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Vet Nursing > Pathology > Flashcards

Pathology Flashcards

All information that was taught to me while attending Vanier College's "Animal Health Technology" Program, located in St-Laurent Montreal.

1
Q

What happens in a lesion

A

Abnormal structural and functional changes

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2
Q

How can you observe a lesion

A

May be observed by:Gross examinationMicroscopic examinationLaboratory methods

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3
Q

What are the three possible types of diagnoses

A

PresumptiveDefinitiveDifferential

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4
Q

What is a prognosis

A

A statement regarding the expected (estimated) outcome of the diseaseHopefully evidence-based

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5
Q

Why do we do necropsies

A

To identify the causes of the diseaseto identify cause of death

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6
Q

What are some causes of cell injury

A

HypoxiaPhysical agentsChemical agentsInfectious agents and their toxinsGenetic mutationsNutritional deficiencies and imbalancesAging

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7
Q

What can cause cell degeneration

A

Increase in water (hydropic degeneration)Increase in other substances(FatAmyloidOther)Can be seem macroscopically in microscopically

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8
Q

What is pyknosis

A

When nuclei is condensed and dense in dead cells

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9
Q

what is karyorrhexis

A

when nuclei breaks up into fragments

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10
Q

what is karyolysis

A

when the nuclei is dissolved

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11
Q

What are terms you use to describe necrosis of an organ or tissue

A

PaleSoftFriableSharply demarcated

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12
Q

What are the types of necrosis

A

coagulation necrosiscaseous necrosisliqufactivegangrenous

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13
Q

What species get coagulation necrosis

A

cows

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14
Q

Describe liqufactive necrosis

A

Mostly in central nervous systemRapid enzymatic dissolution

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15
Q

describe gangrenous necrosis

A

Typically further degraded by bacteria that liquefies (moist gangrene – typically saprophytic bacteria) or produces gas (gas gangrene – typically Clostridium).Dry gangrene – ischemia, mommification

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16
Q

What can cause atrophy

A

Deficient nutritionDecreased workloadDisuseDenervationPressureLoss of endocrine stimulation

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17
Q

What are types of cell adaptation

A

AtrophyHypertrophyHyperplasiaMetaplasia

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18
Q

What is metaplasia

A

When one cell type is replaced by another “more useful”Epithelium of trachea: cilliated  squamousVitamin A deficiency in birdsCan be reversible or can progress to neoplasia

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19
Q

What does intracellular accumulation show

A

Symptom of dysfuntionNormal, in excessAbnormal (endogenous or exogenous)Pigment

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20
Q

What are the endogenous pigments

A

MelaninHemoglobin Derivatives (bilirubin, porphyrin)

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21
Q

what are the exogenous pigments

A

carbon (anthracosis)tattoossilica (silicosis)

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22
Q

What is inflammation

A

Mechanism with a protective biological purpose:To dilute, isolate and eliminate cause of injuryWell organized cascade of fluid and cellular changesCan be harmful

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23
Q

What are the four cardinal signs of inflammation

A

RednessHeatSwellingPain

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24
Q

Describe acute inflammation

A

Short duration (few hours to few days)Mostly fluid changes with neutrophilsFollowed by repair and healing

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25
Q

Describe chronic inflammation

A

Weeks to months (to years)Mostly lymphocytes and macrophagesOften fibrosis and granulation tissueCan be secondary to acute inflammation or direct (mycobacterium, foreign material)

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26
Q

What is serous exudates

A

Low in proteins, clotting factors and cellsBlisters from burns, acute allergic responses

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27
Q

Describe mucous exudates

A

Fluid containing an abundance of mucus and mucin (from a mucus membrane)Chronic allergies (chronic asthma)Autoimmune GI diseases

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28
Q

Describe fibrinous exudate

A

Fluid with high concentration of plasma proteinsBut low leukocytes

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29
Q

Describe purulent/suppurative exudate

A

High proteinsHigh WBC

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30
Q

Describe the systemic reaction in inflammation

A
  1. release of cytokines (pyrogens) from wbc2. hypothalamus is triggered3. causes a fever
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31
Q

When does an abscess occur

A

Occurs when acute inflammation fails to rapidly eliminate stimulus.

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32
Q

What is an abscess

A

Enzymes from neutrophils liquefy affected tissue and neutrophils  pusParticularly myeloperoxidase

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33
Q

What species lacks myeloperoxidase

A

rabbits and reptiles

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34
Q

Describe the difference between acute and chronic inflammation

A

Cells as opposed to fluid

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35
Q

What is a particular feature of chronic inflammation

A

granulomas

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36
Q

What is equine proud flesh

A

hypertrophic scar

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37
Q

Describe equine proud flesh

A

Exuberant proliferation of fibroblats and collagenNot well understoodDisregulation of cytokines & Growth factors most likely

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38
Q

Describe IBD

A

Idiopathic. Classified by the region of the gastrointestinal tract (GIT) affected and by the predominant inflammatory cell type. Lymphocytic-plasmacytic inflammation is most commonly found, followed by eosinophilic inflammation. IBD is believed to be immune-mediated in origin.normal intestinal mucosa serves as a barrier and controls exposure of antigens to the GI lymphoid tissue (GALT). GALT generates appropriate immune responses (tolerance of harmless antigens).IBD develops when there is a break-down in this process and inappropriate immune responses occur.

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39
Q

Describe the components of the heart

A

÷ Pericardium÷ Myocardium÷ Conduction system÷ Endocardium & Valves

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40
Q

Describe the components of the heart vessels

A

÷ Arteries (distribution) ÷ Veins (collection)÷ Capillaries÷ Lymphatic

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41
Q

How is fluid distribution and homeostasis maintained

A

Physical barriersConcentration GradientPressure Gradient

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42
Q

What is edema

A

Accumulation of excess interstitial fluid

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43
Q

What are the barrier problems

A

increased permeability

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44
Q

What enzymes are associated with inflammation

A

histamine and bradykinin

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45
Q

What can cause barrier problems

A

inflammation, damage and immune mediated

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46
Q

What causes edema

A

infectious (tick born disease, FIP, leptospirosis, etc)immune mediated diseasetoxins

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47
Q

What causes hydrostatic pressure problems

A

portal hypertensionlocalized obstructionfluid overload

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48
Q

What does hydrostatic pressure mean

A

increased pressure

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49
Q

what causes oncotic pressure problems

A

decreased albumin (production or losses)

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50
Q

What are common fluid distribution problems

A

Barrier ProblemsPressure ProblemsDecreased lymphatic drainage

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51
Q

Where can edema be located

A

¡ Alveolar lumen¡ Thoracic cavity¡ Pericardial sac¡ Abdominal cavity ¡ Subcutaneous

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52
Q

Describe the appearance of edema and the histological appearance

A

Clear to slightly yellowtransuadate (low protein and low cells)

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53
Q

Describe physical disruption that cause hemorrhage

A

traumaerosionneoplastic invasionfungi

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54
Q

What minor defects that could cause hemorrhage

A

endotoxemia/infectious agentstoxinsimmune-complexes

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55
Q

What can cause hemorrhage

A

Physical disruptionminor defectsthrombocytopeniacoagulation factor deficiency

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56
Q

What is thrombosis

A

— Formation of inappropriate clot of fibrin and/or platelets along with other blood elements on the wall of a blood vessel / lymphatic / heart.

