, insect and mite hypersensitivity, and food proteins. It presents through multiple manifestations, known as feline cutaneous reaction patterns.

792
Q

How is allergic skin disease categorized in horses?

A

In horses, allergic skin disease includes insect bite hypersensitivity, equine atopic skin disease, food allergy, and contact allergy. Clinical signs include urticaria, pruritus, and secondary infections, along with behavioral changes.

793
Q

Describe immune-mediated diseases in farm and exotic species.

A

Immune-mediated diseases in these species can include parasite-induced hypersensitivity, atopic dermatitis diagnosed in sheep and goats, and hypersensitivity being a major component of clinical signs, varying from protective to unhelpful.

794
Q

What is the diagnostic plan for animals suspected of having immune-mediated or autoimmune skin disease?

A

The diagnostic plan involves accurate diagnosis through exclusion of common differential diagnoses, confirmation of the correct histological pattern on histopathology, and occasionally relying on exclusion alone. It includes careful history taking, rule out common differential diagnoses through tests like skin scrapes, hair plucks, dermatophyte culture, cytology, and test treatments.

795
Q

Summarize the key points about immune-mediated and autoimmune skin diseases.

A

These diseases are rare, resulting from aberrant immune function due to a failure of tolerance, leading to tissue damage. The tissue or antigen involved determines the clinical signs, which are systemic in nature and usually bilaterally symmetrical. Cutaneous immune-mediated disease may be associated with systemic disease or represent a cutaneous marker of systemic disease.

796
Q

What are the key questions to ask when presented with a Labrador having lesions on the ventrum?

A

Duration and development of the lesions.
Presence of pruritus and its duration.
Health status of in-contact animals and humans.
Parasite control measures in place.
Any recent changes in the environment or contact with other animals.

797
Q

General Approach to Dermatology Patient: Overview

Begin with a comprehensive understanding of dermatologic diseases.
Major causes include: Inflammatory, Immune-Mediated, Infectious, Neoplastic, Nutritional, Degenerative, Anomalous, Metabolic, Toxic, Traumatic, Vascular (DAMNITV framework).
Importance of signalment, history (general and dermatological), and clinical examination.§

A

Differential Diagnosis Approach:

Incorporate DAMNITV to formulate potential causes.
Inflammatory and Immune-Mediated conditions often predominate.
Infectious causes include parasites, bacteria, fungi, protozoa, and viruses.
Diagnostic Tests:

Coat brushing, skin scrapes, skin cytology, dermatophyte culture, trichograms, Wood’s lamp examination.
Further investigations may include blood tests, skin biopsies, microbial culture, trial therapy (antimicrobial, antiparasitic).
Signalment and History Considerations:

Age, sex, breed-specific predispositions.
General health, lifestyle, housing, and past dermatological history.
Importance of environment, contact with other animals or species, and response to past treatments.
Clinical Examination:

Perform both general and detailed dermatological examinations.
Systematic assessment for any signs of systemic disease affecting the skin.
Examination of less visible areas and mucocutaneous junctions is crucial.
Diagnosis and Treatment:

Aim for a definitive diagnosis through a logical stepwise approach to testing.
Treatment based on diagnosis, considering potential systemic involvement.
Awareness of age-specific diseases (e.g., young animals prone to immunological immaturity diseases, older animals to endocrinopathies and neoplasia).

798
Q

What are the major causes of dermatological disease?

A

DAMNITV framework highlights:

Degenerative
Anomalous
Metabolic
Neoplastic and Nutritional
Inflammatory, Immune-mediated, Infectious, Idiopathic
Toxic
Traumatic
Vascular

799
Q

Why is signalment important in a dermatology case?

A

Signalment provides vital clues about possible dermatologic conditions based on age, sex, and breed, which can influence predispositions to certain diseases.

800
Q

What are some initial diagnostic tests commonly used in dermatology?

A

Coat brushing
Skin scrapes
Skin cytology
Dermatophyte culture
Trichograms
Wood’s lamp examination

801
Q

What is the general approach to diagnosing a dermatologic condition?

A

Establish what is happening to the skin and why.
Determine if the dermatological disease is primary or secondary.
Conduct a general and dermatological clinical examination.
Formulate a differential diagnosis.
Perform targeted diagnostic tests.
Confirm the diagnosis and initiate appropriate treatment.

802
Q

How do age, sex, and breed influence dermatological diseases?

A

Age: Certain conditions are more common at specific life stages (e.g., demodicosis in young animals).
Sex: Hormonal influences can affect skin condition (e.g., entire males with endocrine changes).
Breed: Specific breeds have predispositions to certain dermatologic conditions.

803
Q

Why is a general health history important in dermatology cases?

A

General health history can reveal systemic diseases that manifest with dermatologic signs, influence the diagnostic plan, and impact treatment options.

804
Q

What are key takeaways from the approach to a dermatology patient?

A

Systematically approach each case without jumping to conclusions.
Dermatological diagnoses often require more than visual inspection.
Follow a structured diagnostic process to accurately identify the cause and provide effective treatment.

805
Q

How can pruritus be recognized in different species?

A

Dogs may scratch, chew, or lick their feet.
Horses may stamp.
Cats may overgroom, leading to self-induced alopecia.
Small furries may exhibit barbering.

806
Q

What are the major causes of pruritus?