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57
Q

What is a thrombosis called when it occurs in the lumen

A

thromboembolism

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58
Q

What can cause endothelial injury/vasculitis

A

¡ Infectious (ex herpes virus, salmonella, aspergillus)¡ Immune-mediated ¡ Toxins

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59
Q

What can cause an alteration in blood flow

A

¡ Mechanical÷ (GDV, external compression) ¡ Cardiac disease¡ Hypovolemia

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60
Q

What can cause hypercoagulability

A

¡ Inflammation¡ Diabete¡ Renal disease¡ Neoplasia¡ Hepatic disease ¡ Cushing’s¡ Hypothyroidism ¡ Heartworm

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61
Q

What are the clinical signs of thromboembolism in the renal arteries

A

decrease in renal function, proteinuria and hematuria oranuria if bilateral

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62
Q

what are the clinical signs of thromboembolism in the pulmonary arteries

A

¡ acute respiratory compromise and a ventilation-perfusion mismatch that can be mild or subclinical depending on the degree of embolization

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63
Q

what are the clinical signs of thromboembolism in the mesenteric arteries

A

¡ gastrointestinal signs and abdominal pain

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64
Q

what are the clinical signs of thromboembolism in the distal limb arteries

A

¡ pain, hardening of the musculature (tetany), and cyanosis

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65
Q

What are the three types of shock

A

¡ Cardiogenic¡ Hypovolemic¡ Blood maldistribution(÷ Septic÷ Anaphylactic ÷ Neurogenic)

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66
Q

What is cariogenic shock

A

Failure of the heart to pump adequate amount of blood ÷ Arrhythmias÷ Cardiomyopathy÷ Pericardial tamponade÷ Anesthesia

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67
Q

How is cardiogenic shock characterized

A

Loud murmurs, tachycardia or bradycardia, arrrhythmias, and weak heart sounds

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68
Q

What is hypovolemic shock

A

¡ Reduced circulating blood volume ÷ Fluid loss: vomiting, diarrhea, burns ÷ Blood loss (>35%)

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69
Q

How is hypovolemic shock characterized

A

tachycardia, pale mucous membranes, and tachypnea

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70
Q

What is blood maldistribution

A

¡ Pooling of blood in peripheral tissues from vasodilation

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71
Q

what is anaphylactic shock

A

¡ Widespread mast cell degranulation ¡ USUALLY CAUSED BY: Vaccine, insect/plant, drugs

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72
Q

What is neurogenic shock

A

¡ Autonomic nerve discharge ¡ CAUSED BY: Electrocution, stress, fear

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73
Q

What is septic shock

A

¡ Infectious organism released inflammation mediator

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74
Q

What is congestive heart failure

A

Inability of the heart to maintain normal ¡ systemic blood pressure¡ normal cardiac output (normal tissue blood flow) ¡ normal filling pressure

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75
Q

Why does congestive heart failure occur

A

results from severe heart disease

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76
Q

What does right sided heart failure cause

A

¡ Hepatomegaly & splenomegaly ¡ Ascites

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77
Q

What does left sided heart failure cause

A

Pulmonary congestion and edema

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78
Q

What can cause pericardial effusion

A

¡ Cardiac hemangiosarcoma÷ Highly malignant ¡ Idiopathic÷ Golden Retriever ¡ Acute vs Chronic¡ Pericardiocenthesis

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79
Q

Describe dilated cardiomyopathy

A

¡ Large breed dog (e.g. Doberman, Irish Wolfhound)¡ Familial pattern¡ Etiology not well understood¡ Adult onset÷ May have murmur, arrhythmias, tachycardia¡ Taurine-deficient cats

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80
Q

Describe myocardium

A

Hypertrophic cardiomyopathy¡ Main Coons¡ Etiology not completely clear¡ Young adult, middle-age cat÷ Mostly asymptomatic with murmur of gallop¡ Associated with arterial thromboembolism¡ Hyperthyroidism can cause a form of DCM (reversible)

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81
Q

Describe arrhythmogenic cardiomyopathy of the boxer

A

¡ Ventricular arrhythmias, syncope, sudden death¡ Familial disease÷ Not well understood, difficult to breed out

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82
Q

Describe sick sinus syndrome

A

¡ West Highland white terrier, Miniature schnauzer, Americancocker spaniel, Boxer, Dachshund, Pug¡ Idiopathic¡ Adult onset÷ Most of these dogs show overt clinical signs (syncope, episodicweakness) at the time of diagnosis¡ Pacemaker

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83
Q

Describe myxomatous valvular degeneration

A

¡ Progressive degeneration of the atrioventricular valves¡ Older dogs¡ Small- to medium-size breeds (Papillon, Poodle, Chihuahua,Dachshund, Cavalier King Charles Spaniel)¡ Slow progression to heart failure¡ Progressive murmur

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84
Q

Describe patent ductus arteriosus

A

¡ Mostly dogs¡ Congenital, can be genetic¡ Female; pomeranian, poodle (proved heritable cause), Keeshond, Bichon frise, Chihuahua, Maltese, Shetland sheepdog¡ Continuous murmur¡ Sx or Coil

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85
Q

Describe valve stenosis

A

¡ Pulmonary valve (smaller breeds)¡ Aortic valve (larger breeds) ¡ Loud murmur¡ Not as easy to correct if severe

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86
Q

describe fibrocartilaginous embolism

A

¡ Vascular thrombosis and infarction of the spinal cord¡ Sudden onset, usually one side worst¡ Non-chondrodystrophoid¡ If deep pain sensation remains, many animals will recover useful spinal function

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87
Q

describe intestinal lymphangiectasia

A

Dilatation of lymphatic vessels and obstruction of normallymph flow.¡ Intestinal lymphatic dysfunction leads to leakage of protein- rich lymph into the intestinal lumen.÷ Common causes of protein-losing enteropathy (PLE) in dogs¡ Primary: idiopathic¡ Secondary:÷ Inflammatory disease ÷ Neoplasia÷ Heart failure

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88
Q

What are the signs of intestinal lymphangiectasia

A

÷ vomiting, diarrhea (usually small bowel), weight loss, lethargy, anorexia÷ peripheral edema, abdominal distension from ascites

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89
Q

How do you treat intestinal lymphangiectasia

A

diet change, anti-inflammatories

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90
Q

what is the prognosis for intestinal lymphangiectasia

A

prognosis is variable

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91
Q

What causes a rupture of the thoracic duct

A

¡ Cause chylothorax¡ Cytological aspect:¡ Often idiopathic (other: neoplasia, HWD, heart failure)

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92
Q

What is a portosystemic shunt

A

¡ Anomalous vessels that allow normal portal blood (from GIT) to pass directly into the systemic circulation without first passing through the liver¡ Congenital or acquired (older)¡ Failure to thrive, poor weight gain, and small body stature ÷ Seizure-like episodes after a meal¡ Some can be treated with surgery

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93
Q

What does carcinogenic mean

A

Agent that causes mutations resulting in tumor formation

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94
Q

What is oncology

A

The study of neoplasia (diagnosis, treatment)

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95
Q

What are the characteristics of benign neoplasm

A

Well differentiatedThe cells resemble closely the parent tissueLittle or no anaplasiaSlow growthNo basement membrane invasionDo not metastasizeOften encapsulated

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96
Q

How can a benign neoplasm cause disease

A

By compressing sensitive tissuesBy being metabolically activeBy malignant transformation

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97
Q

What are the characteristics of malignant neoplasm

A

Some lack of differentiationAnaplasiaRapid GrowthMany mitotic figuresAbnormal mitotic figuresLocally invasiveInfiltrative growthFrequent metastasisUsually no capsule

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98
Q

What are some names of epithelial tumors

A

AdenomaPapillomaCarcinomaAdenocarcinoma

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99
Q

What are some names of mesenchymal tumors

A

Tissue -omaTissue -sarc0ma

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100
Q

How does a tumor metastasise

A

Invasion of host tissueDissemination through vascular systemImplantation on new surfaces

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101
Q

What are some diagnostic methods for neoplasm

A

radiologycomputed tomographyultrasoundMRINuclear MedicinecytologyDNA, RNA analysis

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102
Q

What do you do radiography for

A

screening test

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103
Q

why do you use computed tomography

A

to characterize and localize lesionidentify metastasissurgery and radiotheraphy planning

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104
Q

Why do we use ultrasound

A

Abdomen: internal structure of organs and to image body cavities when effusionAssess vasculatureUltrasound-guided sampling

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105
Q

Why do we use nuclear medicine

A

administration of radioisotopes

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106
Q

What are the advantages to cytology

A

Relatively low risk of procedures to the animalLower cost compared with biopsySpeed with which results can be obtainedBest to evaluate cellular criteria (ex lymphoma)

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107
Q

what are the disadvantages to cytology

A

Small sample (may not be representative)No tissue architecture

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108
Q

Why do we do DNA and RNA analysis

A

Study mutations to help classify tumorsDiagnostic utility (lymphocytosis)Can help guide therapy

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109
Q

Why do we do grading

A

Done to predict/classify the behavior of the tumor.Different criteria depending on tumor type.Done by pathologist

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110
Q

Why do we do staging

A

Describing or classifying a cancer based on the extent of cancer in the body. Often based on the size of the tumour, presence of metastasisStages are based on specific factors for each type of cancer

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111
Q

What are some clinical effects of neoplasm

A

The pressure exerted by the neoplasm on the surrounding tissues will cause the following effects:PainVessels blockageDyspnea, hypoxiaCompromise organ function

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112
Q

What is cachexia

A

Weakness and wasting of the body due to severe chronic illnessthat cannot be reversed nutritionallyInflammatory cytokines involved

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113
Q

What causes anemia

A

Suppression of erythropoietin synthesis in kidneysHemorrhagesDecreased erythropoiesisErythrocyte fragmentation

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114
Q

What causes hypercalcemia

A

Tumor cell secretionsOsteolytic metastases of neoplasms

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115
Q

What are some causes of cancer

A

Genetic Immunosuppression Chemical carcinogens Viral carcinogens Physical carcinogens Chronic tissue injury

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116
Q

What are some environmental factors that cause cancer

A

Cigarette smokeUltraviolet irradiationUrbanizationDiet

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117
Q

What are the intrinsic factor that cause cancer

A

Oxygen free radicals that result from chronic inflammationIntrinsic errors in DNA replicationevery time a cell divides, each daughter cell is likely to carry at least a few hundred mutations in its DNA Most are silent, but accumulate

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118
Q

describe heritable cancer syndromes

A

Cancers with clear heritable basisNot many described in veterinary literature

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119
Q

Describe genetic Influence in Sporadic Cancers

A

It is Why not all smokers get lung cancer

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120
Q

Describe Presence of distinct heritable traits that segregate with common cancer phenotypes in dogs (animals)

A

Will not cause cancer directly (unlike heritable syndrome)Histiocytic sarcoma in Bernese Mountain dogs

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121
Q

What are the characteristics of the chemical extrinsic factors

A

Very wide varietyMost bind covalently to DNADirect carcinogenIndirect:Require metabolic activation

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122
Q

what are the characteristics of the physical extrinsic factors

A

Sunlightfacial, aural, and nasal planum SCC in white or partially white cats and may also play a similar role in some cutaneous SCC lesions in dogTrauma/InflammationChronic keratitisFeline vaccine associated sarcomaRadiationAt site of radiation therapySurgery/ImplantsAnecdotal reports

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123
Q

what are the characteristics of the hormonal extrinsic factors

A

Canine mammary cancermost common neoplasm of female intact dogsSimilar in cats, but not as well documentedPerianal adenomaoccurs primarily in intact male dogs, whereas perianal adenocarcinoma occurs in both intact and castrated malesResolves after castrationProstate cancerneutered dogs have been shown to be at increased risk

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124
Q

Describe the papilloma virus

A

Usually multiple lesions affecting young dogsMost regress without txt

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125
Q

Describe the feline leukaemia virus

A

Still much to discoverOnly 20% of cats persistently infected with FeLV develop lymphoid cancerTwenty years ago, 70% of lymphomas in cats were believed to be caused by FeLV

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126
Q

describe the FIV virus

A

neoplasms most commonly linked to FIV infectionLymphomas and myeloid tumors (myelogenous leukemia, myeloproliferative disease) few carcinomas and sarcomas Lentiviruses such as FIV not oncogenic in themselvesmarkedly immunosuppressiveaffect normal immunosurveillance of cancerous cells

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127
Q

Describe canine hemangiosarcoma

A

Highly malignant neoplasm that originates from vascular endotheliumAffects middle-age to older dogs, large breedPrimary tumor site:SpleenHeart (right atrium)SubcutisLiverMetastasis:lungs, liver, mesentery, and omentum (hematogenous)Direct spreadFeatures helpful for diagnosis (pertinent staging/grading, etc):Often morphologically altered RBCs are present, such as schistocytes, acanthocytes, and poikilocytesCan present as acute abdomen or cardiac tamponadeOther (complications, prognosis, etc)Highly metastaticWatch for DICIf Splenic, need to remove spleen, but prognosis still poor (better with chemo - 141–179 days)

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128
Q

What is the definition of canine lipoma

A

A benign subcutaneous mass with a soft texture usually localized.

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129
Q

Who does canine lipoma affect

A

Most commonly dogs, rare in cats and horsesBreed predispositionsHypothyroid dogs

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130
Q

What are the clinical signs of canine lipoma

A

Palpation of small, soft mass under the skinShould not cause discomfort to the patientUsually around abdominal region but can be anywhereTendency to develop multiple

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131
Q

How do you diagnose canine lipoma

A

Fine needle aspirationSurgical removal and histopathology

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132
Q

How do you treat canine lipoma

A

Surgical removal can be done but it is not necessary unless it is restricting movement

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133
Q

Describe basal cell tumor

A

Has many specific namesMid to old dog and catMostly on head and neck

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134
Q

Describe follicular tumor

A

Often inflammationOlder dogsCan sometimes squeeze out material

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135
Q

Describe sebaceous adenoma

A

Cauliflower-like tumorOlder cats & dogsideally should be removedmalignant version exists

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136
Q

describe soft tissue sarcoma

A

General name for a number of mesenchymal tumorsMuscle, adipose, neurovascular, fascial, and fibrous tissue Mostly malignant (see grade)Similar pathologic appearance and clinical behavior Solitary tumor in older dogs and catsSkin and subcutaneous sites are most common

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137
Q

describe the soft tissue sarcoma

A

Tend to appear as pseudoencapsulated soft-to-firm tumors, but have poorly defined histologic margins or infiltrate through and along fascial planes, and they are locally invasive.Local recurrence after conservative surgical excision is commonTend to metastasize hematogenously in up to 20% of cases.Regional lymph node metastasis is unusualHistopathologic grade is predictive of metastasis, and resected tumor margins predict local recurrence.Measurable or bulky (>5 cm in diameter) tumors generally have a poor response to chemotherapy and radiation therapy (RT).

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138
Q

describe equine malignant melanoma

A

80% of grey horses over the age of 15 will develop at least one melanoma tumor during their lifetimeCan be fatalThere is no available effective chemotherapy for horses.Tumor of the melanocytes, the cells that produce skin pigment.Most common location: underside of the tail, the perineal and peri-anal regions, penis and sheath in malesCan also be found: ear margins, anywhere on the head, jugular region, new or on the parotid salivary glandIt is also possible that the melanomas can spread internally, most commonly to the serosal surfaces of the liver, spleen, and lungsCan be hard or soft, and appear either solitary or in clustersStart off under the skin until they surface. They can become ulcerated and/or infected

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139
Q

How do melanoma’s develop

A

1- Melanomas develop slowly over years, and remain benign 10-20 years, without metastasis. Most common.2- Benign melanomas that exist for months or years and suddenly develop malignant characteristics and spread rapidly externally and/or internally.3- Melanomas are malignant from the start. Rare.

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140
Q

where can malignant melanoma metastasis to

A

Metastasis: lymph nodes, liver, spleen, skeletal muscle, lungs, and surrounding or within blood vessels throughout the body

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141
Q

Describe feline oral squamous cell carcinoma

A

Most common oral malignancy in the cat Can originates from the jaw bones or the tongueOwners may find a mass in their cat’s mouth which occurs mostly in the back of the mouth or under/on the tongueIt has an ability to grow invasively (locally), but does not tend to metastisizeCan be ulcerative or proliferativeNo breed/sex predisposition, usually affects middle-aged cats

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142
Q

what are the symptoms of the feline oral squamous cell carcinoma

A

mass that can be ulcerativedroolingweight loss, halitosisdifficulty eatingbloody discharge from the mouth

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143
Q

What are the environmental factors that contribute to oral SCC

A

Second Hand Smokeflea collarsDiet

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144
Q

How do you diagnose oral SCC

A

Often not diagnosed until the tumour is advancedOral examinationAn ulcerated, red, locally invasive lesion is highly suggestive of an oral tumor Loose teeth can suggest bone structure is affectedBloodwork to check overall healthRadiographsCan reveal invasion of underlying boneBiopsy of abnormal tissueUsed to confirm the presence of SCC and help stage the tumor Important to obtain a large sample since feline oral SCC are frequently infected, necrotic, or inflamed.

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145
Q

Describe the treatment of feline oral SCC

A

Surgical removal is possible but can be difficult due to the aggressiveness and invasiveness that typically involves the bone. This means part of the jaw would need to be removedRadiation therapy or chemotherapy alone is generally ineffective in the managing oral SCC. The combination of the two can improve quality of life and overall survival time. Pain medication can help reduce discomfort associated with the tumor.

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146
Q

Describe the prognosis of feline oral SCC

A

Extremely poor1 year survival rate is less than 10% even with combinations of radiation therapy and chemotherapyMost cats are euthanized withing 1-3 months because they cannot eat or drink and poor quality of life

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147
Q

What are the malignant oral tumors

A

squamous cell carcinomamelanocyte tumorfibrosarcoma

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148
Q

What are the benign oral tumors

A

epulides

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149
Q

How do you treat oral tumors

A

Surgery and RT are the most common treatments used for the local control of oral tumors.