A

Hypersensitivities (environmental atopy, food-induced atopy, contact allergy)
Parasites (arachnids, mites, insects like fleas and lice)
Microbial infections (bacterial pyoderma, Malassezia dermatitis)
Others (drug reaction, contact irritant, neoplasia, autoimmune diseases)

807
Q

What are the first steps in diagnosing pruritus?

A

Formulate an initial ranked differential diagnosis list based on signalment, history, and clinical exam.
Perform initial diagnostic tests as needed (e.g., coat brushing, skin scrapes, cytology).

808
Q

What is the next step if pruritus persists after initial treatment?

A

Treat any confirmed parasites or microbial infections.
If pruritus resolves, investigate for immunosuppressive/endocrine diseases.
If pruritus persists, consider an exclusion diet trial.

809
Q

What to do if pruritus persists even after an exclusion diet trial?

A

Consider environmental atopic dermatitis (AD) as a diagnosis by exclusion.
Identify allergens for potential immunotherapy or allergen avoidance through intradermal allergy tests or IgE serology.

810
Q

What are the key take-home messages for managing pruritus in dermatology patients?

A

Be systematic in your diagnostic approach.
Eliminate parasites and microbial infections first.
Use diet trials judiciously to rule out food-induced atopy.
Environmental AD is diagnosed by exclusion and requires a comprehensive approach for management.

811
Q

What are the definitions of papules and pustules?

A

Papule: A small, solid elevation of skin less than 1cm in diameter, often erythematous.
Pustule: A small elevation of skin filled with pus, often starting as a papule.

812
Q

What are common causes of pustules and papules?

A

Infections (bacterial, fungal)
Ectoparasites (fleas, mites)
Hypersensitivities (flea, environmental, food)
Autoimmune diseases (e.g., Pemphigus foliaceus).

813
Q

What is the clinical approach to diagnosing pustules and papules?

A

Consider signalment, history, and dermatological examination.
Assess if lesions are follicular and their distribution.
Produce a ranked differential diagnosis list.

814
Q

What diagnostic tests are recommended for pustules and papules?

A

Cytology (possibly with bacterial culture).
Tests for ectoparasites and dermatophytosis.
Consider biopsy if autoimmune diseases are suspected.

815
Q

How are scale and crust defined in dermatology?

A

Scale: Rafts of immature keratinocytes, resulting from hyperkeratosis.
Crust: Dried exudates on the skin surface, often a secondary lesion.

816
Q

What are the common causes of scale and crust?

A

Infections, ectoparasites, hypersensitivities, nutritional deficiencies/metabolic diseases, autoimmune diseases, and rarely, neoplasia.

817
Q

What is the diagnostic approach for animals with scale and crust?

A

Perform cytology and cultures for bacterial and fungal infections.
Rule out ectoparasites and consider biopsy if autoimmune diseases are suspected.
Treat to eliminate secondary infections and control ectoparasites.

818
Q

What are the take-home messages for managing crusting, scaling, pustular, and papular lesions?

A

Focus on microbial infections and ectoparasites first, unless autoimmune disease is suspected.
Formulate a differential diagnosis based on thorough clinical examination and history.
Be systematic in your approach to diagnosis and treatment.

819
Q

What are the definitions and main causes of alopecia?

A

Alopecia: Loss of hair, either partial or complete, which can be primary (failure to grow) or secondary (loss after growth).
True Alopecia: Direct damage to the hair follicle unit.
Apparent Alopecia: Hair shaft is damaged but remains in the follicle.

820
Q

What mechanisms lead to primary alopecia?

A

Lack of stimulation for hair growth, leading to miniaturized or dysplastic hairs that easily break off or shed.

821
Q

What are the various causes of alopecia?

A

Hair follicle inflammation.
Hair cycle abnormalities, often due to endocrine issues.
Hair morphological abnormalities.
Congenital aplasia.

822
Q

What initial steps should be taken when approaching a case of alopecia?

A

Consider species-specific common causes, such as dermatophytosis in certain animals or demodicosis and pyoderma in dogs.
Age of onset is crucial, with differentials including infections in younger animals and endocrinopathies or neoplasia in older animals.

823
Q

Why is signalment important in diagnosing alopecia?

A

Certain conditions are predisposed by species, age, sex, and breed, affecting the diagnostic approach and differential diagnosis.

824
Q

What should be included in the clinical examination for alopecia?

A

Both general and dermatological examinations are essential, looking for systemic abnormalities and assessing the distribution and type of alopecia.

825
Q

How do you differentiate between true and apparent alopecia?

A

A trichogram can help determine if alopecia is true (easily epilated) or apparent (requires effort, with broken distal tips).

826
Q

What tests can help narrow down the differential diagnoses for alopecia?

A

Skin scrapings, especially for demodicosis.
Dermatophyte tests (microscopy/culture).
Trichograms to assess the hair bulb and shaft for signs of disease.

827
Q

What are the key take-home messages for diagnosing and managing alopecia?

A

Differentiate alopecia caused by trauma/self-trauma from other types.
Common causes include folliculitis, demodicosis, pyoderma, and endocrinopathies.
A systematic approach including signalment, history, examination, and targeted tests is crucial.

828
Q

How can you determine if a swelling is actually a skin mass?

A

Consider swellings of non-dermatologic origins such as hernias, oedema, bursitis, emphysema, clostridial infections, and mammary tumors.

829
Q

What are the classifications of skin masses?

A

Inflammatory (infectious and non-infectious).
Neoplastic.
Cysts.

830
Q

What are some infectious causes of skin masses?

A

Abscess/cellulitis, furunculosis, bacterial granulomas, and deep/subcutaneous or systemic fungal granulomas.

831
Q

What are some non-infectious causes of inflammatory skin masses?

A

Urticaria/angioedema, seroma, haematoma, and conditions like eosinophilic granulomas.

832
Q

What are common neoplasms and cysts found on the skin?

A

Skin neoplasms are common in older animals and include lipomas, sebaceous adenomas, mast cell tumors. Cysts are epithelial-lined cavities containing fluid or solid material.

833
Q

What is the diagnostic approach for animals presenting with skin masses and cysts?

A

Use signalment, history, and clinical examination to form a list of ranked differential diagnoses, then investigate using cytology, tissue biopsy (histopathology and/or tissue culture).

834
Q

Why are signalment and history important in diagnosing skin masses?

A

They provide clues about the nature of the mass, considering the species, breed/color, age, and any previous health issues or environmental exposures.

835
Q

What non-dermatological findings can help diagnose skin masses?

A

Look for pyrexia, peripheral lymphadenopathy, and other systemic abnormalities that might be related to the skin mass.

836
Q

What specific aspects should be noted in a dermatological examination of skin masses?

A

Note whether the lesions are solitary or multiple, their location, size, definition, mobility, and any signs of inflammation or drainage.

837
Q

How is cytology used in the investigation of skin masses?

A

Fine needle aspirates (FNA) can differentiate between inflammation, neoplasia, and cyst contents, providing valuable initial information.

838
Q

What is the key message in approaching cutaneous masses?

A

To classify the mass as inflammatory, neoplastic, or cystic, start with a thorough clinical examination, followed by cytology and, if necessary, biopsy for a definitive diagnosis.

839
Q

What should you consider when using dermatological tests?

A

Decide which tests will help narrow down differential diagnoses efficiently and cost-effectively.
Prioritize tests that provide the most useful information quickly and non-invasively.
Ensure good quality and adequate number of samples are taken and correctly interpret the samples, considering the limitations of each test.

840
Q

What are some common diagnostic techniques and their purposes?

A

Techniques include coat comb/brush, acetate tape strip, skin scrapings, trichograms, cytology, Wood’s lamp examination, McKenzie coat brush, and microbiological swab for culture, each targeting different aspects like parasites, microbes, or hair structure.

841
Q

What can cytology reveal in dermatological diagnostics?

A

Cytology, especially fine needle aspirate cytology, can reveal bacteria, yeasts, and other cells (e.g., inflammatory, epithelial, neoplastic) under magnifications of X4-100 (Oil).

842
Q

Why are skin biopsies performed?

A

To establish a definitive diagnosis when less invasive tests are inconclusive.
To rule out certain conditions.
Histopathology and tissue culture are common tests carried out on skin biopsies.

843
Q

How should you prepare and perform a skin biopsy?

A

Choose sedation or general anesthesia based on the animal’s calmness and biopsy site.
Select representative lesions and avoid disturbing the skin surface.
Properly prepare the sample site and decide on the biopsy type (punch, wedge/ellipse, excisional, incisional) based on the lesion.

844
Q

How should biopsy samples be handled and submitted?

A

Handle gently to avoid damaging the sample.
Blot blood and place in 10% formalin.
Provide the pathologist with a brief history and differential diagnosis list.

845
Q

What are the considerations for bacterial and fungal tissue culture from skin biopsies?

A

Withdraw antibiotics and topical antimicrobials before sampling.
Blot the surface with alcohol and allow drying.
Submit punch biopsy in sterile conditions avoiding formalin contamination.

846
Q

Why might biopsy results sometimes seem disappointing?

A

Samples may not be representative of the lesion.
Inflammatory reactions could be affected by therapy.
Unrealistic expectations; not all diseases can be distinguished on biopsy.

847
Q

What is the summary advice for biopsy sampling?

A

Carefully select cases and lesions.
Take high-quality samples without destroying evidence.
Give a brief history and differential diagnosis list to your pathologist.

848
Q

How are skin biopsies interpreted and why are they important?

A

Pattern analysis is used to classify pathological changes based on the type and location of cellular infiltrate.
This helps formulate a specific list of aetiological agents or narrow down categories of disease with a common pathogenesis.

849
Q

What are the take-home messages regarding the use and interpretation of dermatological diagnostics?

A

Knowledge of pattern analysis enhances the utility of skin biopsies, allowing for a more precise diagnosis.
Biopsies should be reserved for cases where they are likely to be most useful,

850
Q

What are the primary aims of dermatologic therapy?

A

To kill or repel parasites using ectoparasiticides.
To control or cure microbial infections with antimicrobials.
To control inflammation and pruritus, particularly for atopic dermatitis and autoimmune diseases.
To moisturize and improve skin barrier function.
To resolve scaling.
To treat otitis externa.

851
Q

How do emollients and moisturizers improve skin barrier function?