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150
Q

What are the symptom of oral melanoma in dogs

A

HalitosisDroolingBleeding from the mouthChange in food preferenceChange in chewing habitsDecrease in appetiteChronic coughingDifficulty swallowingWeight loss

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151
Q

What causes canine oral melanoma

A

idiopathic

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152
Q

How do yu diagnose canine oral melanoma

A

Physical exam: Blood tests, UA, X-rays, abdominal ultrasound, MRI, fluid biopsyOlder dogs will have dark pigmented areas on the tongue, mouth and gums. Look for anything unusual in the mouth pigmented or non-pigmented fleshy masses. Metastasis: Head, neck, lymph nodes, liver, lungs, kidneys and sometimes bone tissue

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153
Q

how do you treat canine oral melanoma

A

Removal of tumor: Sometimes hard to completely remove because it may spread to the bone in the mouth. Can return even if completely removed. Resistant to chemo.Radiation: Remission in 70% of patients. Reoccurrence and spread still possible.New vaccine restricted availability.

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154
Q

what is the prognosis from canine oral melanoma

A

5-7 months, but; Stage 1: 1 yearStage 2: 6 monthsStage 3: 3 monthsStage 4: 1 month

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155
Q

describe nasopharyngeal polyps in cats

A

Nonneoplastic, inflammatory massesoriginating from either the middle ear or eustachian tubecan extend into the external ear canal or nasopharynxYounger catsIdiopathic

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156
Q

Describe the tumors of the liver

A

Primary tumors rarePrognosis variableMetastasis are frequentNodular hyperplasiacommon diagnosis in older dogsbenign and probably does not represent a preneoplastic lesion

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157
Q

describe feline intestinal lymphoma

A

Can present as:a purely intestinal infiltrationor a combination of intestinal, mesenteric lymph nodes and liver involvementTumors can be solitary but more commonly diffuse throughout the intestinesCommonOlder cats, mostly small intestineOften preceded by IBD

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158
Q

Describe perianal adenomas in animals

A

Benign sex-hormone dependent (spayed female, intact male)

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159
Q

Describe apocrine gland adenocarcinoma

A

Tiny primary tumor (often pea-size)About 50% metastasis at diagnosisHypercalcemia (PU/PD)

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160
Q

Describe canine chondrosarcoma

A

Chondrosarcoma is a form bone cancer in dogsThe cancer starts in the cartilage and connective tissue found in joints, and/or ribs and nose. It can cause bones to fracture easily as the tumour invades the bones. It is mostly common in older dogs

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161
Q

How do you treat canine chondrosarcoma

A

Better prognosis if caught early and treated aggressively. Amputation of the affected limb if no metastasis has occurred. Radiation therapy if located in the nose. Removal of the affected rib and portion of the lung if tumour is on rib followed by chemotherapy. Inoperable tumours are treated with radiotherapy to try to prolong the life span.Surgery is the only known affective treatment.

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162
Q

How do you diagnose canine chondrosarcoma

A

XraysCBCLymph biopsyBiopsy of tumourCT scan

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163
Q

describe canine osteosarcoma

A

Most common bone tumor found in dogs5% of all canine tumorsMalignantCan effect any breedMost common in large or giant breeds.Middle aged or elderly

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164
Q

What are the primary osteosarcoma tumor sites

A

Bordering the scapula Tarsus CarpusStifleCommonly near growth plates

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165
Q

Where does canine osteosarcoma metastasize to

A

Lungsother bones lymph nodes

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166
Q

What are the risk factors associated with canine osteosarcoma

A

Slightly more in females than malesHigher in castrated males and spayed females (compared to intact)

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167
Q

What are the symptoms of canine osteosarcoma

A

LamenessPeriosteal inflammationMicrofracturesPathologic factorsSwelling

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168
Q

how do you diagnose canine osteosarcoma

A

Orthopedic, neurologic and physical examinationX-rays (if lesion is in question – do a biopsy)Biopsy through aspirationBone scan

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169
Q

how do you treat canine osteosarcoma

A

Aggressive treatment planRadiation therapy – palliative care not curativeCurative options include a combination of surgery, radiation therapy and chemotherapyStandard treatment is amputation

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170
Q

what is the prognosis for osteosarcoma

A

Very good prognosis with amputation: resolves 100% of the pain

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171
Q

What is the aetiology and pathogenesis of insulinomas

A

Insulinomas are tumors of the pancreatic β cells (type of islet cell) which produce insulin These tumors cause increased insulin production which result in hypoglycemiaThe tumors respond to normal provocative stimuli that encourage a rise in insulin, but fail to respond to negative feedback when the insulin levels are too highInsulinomas are very common in middle-aged and older ferrets ( greater than 3 years of age)

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172
Q

What are the clinical signs of insulinomas

A

Hypoglycemia will result in neurological signs such as mental dullness, sluggishness, lethargy, ataxia, seizures and comaProlonged, severe hypoglycemia can result in cerebral hypoxia and cerebral lesionsOther possible symptoms are nausea (which can cause the ferret to paw at its mouth), depression, hypersalivation, staggering, tachycardia, hypothermia, tremors, muscle fasciculations, nervousness and irritabilityOwners may report that the ferret tends to sleep more frequently, be difficult to wake up, or stops in its tracks with a dazed appearanceIt is important to note that these symptoms can come and go as blood sugar levels rise and drop

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173
Q

how do you diagnose insulinomas

A

One of the most common illnesses diagnosed in ferretsWill be diagnosed using clinical signs, history, physical exam, blood glucose levels and insulin levels

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174
Q

How do you treat ferret insulinoma

A

Surgery to remove the tumors (the tumors often grow back so several surgeries will likely be required)Medication to manage insulin and glucagon levels (the dose will need to be increased as the illness progresses)Diet is another huge component to managing this disease. All ferrets should be fed a high-protein ferret food, but this is especially important in sick ferrets

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175
Q

what is the prognosis for ferret insulinomas

A

Most insulinomas are eventually fatalThis is either because of hypoglycemic induced complications or because the tumors have spread to other organsAll that can be done is attempt to maintain a good quality of life for the ferret for as long as possible

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176
Q

describe pituitary adenoma

A

Common pituitary neoplasia of older dogsMost common cause of cushing in horses.Pituitary tumors account for approximately 15% of intracranial tumors Frequently associated with either: -hyperadronocorticism
 - Diabetes Insipitus

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177
Q

What are the clinical signs of pituitary adenoma

A

Non-neurological: weight loss, PU/PD, lethargy
 Neurological signs: cranial compression is rare but pressure on the optic chiasma may cause ocular changes

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178
Q

how do you diagnose pituitary adenoma

A

imagining with CT or MRI may be difficult, but a definitive diagnosis is usually done with a intraoperative or postmortem biopsyDifferential diagnosis: lymphoma, hypothalamic-pituitary trauma, dorsally expanding cysts, congenital malformations, inflammatory granuloma, etc.

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179
Q

how do you treat pituitary adenoma

A

corrective hormonal therapy or hypophysectomy (removal of the pituitary gland)

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180
Q

what is the prognosis for pituitary adenoma

A

Prognosis depends upon the type and size of the tumour.The prognosis for a pituitary tumor (if the client is willing to do treatments) is usually fairly good as the treatments are quite effective.In serious unnoticed cases The entire hypothalamus may become compressed and replaced by the tumor.

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181
Q

How can you determine whether cushings disease is caused by the pituitary or the adrenal adenoma

A

If there is no change in Cortisol levels being released by the adrenal gland, then it is an Adrenal Adenoma.If there is suppression of the adrenal gland, then the Cushing’s is being caused by a Pituitary Adenoma.