A

Emollients soften, lubricate, and soothe the skin, acting as occlusives to “seal in” water content and reduce trans-epidermal water loss. Examples include lanolin, coconut oil, and Vaseline.
Moisturizers increase the water content of the stratum corneum, containing ingredients like colloidal oatmeal, aloe vera, urea, glycerine, and sodium or ammonium lactate.

852
Q

What is the action of keratolytic and keratoplastic agents in controlling skin scale?

A

Keratolytics reduce cohesion between cells of the stratum corneum, facilitating the removal of scales.
Keratoplastics restore normal epidermal epithelialization and keratinization and reduce epithelial turnover. Common agents include sulfur, salicylic acid, and ammonium lactate.

853
Q

What are important considerations in treating otitis externa?

A

Ear infections are often secondary to underlying issues, like allergies.
Early intervention with topical corticosteroids and antimicrobial cleaners can control microbial overgrowth and inflammation without the need for antibiotics.
Cytology is essential for establishing treatment.

854
Q

What factors influence the selection of polypharmacy ear drops/creams for otitis externa?

A

The presence of organisms as identified by cytology and/or culture.
The level of inflammatory activity, selecting the lowest potency glucocorticoid likely to be effective.
The potential for ototoxicity if the tympanic membrane is ruptured.
The nature of the exudate, with some agents being inactivated by pus.

855
Q

What are the components and actions of ear cleaners?

A

Cerumenolytics dissolve or soften cerumen.
Antimicrobials control microbial growth.
Surfactants emulsify debris.
Astringents dry the ear canal.
Select a product based on the action required and the safety profile, especially if the tympanic membrane is likely to be perforated.

856
Q

What are the pros and cons of topical therapy?

A

Pros:

Direct delivery to skin allows for higher drug concentration.
Can target therapy to specific areas.
Cons:

Labor-intensive, affecting compliance.
May be difficult to apply based on the animal’s tolerance or the area of the body affected.

857
Q

What are key points in selecting dermatologic therapeutics?

A

Understand the actions of drugs to select the most appropriate product.
Consider both patient and owner factors in product selection, aiming for formulations with maximum persistence and ease of use.

858
Q

What are the common bacterial skin diseases in small animals and their preferred treatments?

A

Bite and traumatic wounds, surface pyoderma, superficial pyoderma, deep pyoderma, and otitis externa are common.
Treatments focus on using topical antibacterials/antibiotics where possible and choosing the narrowest spectrum and lowest EMA Category antibiotic likely to be effective.

859
Q

What are the general principles of antibacterial therapy for skin diseases?

A

Ensure bacteria are involved via cytology.
Use topical treatments to minimize systemic antibiotic use.
Correct the underlying cause of the infection.

860
Q

How are superficial bacterial skin infections treated?

A

Prefer topical antibacterials (e.g., chlorhexidine, silver sulfadiazine) if possible.
Correct the underlying cause of the infection.

861
Q

What is the recommended treatment for deep pyoderma/cellulitis?

A

Systemic antibiotics are recommended, ideally based on bacterial culture and susceptibility testing.
TMPS (trimethoprim-sulfamethoxazole) is often used where possible, with treatment duration varying by severity.

862
Q

What considerations are important when treating otitis externa?

A

Selection of ear drops/creams should be based on organism present, level of inflammatory activity required, potential for ototoxicity, nature of exudate, and frequency of application for compliance.

863
Q

How is dermatophytosis treated in animals?

A

Identify the fungus and predisposing conditions.
Use topical antifungal rinse/shampoo and clean the environment.
Consider systemic therapy for small animals but not always for farm species.

864
Q

What treatments are available for Malassezia infections?

A

Topical antifungals are the mainstay of treatment, including miconazole and clotrimazole.
Systemic antifungals like ketoconazole (for dogs, not cats) and itraconazole may be used, with monitoring for side effects.

865
Q

What are the key take-home messages for using antimicrobials in treating skin infections?

A

Perform appropriate diagnostics before treatment.
Prefer topical treatments where possible.
If systemic antibiotics are necessary, choose the narrowest spectrum effective drug.
Treat for an adequate duration to fully resolve the infection but no longer than necessary.
Always address any underlying causes to prevent recurrence.

866
Q

What are the key components of multimodal therapy for atopic dermatitis?

A

Control of inflammation and pruritus.
Allergen avoidance and allergen-specific immunotherapy (ASIT).
Improving the skin barrier.
Control of flare factors.

867
Q

How are glucocorticoids used in the treatment of atopic dermatitis?

A

Prednisolone is commonly used for its rapid, effective anti-inflammatory action but with caution due to potential long-term side effects.
The goal is to use the lowest effective dose and possibly taper to an alternate-day regimen to minimize side effects.

868
Q

What are the benefits of using Oclacitinib (Apoquel) and Lokivetmab (Cytopoint) in treating atopic dermatitis?

A

Oclacitinib (Apoquel) blocks the JAK-1 pathway, offering good antipruritic and some anti-inflammatory action with a favorable long-term safety profile.
Lokivetmab (Cytopoint) is a monoclonal antibody targeting IL-31, providing targeted therapy with a good safety profile and effective antipruritic action.

869
Q

What role does Ciclosporin play in the treatment of atopic dermatitis?

A

Ciclosporin is a potent anti-inflammatory agent used in the treatment of atopic dermatitis, especially for its effectiveness in the long term, though it has a slow onset of action and is costly.

870
Q

What are the phases of therapy for autoimmune skin diseases?

A

Induction: Rapid control of lesions using systemic glucocorticoids at immunosuppressive doses.
Titration: Tapering to the lowest effective maintenance dose, adding adjunctive treatments as necessary.
Maintenance: Maintaining remission with minimal adverse effects, possibly using adjunctive therapies to enable glucocorticoid reduction.
Monitoring: Regular check-ups to monitor lesion control and drug side effects.

871
Q

What adjunctive treatments are used in autoimmune skin diseases?

A

Azathioprine (not for cats), chlorambucil, mycophenolate mofetil, ciclosporin, and potentially oclacitinib.
These drugs may be slow to take effect, so they are often used alongside steroids from the start.

872
Q

What are the take-home messages for managing atopic dermatitis and autoimmune skin diseases?

A

Multimodal therapy is crucial, with no “one size fits all” approach.
For atopic dermatitis, control of inflammation, pruritus, and flare factors, alongside improving skin barrier function, is key.
For autoimmune diseases, the goal is rapid lesion control followed by maintenance of remission with minimal drug side effects, requiring close monitoring and potentially lifelong management.

873
Q

What is the JAK-1 pathway and its significance in veterinary medicine?

A

The Janus Kinase (JAK) pathway is a critical signaling mechanism involved in the immune response, hematopoiesis, and inflammation in animals. JAK-1, a member of the Janus kinase family, plays a pivotal role in transmitting signals from various cytokines and growth factors to the cell nucleus, influencing gene expression. In veterinary medicine, the JAK-1 pathway’s significance lies primarily in its role in mediating the effects of cytokines involved in allergic responses, such as interleukin-31 (IL-31), which is directly associated with pruritus (itching) in animals, especially dogs.

Oclacitinib (Apoquel) is a selective inhibitor of the JAK-1 pathway, providing a targeted approach to managing allergic dermatitis, including atopic dermatitis in dogs, by effectively reducing inflammation and pruritus without the extensive side effects associated with glucocorticoids. By blocking JAK-1, oclacitinib prevents the action of pro-inflammatory cytokines, thereby offering a novel and specific mechanism to control allergic symptoms and improve the quality of life for affected animals.

874
Q

What are the purposes of the breeding soundness and clinical examination of the female reproductive tract?

A

To document normality (BSE), estimate breeding time, confirm pregnancy, detect abnormalities (causes of infertility), and manage parturition.

875
Q

Why is taking a relevant and specific clinical history important in the examination of the female reproductive tract?

A

Climate, nutrition, stress, and teratogens may impact reproductive health, and history should be specific to the species’ age and clinical presentation.

876
Q

What key information must be considered before any examination of the female reproductive tract?

A

Previous pregnancies, the possibility of current pregnancy, and the timing of the examination to avoid missing early pregnancies.

877
Q

What aspects of previous breeding records are important to establish before examination?

A

Puberty status, inter-oestrus intervals, and whether they are normal, prolonged, or shortened.

878
Q

What precautions should be taken to assess infectious disease risks before examining a female animal?

A

Consider zoonotic risks, transmission of venereal or other pathogens, and any notifiable conditions like Contagious Equine Metritis in mares.

879
Q

What pre-mating vaccinations or plans should be considered?

A

Relevant vaccinations for diseases like Salmonella in birds, Clostridial vaccination in ewes and pigs, and Canine herpes virus post-mating to prevent abortion.

880
Q

What types of screening may be required at the start of an examination?

A

Bacteriological and virological screenings like CEMO, Klebsiella, Pseudomonas in mares, and FeLV in queens. Genetic tests for diseases like polycystic kidney disease in cats.

881
Q

What is checked in a general clinical examination to ensure a female can get pregnant and carry to term?

A

Body condition, dentition, feet, ventral hernias, and hereditary defects like hip dysplasia in dogs.

882
Q

What aspects are examined in the mammary glands?

A

The correct number of teats, evidence of the estrous cycle stage, presence of current or previous disease.

883
Q

What is looked for in the examination of the perineum?

A

Normal alignment of vulval lips, evidence of venereal pathogens, and conditions like Coital exanthema in mares or Infectious pustular vulvovaginitis in cows.

884
Q

What factors are assessed during the examination of the vulva?

A

Normality or abnormalities, previous injuries or surgeries, presence of normal or abnormal discharge.

885
Q

What procedures are involved in the examination of the vestibule, vagina, and cervix?

A

Clean vulval lips, sterile manual/digital or speculum examination, and vaginoscopic exams for conditions like urovagina.

886
Q

What are the key points in examining the cervix?

A

Evaluation of the cervical opening, estimation of the cycle stage, normal vs. abnormal conditions like discharge or previous trauma.

887
Q

What methods are used in the examination of the uterus?

A

Trans-rectal and trans-abdominal palpation, radiography, ultrasonography, uterine cytology/microbiology, endoscopic examination, and biopsy.

888
Q

What are the purposes of breeding soundness and clinical examination of the male reproductive tract?

A

To document normality (BSE), determine prognosis for fertility (fertile, infertile, sterile), and detect abnormalities not necessarily related to fertility.

889
Q

Why is taking a relevant and specific clinical history important in the examination of the male reproductive tract?