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182
Q

Describe pheochromocytoma

A

Adrenal gland tumorOlder dogsSecretes catecholamines (episodic)episodic collapse, panting, anxiety, restlessness, exercise intoleranceMalignant (40% metastasize)Good prognosis is no metastasis

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183
Q

Describe thyroid gland adenomas in dogs

A

Often benign adenoma found at necropsyMalignant:If clinical signs of hyperthyroidism (most non-functional)Older dogsFrequent metastasis

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184
Q

Describe hyperthyroidism

A

Multinodular adenomatous hyperplasiaCarcinoma rare

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185
Q

describe insulinoma

A

Pancreatic Beta-Cell TumorsHallmark of insulinomanormal or elevated blood insulin concentration in the presence of low blood glucose levelsOften malignant50% metastasisMedium and large breed dogs, older

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186
Q

What are the clinical signs of insulinoma

A

weakness, ataxia, collapse, disorientation, behavioral changes, and seizures

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187
Q

How do you treat insulinoma

A

Medical and surgical treatmentprognosis for dogs with insulinomas is good in the short term but guarded to poor in the long term

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188
Q

What is a gastrinoma

A

Often pancreatic, secretes gastrinGastric acid hypersecretionMiddle-aged dogs and older catsNon-specific clinical signsvomiting and weight lossmelena, abdominal pain, anorexia, hematemesis, hematochezia, and diarrheaOften metastasis at diagnosis

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189
Q

What is a transitional cell carcinoma

A

Fairly common malignant tumorLocated in the trigone region of the bladder15% metastasis at diagnosis30% of dogs have abnormal cells in urine

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190
Q

What are the signs of the transitional cell carcinoma

A

hematuria, dysuria, pollakiurialess commonly: lameness caused by bone metastasis

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191
Q

What is canine lymphoma

A

Is a common type of cancer in dogs. Unregulated growth of malignant lymphocytes that often affects; lymph nodes, bone marrow, liver, and spleen.Can also be seen in the eyes, skin, and gastrointestinal tract.It can be small cell lymphoma; progresses very slowly and is difficult to treat. There is also large cell lymphoma; progresses quickly but responds very well to chemotherapy.

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192
Q

What are the 5 stages of canine lymphoma

A

Stage I: Ailment restricted to a single lymph node.Stage II: Regional lymphadenopathy (restricted to one side of diaphragm).Stage III: Generalized lymphadenopathy (enlargement of lymph nodes)Stage IV: Enlargement of the liver and spleen or hepatosplenomegaly (with or without lymphadenopathy).Stage V: Bone marrow, CNS (Central Nervous System), or involvement of other extranodal sites.

193
Q

what are the symptoms of canine lymphoma

A

Firm, enlarged, non-painful lymph nodes. Other common symptoms include loss of appetite, lethargy, weight loss, swelling of the face or legs (edema), and occasionally increased thirst and urination.

194
Q

how do we diagnose canine lymphoma

A

Best way is to perform a biopsy; you are able to differentiate between T and B cells with special stain because they respond differently to treatment.

195
Q

how do we treat canine lymphoma

A

Most effective therapy is chemotherapy. In some situations, surgery or radiation therapy may also be recommended.

196
Q

what is the prognosis for canine lymphoma

A

Depends on what type of lymphoma the dog has and the type of chemotherapy. The average for multicentric lymphoma is 9-13 months.

197
Q

describe leukemia

A

Many different types of leukemiaMyeloid: white blood cellsErythroid: RBCAll from bone marrowCan be acute or chronicAcute: high cell counts, immature cellsChronic: moderate cell counts, mature cellsBone marrow examination important

198
Q

what are the signs of multiple myeloma

A

Bleeding (nose, gums)LamenessPU/PDElevated globulins

199
Q

describe the prognosis of multiple myeloma

A

Dog: good for initial control of tumor and a return to good quality of life (median 540 days)Cats: 4 months

200
Q

describe plasmacytoma

A

Local & Benign form of plasma cell tumorOlder dogsLimb, head, lipsConservative surgical excision

201
Q

describeb mast cell tumors in dogs

A

Mast cells are found in the connective tissues mostly in the vessels and nerves that are located close to the external surfaces.Boxers, bulldogs, pugs, and Boston terriers appear to be more susceptible to mast cell tumors than other breeds. Dogs affected with a mast cell tumor are around 8 years old but studies show that there has been cases of mast cell tumor seen in less than 1 year old dogs

202
Q

where is the primary tumor site for mastocytoma

A

skin, nose, mouth, lungs

203
Q

describe the metastasis of mast cells

A

Depending on the stages, stage 2 will metastasize into surrounding lymph nodes and stage 4 will metastasize to other organs.

204
Q

How do you diagnose mast cell tumors

A

Fine needle aspiration CytologyBiopsysurgical removalradiation therapy (if metastasis occurs)

205
Q

What is the prognosis for a mast cell tumor

A

The prognosis will depend on the growth of the tumorIf the tumor grows more than 1 cm per week, the animal only has 25% chances of surviving more than 30 weeksIf the tumor is located at one specific area and does not grow rapidly for several months, it is known to be benign

206
Q

What are some complications associated with mast cell tumor

A

In some cases, you might noticed an enlargement of the lymph nodes located around the area of the tumor Some masses can be inflammed and itchy due to high level of histamines in the actual tumor
Enlarged liver and enlarged spleen are characteristic of wide-spread mast cell cancer

207
Q

What is a thymoma

A

Older (9-10 yo) dogs (and cats)Neoplasms of thymic epithelial cellsBenign vs malignant based on surgery

208
Q

What are the clinical signs of a thymoma

A

Lethargy, coughing, tachypnea, and dyspnea

209
Q

What can a thymoma cause in some animals

A

myasthenia gravis (in 40% of dogs)

210
Q

What is myasthenia gravis

A

Autoimmune disease of the neuromuscular junction causing muscular weakness and excessive fatiguabilityMegaoesophagus (regurgitation)3% of dogs with MG have a cranial mediastinal mass

211
Q

What are histiocytic diseases

A

Neoplasia of macrophage (and related cells)

212
Q

What is a histiocytoma

A

Nodular skin tumor of young dogs (head/neck)Very commonBenign, regresses spontaneously

213
Q

What is a histolytic sarcoma

A

Bernese Mountain dogs, rottweilers, retrieversSpleen, liver, lungsVery poor prognosis

214
Q

Describe mammary tumors in dogs

A

Common in intact femalesHeterogenous group of tumors (10+)More research neededImpacts the course of action/treatmentMetastasis common

215
Q

Describe mammary tumors in cats

A

Siamese cat younger, overrepresentedIntact catsThe vast majority of feline mammary tumors are malignant (85% to 95%)with an aggressive biologic behavior, lymphatic invasion and lymph node metastasis are more common at the time of initial diagnosis than in dogsNeeds aggressive surgery

216
Q

Describe a canine prostate tumor

A

Older dogs, intact and neutered (slightly more)At the time of diagnosisMost tumor are locally invasive High propensity for regional and distant metastasisBones (lumbar vertebra and pelvis)

217
Q

what are the signs of a canine prostate tumor

A

hematuria, dysuria, stranguria, dyschezia, tenesmus

218
Q

What are the components of the immune system

A

Cellsrecognition moleculessoluble factors

219
Q

Describe nonspecific immunity

A

First line of defence, non specific

220
Q

Describe the anatomic and physiologic portion of nonspecific immunity

A

skin, mucosa, ciliastomach pH, Body Temperature

221
Q

Describe the cellular portion of the nonspecific immunity

A

phagocytic cells, NK cells

222
Q

describe the molecular portion of the nonspecific immunity

A

inflammationcomplement system

223
Q

Where do the cells from the nonspecific immunity come from

A

recruited by the molecules of inflammation

224
Q

What is the function of the cells of the nonspecific immunity

A

ingest + destroy pathogensneutralize toxins

225
Q

Describe the self/nonself identification by neutrophils, monocytes, tissue macrophages, NK cells

A

Express membrane receptors that innately recognize several pathogens (pathogen recognition receptors)Recognizes PAMPs (pathogen-associated molecular patterns)Also DAMPS (damage associated molecular patterns)

226
Q

Describe the cell mediated specific immunity

A

T-Lymphocytes for intracellular pathogensB-Lymphocytes for extracellular pathogens and toxins

227
Q

Describe the characteristics of specific immunity

A

SpecificityDiversityMemorySelf/non-self recognitionMHC molecules

228
Q

Describe T Lymphocytes

A

Contains T Cell ReceptorTCR can only recognize antigen in combination with a MHC molecule. Each T Lymphocyte expresses a different TCR

229
Q

What is the CD4 T Lymphocyte

A

Helper T lymphocytesRecognizes MHC class II: found on antigen presenting cells

230
Q

What is the CD8 T Lymphocyte

A

Cytotoxic T Lymphocytes: Recognizes MHC class I: found on all nucleated cells

231
Q

What is a signal 2 lymphocyte:

A

important for tolerance and auto-immunity

232
Q

What do T-Lymphocytes do when activated

A

Expand clonaldifferentiate into: Effector Cells or Memory cells

233
Q

Describe the antigen receptor in B Lymphocytes

A

Membrane-bound immunoglobulin. The immunoglobulin gene can rearrange- antigen recognition diversity.