A

It helps understand the reason for presentation, especially regarding fertility, including puberty status and previous breeding success.

890
Q

What precautions should be taken before examining a male animal for breeding soundness?

A

Assess for infectious disease risk, the need for bacteriological or virological screening, and any required genetic tests.

891
Q

What is assessed in the general clinical examination of a male animal for breeding soundness?

A

Age, body size, puberty status, masculinised appearance, musculoskeletal disease, concurrent illness, and hereditary defects like hip dysplasia.

892
Q

How is libido observed in a male animal during a breeding soundness examination?

A

By observing interaction with an estrous female in the normal mating environment, including interest in the female, mounting behavior, erection, intromission, ejaculation, and interest after mounting.

893
Q

What factors are assessed during the examination of the scrotum?

A

Normal or abnormal scrotal skin, mobility of testes within the scrotum, absence of abnormal contents, and ultrasound for abnormalities like hernia or fluid.

894
Q

What aspects are examined in the testes during a breeding soundness evaluation?

A

Palpation for size, texture, tone, and evenness; measurement of scrotal width/circumference; and ultrasound examination for volume and abnormalities.

895
Q

What is examined in the sheath of a male animal during breeding soundness evaluation?

A

Normal appearance and direction, mobility of the penis, preputial skin condition, size of orifice, presence of discharge, and ability to protrude penile tip.

896
Q

What is assessed during the examination of the penis in breeding soundness evaluation?

A

Examination in non-erect and erect state, absence of penile-preputial adhesions, and penile deviations.

897
Q

How are the accessory glands examined in a male breeding soundness evaluation?

A

Detection of normality or abnormality using semen collection, rectal palpation, radiography, ultrasonography, and lavage techniques.

898
Q

What aspects are evaluated during the collection of ejaculate in a breeding soundness examination?

A

Number, motility, morphology, live staining, and presence of other cells.

899
Q

What tests are included in endocrinological testing during a breeding soundness evaluation?

A

hCG stimulation test, GnRH stimulation test, and measurement of basal oestrone sulphate in stallions. Serial plasma testosterone measurement in dogs.

900
Q

What specific aspects are examined in breeding soundness evaluations across different species (Stallion, Bull, Ram/Boar, Dog, Tom Cat)?

A

Libido, examination of scrotum, testes, epididymides, sheath, penis, urethra, accessory glands, semen examination, and basal hormone and stimulation tests. Methods vary according to species’ anatomy and size.

901
Q

What signifies oestrus in females and how does it vary across species?

A

The female becomes sexually receptive, signaled by “standing to be mated by the male.” Oestrus intensity, length, and timing of ovulation relative to oestrus vary across species.

902
Q

When does oestrus occur after events like parturition or seasonal anoestrus?

A

: Oestrus occurs once puberty is initiated, after parturition/lactational anoestrus, and the resumption of cyclicity after seasonal anoestrus, typically in the latter part of the follicular phase.

903
Q

What are considerations for determining the optimal time to mate?

A

Considerations include the introduction of a specific male, controlled mating, artificial insemination, the period of pre-ovulatory follicle growth, and increasing oestradiol that induces oestrus and the LH surge.

904
Q

What is the difference between the fertile and fertilisation periods in females?

A

The fertilisation period is when oocytes are available to be fertilised by sperm, shortly after ovulation. The fertile period is when mating could result in pregnancy.

905
Q

What hormones are monitored to predict oestrus and ovulation?

A

Progesterone (indicates follicular phase onset and ovulation in dogs), oestradiol (elevated during the follicular phase), and LH (surge triggers ovulation).

906
Q

How is ultrasound used to monitor ovarian structures for breeding timing?

A

Ultrasound checks for the absence of the corpus luteum, follicular size, and morphology. Optimal ovulation timing can be inferred from changes in follicle shape and size.

907
Q

What can rectal palpation of the reproductive tract reveal about fertility status?

A

It helps assess the reproductive tract’s condition, influenced by oestrogen and progesterone dominance, indicating readiness for breeding in mares and cows.

908
Q

What is the significance of vulval softening and vaginal cytology in dogs?

A

These are indicators of the stage of the oestrous cycle, helping determine the optimal time for mating or artificial insemination.

909
Q

How can ovulation be pharmacologically controlled?

A

Using GnRH to induce an LH surge or HCG for direct ovulation induction. This allows for timing mating or artificial insemination more accurately.

910
Q

What are general principles important for diagnosing pregnancy across species?

A

Absence of oestrus post-mating, detection of pregnancy-specific protein/endocrinological changes, and direct or indirect detection of the fetus or fetal membranes (e.g., ultrasound, radiography).

911
Q

What are key signs and hormonal changes associated with pregnancy?

A

Pregnancy-associated glycoproteins, stable progesterone levels post-mating, species-specific hormone secretion (e.g., placental estrogens, relaxin), and physical/maternal changes due to pregnancy.

912
Q

How is pregnancy diagnosed in mares, considering hormonal concentration changes?

A

Tracking hormone concentration changes, fetal mineralization, the presence of the corpus luteum, placental function, and eCG levels.

913
Q

What techniques are used for pregnancy diagnosis in mares and their timing?

A

Transrectal ultrasound from day 12, palpation from day 21, eCG from day 60-120, and transrectal ballottement from day 80.