234
Q

What happens to B Lymphocytes when activated

A

Expand clonallyDifferentiates into:Effector cells plasma cell (antibody secreting)Needs the action of T-helper lymphocyteMemory cells

235
Q

What is the function of a macrophage

A

PhagocytosisAntigen presentation to T-LymphocyteMHC class II

236
Q

What is the function of a dendritic cell

A

Very efficient antigen presenting cellCapture antigens in circulation and present to T-Lymphocytes in lymph nodes

237
Q

Describe a Type 1 hypersensitivity

A

Immediate hypersensitivityMisdirected/innapropriate responseoccurs within minutes of exposure

238
Q

Describe the type 1’s immediate hypersensitivity

A

IgE mediatedAgainst: Environmental antigens (allergens)Parasite antigen

239
Q

What does a type 1 hypersensitivity reaction require

A

Need to be previously SENSITIZEDMediated by mast cells

240
Q

What does mast-cell degranulation in a type 1 hypersensitivity reaction result in

A

VasodilationEdemaSmooth muscle contractionMucus productionInflammation

241
Q

Describe the systemic reaction in a type 1 hypersensitivity

A

Anaphylaxis

242
Q

Describe the localized type 1 hypersensitivity reaction

A

Skin, mucosa, GITAtopy, allergic rhinitis

243
Q

What is allergic dermatitis

A

cutaneous manifestation of type I hypersensitivityInhalation, ingestion, percutaneous

244
Q

What do you call an allergic dermatitis with a genetic predisposition

A

atopic dermatitis

245
Q

Describe a flea bite hypersensitivity

A

Most common hypersensitivity in cats & dogsVery pruritic dermatitis (mostly on back)

246
Q

What is urticaria and angiodema

A

Most often in horses and dogsMultifocal or localized areas of edemaUrticaria: superficialEdema: deep dermis and subcutis

247
Q

What are the immunologic causes of Urticaria and Angioedema

A

food, drug, antisera, insect bites

248
Q

what are the non immunologic causes of urticaria and angiodema

A

heat, exercise, stress

249
Q

Describe a cytotoxic hypersensitivity

A

Development of antibodies against self cells or tissueMay be from self antigen or exogenous antigen adsorbed to self

250
Q

What does a cytotoxic hypersensitivity cause

A

IMHA, ITP (cytotoxic)Myasthenia gravis (altered function)

251
Q

What immune complexes are involved in a type 2 hypersensitivity

A

IgM and IgG

252
Q

What does a type 2 hypersensitivity reaction require

A

a sensitized host

253
Q

What enhanced phagocytosis of antigen by macrophages in type 2 hypersensitivity

A

opsonization by antibodies or complements

254
Q

How can an antibody activate the complement system and what happens when it does it

A

Antibody can activate the complement system, via the classical pathway, resulting in the elaboration of inflammatory mediators

255
Q

What can antibodies against cell receptors do

A

activate or inhibit cell function. ex: TSH

256
Q

What is immune mediated hemolytic anemia

A

Common, life-threatening acute anemiaYoung middle-aged females, cocker spanielsUsually idiopathicInfection, drugs, neoplasia

257
Q

What is neonatal isoerythrolysis

A

A form of IMHAColostrum derived maternal antibodiesAttacks newborn’s RBCCommon in horsesImmunosensitization of mother to incompatible blood type from stallion8-10h after birth up to 4-5 days

258
Q

what is pemphigus (foliaceous)

A

Most common and milder form of pemphigusOften adverse reaction to drugsAutoantibodies against a protein in desmosomesPustules with acantholytic keratinocytes

259
Q

What are three different type 2 hypersensitives

A

Immune Mediated Hemolytic AnemiaNeonatal isoerythrolysisPemphigus

260
Q

Describe a type 3 hypersensitivity

A

Immune-complex hypersensitivityAntigen-antibody complexes that activate complement and cause damageSimilar to type IIType II: antigen directed against selfType III: antigen just get “stuck” to tissue

261
Q

What happens when immune complexes are deposited into tissues

A

Activation of complement systemtissue DAmage

262
Q

Why do antibody antigen complexes go wrong

A

Improper atb/ag ratioWeak, chronic atb responseToo many atb-ag complexes

263
Q

What is type 3 hypersensitivity caused by

A

chronic/persistant infectionforeign antigen inhalation

264
Q

Where do antibody-antigen complexes accumulate in

A

Blood vesselsSynovial membranesGlomeruliChoroid plexus (brain)

265
Q

What is systemic lupus erythematous

A

Multiorgan disease (dogs; rarely cat & horse)Defective T-Lymphocyte suppression results in B-Lymphocyte hyperactivity

266
Q

What are the predisposing factors for systemic lupus erythematous

A

GeneticsViral infectionHormonesUV light

267
Q

Describe how systemic lupus erythematous affects the body

A

Formation of autoantibodies to a variety of antigens, including nucleic acidOrgan specific antigensClotting factorsCells (RBC, platelets, leukocytes)Main damage: atb-ag complexesMany tissue, notably skin (intensified by UV light)

268
Q

What are the skin symptoms of systemic lupus erythematous

A

Local or generalizedErythema, depigmentation, alopecia, crusting

269
Q

What are the systemic signs of systemic lupus erythematous

A

PolyarthritisFeverAnemia, thrombocytopeniaProteinuria

270
Q

What causes equine infectious anemia

A

caused by the lentivirus

271
Q

how does the lentivirus cause equine infectious anemia

A

infects monocytes and macrophages

272
Q

what does equine infectious anemia do to the body

A

Immune-mediated (atb-atg complexes deposition)Decreased erythropoiesis

273
Q

how do you diagnose equine infectious anemia

A

coggins test for diagnostic

274
Q

describe a type 4 hypersensitivity

A

Delayed-type hypersensitivityCell mediated hypersensitivityInteraction between T-lymphocytes and specific antigensSensitized T-lymphocytesResponse is 24-48h after exposureGranuloma formationUnlike type I, II & III: NOT dependent on antibody

275
Q

describe tuberculosis

A

Caused by acid-fast bacilli of the genus Mycobacterium. Chronic, debilitating diseaseOccasional acute, rapidly progressive course. Affects practically all species of vertebratesMycobacterium Tuberculosis and othersOften the body is unable to clear the infectionChronic Granuloma formation

276
Q

Describe johne’s disease

A

Mycobacterium paratuberculosis.Chronic, contagious granulomatous enteritisOften in cattlePersistent diarrhea, progressive weight loss, debilitation, and eventually deathThickened and corrugated intestine with enlarged and edematous neighboring lymph nodesGranulomas

277
Q

What is auto-immune thyroiditis

A

Chronic and progressive lymphocytic infiltration and subsequent destruction of the thyroid gland

278
Q

Who is predisposed to getting auto-immune thyroiditis

A

Doberman Pinschers, Beagles, Golden Retrievers, and Akitas

279
Q

What is special about auto-immune thyroiditis

A

Probably has both humoral (Type II - cytotoxic) and cell-mediated (Type IV - delayed) componentsMHC probably involved

280
Q

What is bovine/canine leukocyte adhesion deficiency

A

Genetic, congenital anomaly of leukocytesPrevents leucocytes from migrating from the blood in the tissuesVery high neutrophiliaAnimals are highly susceptible to infectionDie very young

281
Q

Describe feline infectious peritonitis

A

Mutation of benign enteric coronavirus to FIP virusInfects monocytes & macrophages and spreads through bloodType III (immune complex)VasculitisType IV (delayed) also likelyGranulomas

282
Q

Describe keratitis sicca

A

Due to an aqueous tear deficiencyUsually results in persistent, mucopurulent conjunctivitis and corneal ulceration and scarringDogs, cats & horsesDogs: often autoimmune dacryoadenitis of both the lacrimal and nictitans glandsNot well understood

283
Q

What causes infection

A

bacteria, viruses, fungi, protozoa, prions

284
Q

what are the steps of infection

A

Chronologic sequence of eventsPortal of entryRegulated by virulence factors

285
Q

are most infectious agents targeting specific cells or organs

A

yes

286
Q

How does the infectious agent get into the body

A

Mucosae (respiratory, alimentary, lower urinary, reproductive, ear/eye)Subcutaneous tissues

287
Q

what are the bodies cells that help to stop infectious agents initial multiplication

A

Macrophage, lymphocytes, dendritic cells

288
Q

where does the infectious agent go after initial multiplication

A

Then local (submucosa, subcutis), regional (lymph node), systemic spread

289
Q

what does the mucus protective layer of the body do

A

Prevents direct adherenceBlocks/traps organismsCan facilitate action of phagocytesDelivers antigens to local lymphoid tissueKeeps antimicrobial substances and atb close to mucosa

290
Q

what can cause changes in goblet cell function and chemical composition of mucus that can lower protection

A

DehydrationShippingHumidityVentilationWeather changes

291
Q

how have microorganisms evolved to take advantage of our mucus protective layer

A

Source of food (carbohydrates, peptides)If able to colonize inner mucus: prevents expulsionCan specifically adhere to molecules in mucusMicrobial mucolysis ability is virulence factor

292
Q

how do you ingest an infectious agent

A

via infectious fomites

293
Q

where is the thickest layer of mucus protective layer

A

in the colon

294
Q

where is the thinnest layer of the mucus protective layer

A

in the jejunum

295
Q

what is located in the protective mucosal fluids

A

gastric acid, lyzozymes

296
Q

describe inhaling a fomite

A

Nostrils  Nasal turbinates, pharynx or lower airwaysDepends on size, shape, weightVirus > prions > bacteria > fungi > ProtozoaBUT mostly inhaled with fomites!Air turbulence in turbinates increases deposition

297
Q

describe the mucuciliary apparatus

A

Biphasic mucus layerTip of cilia in gelNasal cavity & sinus:Moves downwardConductive respiratory:Moves upwardUltimately swallowedInjury to epithelial cells (influenza, rhino) can disrupt and cause secondary bacterial infections

298
Q

describe infectious agent cutaneous penetration

A

Via abrasions, scratches, bite wounds, insect biteLimited range of host targets but limited defenses

299
Q

describe the pathogenicity of the infectious agents

A

Regulated by virulence factorsIn bacterial genesTheir expression permits bacteria to Colonize mucosae, Infect cells,Grow and replicate,Cause cell death

300
Q

what infectious agents have good motility

A

spirochetes

301
Q

what infectious agents can digest the mucus layer

A

clostridium

302
Q

describe colonization of an infectious agent

A

Adhesion of sufficient amount of bacteriaVia:Fimbria/PilusAdhesion moleculesNeeds to be faster than cell renewal

303
Q

describe spreading of an infectious agent

A

SpreadingDestruction of collagen, tight junctions between cellsProvides safe spot for bacteria

304
Q

describe the toxins released by infectious agents

A

Exotoxins (gram +), endotoxins (gram -) (LPS: lipopolysaccharide)Damages cells and extra-cellular matrixKills cells via cytolysis or activation of complement

305
Q

since Viruses are unable to produce energy and contain a limited number of enzymes what are they considered

A

obligate intracellular parasites

306
Q

how have viruses evolved

A

Have evolved to target specific cells in animals to sustain theirs needsNot as many virulence factornot as complex as bacteria.

307
Q

describe permissive viral target cells

A

Allows for viral replication

308
Q

describe non permissive viral target cells

A

no replication – used as reservoirCan become permissive (ex with cell maturation or activation)

309
Q

describe step 1 of the viral replication cycle

A
  1. Attachement and EntryDetermines which organs are infectedViruses bind to normally expressed receptors
310
Q

describe step 2 of the viral replication cycle

A
  1. Replication stageHow much of the cell is hijackedOrganelles, genome, otherHow much cell dysfunction, cell death
311
Q

describe step 3 of the viral replication cycle

A
  1. SheddingHow the virus exits determines cell’s fateIf cell killed or lysed  causes more severe disease
312
Q

describe parvovirus viral replication

A

Infects intestinal crypt epithelial cellsReceptors on basolateral surfaceSo coming in from circulation, not directly from intestineM-cell  Peyer’s patch  circulationNot most direct; prevents contact with protective mechanism, tight junctions

313
Q

how do non-enveloped viruses attach to cells

A

They attach to host cells using a protein coat (viral coat, capsid, capsomeres) Usually kill infected cells to release newly formed virus.

314
Q

how do enveloped viruses attach to cells

A

They attach to host cells using a viral envelope Usually do not kill infected cells to release newly formed virus.

315
Q

what are the innate host cell defences against viruses

A

InflammationInterferon

316
Q

what are the host cell mediated immunity against viruses

A

NK and cytotoxic T cellsAntibodies important only for subsequent infections

317
Q

what is the aetiology and pathogenesis of canine brucellosis

A

contagious diseased caused by the bacteria. any breed/age can be affected by common in mature dogs. affects reproductive system and organs. ZOONOTIC

318
Q

how is brucellosis transmitted

A

mucosa and broken skin. via infected fluids

319
Q

what are the clinical signs of canine brucellosis

A

lethargyswollen lymph nodesdifficulty walkingback painvaginal discharge etc

320
Q

how do you diagnose canine brucellosis

A

spinal xraycytologyserology

321
Q

how do you treat brucellosis

A

ATB tests

322
Q

how do you prevent brucellosis

A

spay and neuter

323
Q

what does equine herpes virus cause

A

abortion 2-12 weeks after infection. if no abortion the foals have viral pneumonitis.

324
Q

how is equine herpes virus transmitted

A

contact with aborted fetus, fetal fluids and placenta + also through aerosol secretions from coughing horse

325
Q

what are the clinical signs of equine herpes virus

A

can be subclinical in adults.- nasal discharge
- incoordination 
- hind limb weakness 
- loss of tail tone 
- lethargy 
- urine dribbling 
- head tilt 
- poor balance
- inability to rise.

326
Q

how do you diagnose equine herpes virus

A

Diagnosis: nasopharyngeal swab of the horse, blood samples for PCR or virus isolation, or tissue from the aborted fetus for detection of antibody titers.

327
Q

how do you treat equine herpes virus

A

Treatment: Supportive care and treatment of the symptoms. NSAIDS used to reduce fever, pain and inflammation. In uncomplicated cases, will recover in a few weeks.

328
Q

what is the prognosis for equine herpes virus

A

Prognosis: poor if the horse is recumbent for an extended period of time.

329
Q

how do you prevent equine herpes virus

A

Prevention: 2 types of vaccines, controversial. Vaccines might actually reduce the severity and duration of the disease but it will not prevent it. There’s modified live(intra-nasal, faster protection) and killed(IM).

330
Q

what is bordatella

A

Bordetella is a very contagious respiratory disease possible in both cats and dogs caused by a bacteria named Bordetella bronchiseptica The bacteria will cause inflammation of the trachea and bronchi

331
Q

how is bordatella transmitted

A

Direct contact (licking, nuzzling)Air (coughing, sneezing)Contaminated fomites (bowls, toys)

332
Q

what are the mild clinical signs of bordatella

A

Dry, hacking cough in dogs (owners will often refer to the coughing as a foreigh material stuck in the throat) RetchingSneezingNasal discharge

333
Q

what are the severe clinical signs of bordatella

A

PneumoniaFever LethargyInnappetence

334
Q

what is the treatment for bordatella

A

No medication px when an animal comes in with bordetella. rest for 14 days and reevaluation if no improvement. If productive cough= no anti-tussive pxIf non productive cough = anti-tussive can be px

335
Q

what are the risk factors for bordatella

A

Risk factors Shelter animals, rescue centers animals, breeding kennel animals or pet store animals

336
Q

what are the methods of preventing bordatella

A

vaccine once a year

337
Q

what is leishmania

A

is an intracelluar protozoan parasite that causes the zoonotic disease Leishmaniasis.

338
Q

how is leishmania spread

A

Spread through Sand Fly bites, with vertical transmission unlikely but possible.

339
Q

who is affected by leishmaniasis

A

Primarily effects dogs, but humans, cats, rodents and horses can also be infected.Leishmaniasis is a major zoonitic endemic between humans and canines

340
Q

what is the pathogenesis for leishmaniasis

A

Predisposing factors: Age, genetics, nutrition and general immune statusIncubation period: Months to yearsParasite travels from the skin throughout the host’s body Cutaneous and/or visceral lesions:Skin, kidneys, spleen, liver, eyes, jointsGranulomatous inflammationMediated by CD4 T lymphocytes

341
Q

what are the symptoms of leishmaniasis

A

Dermal lesions (nodules, scaling, alopecia, brittle hair coat, may be ulcerative)LymphadenomegalyOcular abnormalitiesEpistaxisWeight loss & anorexiaExercise intolerance/lethargy

342
Q

what are the methods of diagnosis leishmaniasis

A

Clinical SignsCBCBiochemHystologyCytology

343
Q

how do you treat leishmaniasis

A

SC injections of Meglumine Antimoniate (4-8 wks)PO Zyloprim (6-12 months)Tx may only be temporary and may not eliminate the parasite, leaving the animals carriers for life, with the potential for relapse.Carriers can be infectious to sand flies, restarting the cycle.