914
Q

What methods and timings are involved in diagnosing pregnancy in cows?

A

Early pregnancy factor from day 3, transrectal ultrasound from day 14, milk/plasma progesterone levels, transrectal palpation from day 35, and oestrone sulfate in milk from day 100.

915
Q

How is pregnancy diagnosed in ewes?

A

Transabdominal ultrasound from day 30, later detection of cotyledons/caruncles, foetal pulse detection with Doppler ultrasound from day 80, and abdominal enlargement from day 100.

916
Q

Describe the process and timing for pregnancy diagnosis in sows.

A

Observing failure to return to oestrus by day 18-24, elevated plasma progesterone by day 22-24, transabdominal ultrasound from day 20, and foetal pulse detection from day 30.

917
Q

What methods are used to diagnose pregnancy in bitches and their timing?

A

Transabdominal ultrasound from day 25, plasma relaxin from day 25, abdominal palpation for swellings from day 28, and radiographic examination from day 45.

918
Q

How is pregnancy diagnosed in queens?

A

Transabdominal ultrasound and plasma relaxin from day 25, abdominal palpation from day 28, and radiographic examination from day 45.

919
Q

How do pregnancy diagnosis protocols vary by species and management intensity?

A

In cows, ultrasound examination is common at 4 weeks post-mating/AI. In mares on a stud farm, ultrasound exams are typical at days 14, 21, and 35.

920
Q

What is the difference between conception failure and embryonic death?

A

Conception failure occurs when no fertilization happens, often due to mis-timing of mating or ovulation issues. Embryonic death refers to the loss of an embryo before organogenesis, even after fertilization, due to factors like male infertility, chromosomal abnormalities, or issues during early development.

921
Q

: What characterizes early pregnancy loss in cattle?

A

Early pregnancy loss, up to 40% in some cases, is significant in cattle, especially dairy cows, due to high yield/NEB (Negative Energy Balance) and has a high economic cost.

922
Q

How common is embryonic death in sheep, and what factors influence it?

A

Embryonic death is uncommon in sheep, which generally have good fertility. Management issues can reduce twinning rates.

923
Q

What issues are associated with early pregnancy failure in pigs?

A

Early pregnancy failure in pigs is significant and associated with ovarian pathologies after weaning, impacting litter size due to limited uterine capacity.

924
Q

Describe early pregnancy failure in horses.

A

Horses experience significant early pregnancy loss, up to 24%, with most losses occurring before day 12. Loss after this period can still occur, often associated with a lack of embryonic mobility.

925
Q

What factors contribute to conception failure in cattle?

A

Conception failure in cattle can be due to metabolic or physical stress, ovarian pathologies, poor estrus detection, and mis-timing of artificial insemination.

926
Q

How does nutrition affect early pregnancy failure in cattle?

A

Negative energy balance, high NEFA or urea levels, and specific nutrient deficiencies can toxically affect the oocyte/embryo, leading to early pregnancy failure.

927
Q

What strategies can maximize offspring per ewe in sheep, and how does embryonic death affect this?

A

Maximizing offspring involves managing multiple conceptions, nutrition (flushing), and avoiding infectious diseases or management strategies that can lead to increased estrus return or empty rates at pregnancy diagnosis.

928
Q

What causes failure to establish pregnancy in pigs?

A

Factors include seasonal effects on fertility, ovulation failure (e.g., cystic ovarian disease), genetic aspects affecting uterine capacity, and infectious causes like Porcine Parvovirus.

929
Q

What are some causes of early pregnancy failure in mares?

A

Causes include age-related factors, nutritional or physical stress, uterine or uterine tube pathologies, inflammatory conditions, and specific infectious diseases.

930
Q

What are the definitions of resorption, fetal death, mummification, and maceration?

A

Resorption is the death and absorption of the embryo. Fetal death can lead to expulsion, mummification (dehydrated and preserved fetus due to high progesterone and no bacteria), or maceration (autolysis or putrification of the fetus not expelled). Stillbirth is when a fetus reaches term but dies during delivery.

931
Q

What are common non-infectious and infectious causes of pregnancy loss?

A

Non-infectious causes include genetic abnormalities, uterine disease, stress, maternal illness, and nutritional phytotoxins. Infectious causes include exposure to pathogens, recrudescence of latent viral infections, ascending infections, and few venereal pathogens causing abortion.

932
Q

Why is pregnancy loss significant in animals?

A

Pregnancy loss can affect other animals in the group or herd, often involves systemic illness in infectious cases, leads to significant financial losses (cost of treatment, lost production, mortality, prevention), and many infectious causes are potential zoonotic diseases.

933
Q

What are the mechanisms for the expulsion of a dead fetus?

A

Fetal expulsion requires a decline in progesterone and the onset of uterine contractions. If the corpus luteum is not present, expulsion is more likely. If it remains, mummification can occur unless bacteria/inflammation triggers prostaglandin release.

934
Q

How does the presence or absence of the corpus luteum affect the fate of a dead fetus?

A

The absence of the corpus luteum typically leads to expulsion, while its presence can lead to mummification. Bacterial infection or inflammation can induce prostaglandin release, leading to expulsion.

935
Q

What happens in the case of embryonic death and fetal abortion in cows?

A

Embryonic death may result in resorption or pyometra and often goes unnoticed. Fetal death without a corpus luteum leads to expulsion, while with a corpus luteum, it may lead to mummification unless bacterial infection or inflammation induces prostaglandin release.

936
Q

What is the role of exogenous prostaglandins in the context of fetal abortion?

A

Exogenous prostaglandins can induce resorption or abortion by lowering progesterone levels but do not terminate late pregnancy or induce parturition effectively.

937
Q

Leptospiral abortion/stillbirth in cows

A

A bacterial disease causing abortion or stillbirth, transmitted through infected urine or contaminated water.

938
Q

Contagious equine metritis (CEM) in mares:

A

A bacterial sexually transmitted disease caused by Taylorella equigenitalis, leading to inflammation of the reproductive tract but not necessarily abortion.

939
Q

Leptospirosis in bulls:

A

infectious disease risk, potentially leading to Leptospiral abortion/stillbirth in cows.

940
Q

What diseases can cause fetal abortion?

A

Infectious causes of abortion in various species, including viral, bacterial (Campylobacteriosis in cattle), and fungal pathogens. Zoonotic potential of some of these pathogens is noted.
Non-infectious causes include genetic abnormalities, uterine disease, and stress.

941
Q

What diseases can lead to conception failure and embryonic resorption?

A

Specific diseases causing embryonic death in sheep such as toxoplasmosis, Schmallenberg virus, and Border disease.
Cystic ovarian disease in pigs as a cause of ovulation failure.

942
Q

What are common conditions occurring immediately post-partum?

A

Haemorrhage, trauma/lacerations/contusions, prolapse, placental retention, metritis, and recumbency/nerve damage.

943
Q

What can cause post-partum haemorrhage?

A

Profuse bleeding due to umbilicus breakage, uterine or vaginal laceration, and minor seepage from placental attachment sites.

944
Q

What results from trauma, lacerations, or contusions during delivery?

A

Bruising of the vestibule or vulva wall, perineal laceration common in cows and mares, classified by severity from first to third degree.

945
Q

What are types of prolapses seen post-partum?

A

Bladder prolapse through a vaginal tear or eversion through the urethra, distinguished by the visibility of the bladder’s external or internal surface.

946
Q

When is prolapse of the vagina and cervix most commonly seen?

A

Most commonly seen in late pregnancy, not post-partum, with variations across species in prevalence and timing.

947
Q

What are the specifics of post-partum uterine prolapse in different species?

A

Common in cows and ewes post-partum, less common in sows, rare in mares, bitches, and queens, with aetiology linked to factors like hypocalcaemia.

948
Q

How common are retained foetal membranes across species, and what are the consequences?

A

Varies by species; common in cows with significant impact on metritis-endometritis-pyometra complex, less common in mares with severe consequences, uncommon in ewes, bitches, and queens with varying treatments and impacts.

949
Q

What causes post-partum metritis, and how is it treated?

A

: Associated with dystocia, assisted parturition, placental retention; treatments include fluid therapy, NSAIDs, antibiotics, oxytocin or PG administration, calcium administration, and possibly uterine lavage.

950
Q

Which species is most affected by recumbency/nerve damage post-partum, and what are common issues?

A

Cows are most commonly affected, with issues like gluteal and obturator paralysis. Treatments include NSAIDs, hobbling, and general nursing.

951
Q

What are common causes of dystocia in cows?

A

Early breeding, breed (e.g., Holstein high incidence), feto-maternal disproportion, faulty disposition, twin pregnancies, fetal monsters, and maternal dystocia due to hypocalcaemia or incomplete cervix dilation.

952
Q

What are common causes of dystocia in mares?

A

: Faulty disposition due to fetus rotation, short second stage parturition leading to obstructive dystocia, and twins at term being rare due to earlier loss.

953
Q

What are common causes of dystocia in dogs?

A

Primary uterine inertia (75% of cases), faulty disposition, feto-maternal disproportion (common in brachycephalic breeds), and large fetal head relative to pelvic inlet.

954
Q

What are common causes of dystocia in cats?

A

Primary uterine inertia, faulty disposition, fetal monsters, and previous pelvic trauma narrowing the birth canal.

955
Q

What are common causes of dystocia in sheep?

A

: Breed differences, litter size, feto-maternal disproportion, and faulty disposition.

956
Q

What are common causes of dystocia in sows?

A

Less common than other species, with around 40% of cases being uterine inertia and simultaneous presentation being common.

957
Q

What factors influence the choice of treatment plan for dystocia?

A

Deliverability of the fetus, fetal vitality, dam’s condition, potential response to medical treatment, manipulation duration, and number of remaining fetuses.

958
Q

What is the goal of manipulation in dystocia cases?

A

Deliver the fetus, return it to a normal disposition, ascertain fetal vitality, and ensure the dam is not significantly debilitated.

959
Q

When is fetotomy considered in dystocia cases?

A

When the fetus can be delivered with cuts, there’s no current damage to the female tract, the fetus is not viable, and the dam is too debilitated for caesarean.

960
Q

What are the indications for a caesarean operation?

A

Inability to deliver the fetus by manipulation and traction, large litter risk in polytocous species, uterine torsion, incomplete cervix dilation, and as an elective procedure for specific breeds or conditions.

961
Q
A