344
Q

what is erysipelas caused by

A

Caused by a bacteria called Erysipelothrix rhusiopathiae that is:Gram-positive

345
Q

who does erysipelas effect

A

Affects swine 50% of pigs in production are affected

346
Q

where is the erysipelas bacteria found

A

The organism commonly resides in the tonsillar tissue

347
Q

how is erysipelas transmitted

A

Organism is shed by carriers in the feces Oronasal secretions

348
Q

what are the clinical signs of an acute erysipelas infection

A

Sudden and unexpected death from septicemiaPainful jointsSkin lesions often described as diamond skin

349
Q

what are the signs of a chronic erysipelas infection

A

Tends to follow acute infectionsOne form is characterized by enlarged joints and lameness Also has diamond skin disease that can progress to necrosis

350
Q

how do you diagnose erysipelas

A

Skin lesionsSkin discoloration and erythema of the ears, snout, and lateral or dorsal regions of the bodyGram stain the tissue sample of affected tissueAcute more difficult to diagnose

351
Q

how do you treat/prognosis of erysipelas

A

Penicillin treatment at 12 hour intervals for a minimum of 3 daysFever associated with acute infections treated with NSAIDS Treatment usually ineffective and costly (Poor prognosis)

352
Q

what is ehrlichia

A

Ehrlichia is an obligate intracellular bacterium

353
Q

what is ehrlichia responsible for the transmission of

A

a group of tick-borne illnesses known as Ehrlichiosis (zoonosis)

354
Q

describe the ethiology of ehrlichia

A

Once transmitted, Ehrlichia most commonly infects monocytes. They are able to guarantee their survival because they possess the capability to reprogram the systems and mechanisms of defense employed by the host cell.Ehrlichia can cause an acute or chronic infection. Is zoonotic passed through tick bites, causes similar symptoms as in dogs, but can be fatal in immune compromised patients

355
Q

what are the signs and symptoms of ehrlichia

A

Fever, Lethargy, Loss of appetite, Weight Lossabnormal bleeding (e.g., nosebleeds, bleeding under skin – looks like little spots or patches of bruising)enlarged lymph nodes, enlarged spleenpain and stiffness (due to arthritis and muscle pain)Coughing, Discharge from the eyes and/or nosevomiting and diarrheainflammation of the eyeneurological symptoms (e.g., incoordination, depression, paralysis, etc.)

356
Q

how do you diagnose ehrlichia

A

Blood counts and hematological tests are crucial to the diagnosis of Canine monocytic ehrlichiosis. Critical signs of ehrlichia infections are: - Low blood counts - thrombocytopenia

357
Q

what is the etiology of distemper

A

Direct or indirect (fomite), inhalant transmission Improper attenuated vaccines in rare casesMost common cause is coming in direct contact with infected animals such as raccoons, foxes and skunks.

358
Q

what is the pathogenesis of distemper

A

Initially attacks tonsils and lymph nodes and replicates in those specific tissue for about a week. Then attacks the Respiratory, urogenital, gastrointestinal & nervous system

359
Q

who does distemper affect

A

Dogs Ferrets Wolves FoxesSkunks RacoonsUnvaccinated dogs are more at risk for contracting the disease

360
Q

what are the clinical signs of the first stage of distemper

A

Early symptoms includeHigh fever 39.7°CRed eyesWatery discharge from the nose and eyesFollowing SymptomsLethargic and weakUsually become anorexic May have persistent coughing, vomiting and/or diarrhea

361
Q

what are the clinical signs of the later stages of distemper

A

The virus attacks the nervous system effecting the brain and spinal cordMay start having fits, seizures, paralysis, and attacks of hysteria In some strains it can cause abnormal thickening of the pads of feet AKA Hard Pad Disease Secondary bacterial infection may increase the animals vulnerablity to the disease

362
Q

what is the prognosis for distemper

A

No cure Recovery is possible but seizures and other severe changes to the CNS may be fatal 2-3 months after recovery Chance of survival depends on the strain and the dogs immune system Young unvaccinated puppies and non-immunized older dogs are more susceptible.

363
Q

how do you diagnose distemper

A

Biochemical tests Urinalysis Low lymphocytes Serology test : won’t be able to differentiate between vaccinated antibodies or exposure to virus Viral antigens may be detected in urine sediment or vaginal imprints Skin with hair, nasal mucous and foot pad epithelium may be tested for antibodies CT and MRI can be used to examine the brain to view any lesions that may have developed

364
Q

how do you treat distemper

A

Supportive treatment Iv fluidsAntibiotics to control secondary bacterial infection Phenobarbital and potassium bromide to control convulsions and seizuresNo antiviral drugs that are effective in treating the disease

365
Q

how do you prevent distemper

A

VaccinationRarely seen in pet dogs because of judicious vaccine protocolsPart of core vaccinations

366
Q

what is the aetiology and pathogenesis of the avian newcastle disease

A

RNA virusMost important virus in poultry Chickens are most susceptible, waterfowl are least susceptible

367
Q

what is the epidemiology and transmission of newcastle disease

A

Endemic in poultry in most of Asia, Africa, and some countries of North/South AmericaUSA and Canada are free of the virulent strains poultry (import restrictions and destruction of infected poultry)Infected birds shed virus in exhaled air, respiratory discharges, and fecesShed during incubation, clinical stageChickens are often infected by aerosols and ingesting contaminated food and waterYoung chickens are most susceptible

368
Q

what are the clinical signs of newcastle disease

A

Rapid onset, symptoms appear throughout the flock within 2-12 days (avg 5) after aerosol exposureOnset is slower if contracted through fecal-oral routeSigns depend on whether the virus has affected the respiratory, digestive, or nervous systemRespiratory: gasping, sneezing, coughing, ralesNervous: tremors, paralyzed wings and legs, twisted necks, circling, clonic spasms, complete paralysisGI: diarrhea, inappetenceMay see complete or partial cessation of egg productionMortality is variable but can be as high as 100% with virulent infections

369
Q

what is the diagnosis and prevention of newcastle disease

A

Diagnosed through oropharyngeal or cloacal swabsVaccine available, but the vaccines do not provide sterile immunity ZOONOTIC RISKAll strains can produce a transitory conjuctivitis in humans, usually only when exposed to high quantities of the virus (lab workers and vaccination teams)

370
Q

what is foot and mouth disease

A

A reportable, zoonotic, highly contagious viral disease (7 strains) of cattle and swine, which also affects sheep, goats, deer, and other cloven-hoofed ruminants. Giraffes and elephants can also be affected.Mostly found in endemic countries like the Middle East, Africa, Asia, and in parts of South AmericaThe disease is characterized by fever and vesicles in the mouth and on the muzzle, teats, and feetIt can be spread by direct (milk, semen, secretions) and indirect contact (people, air current)

371
Q

what is the pathogenicity of foot and mouth disease

A

In endemic countries, there is 100% morbidity with low mortality, except in the case of young animalsThe primary site of infection is in the mucosa of the pharynx, the virus then goes through the lymphatics and replicates in the mouth, muzzle, feet, teats, and damaged skin.Animals that are infected and vaccinated can still carry the disease (cattle up to 3.5 years)

372
Q

what are the symptoms and treatment of foot and mouth disease

A

Lameness, pyrexia, vesicles in mouth cavity and feet, decreased milk production, frothing of mouth, teat blisters, and decreased appetiteThere is no treatment, only supportive careIll animals can recover, however they are usually culled, as so the ones who are susceptible. They must be incinerated.

373
Q

how do you prevent foot and mouth disease

A

Export restrictions can be instilled to reduce risk of infection in endemic countriesA full quarantine must be implementedFull disinfection of infected areas must be performed immediatelyInfected milk can be disinfected by boiling for 20 minutesVaccination may be provided, however must closely match the strain of the virus, as there is no universal vaccine.The inactivated vx only protects for 4-6 months against clinical signs only

374
Q

what is helicobacter

A

Affects cats and dogsFound in gastric tissues and intestinal tractTransmission is unknown, reservoirs unknownConcern of zoonotic transmission

375
Q

what are the clinical signs of helicobacter

A

100% of healthy cats and dogs are positive.Infection reported in vomiting cats and dogsSigns: Gastritis, vomiting and diarrheaNo direct relationship between symptoms and infection has been identified

376
Q

how do you diagnose helicobacter

A

Upper GI endoscopy ( taking brush samples) or laparotomy Brush samples: Can cover large area of the stomach therefore high sensitivity. Sample viewed under 100x magnification.Multiple biopsies must be taken in the stomach and stained with H&E stain to identify organism.Cytology and histopathology cannot identify specific species but high sensitivity and specificity for Helicobacter.

377
Q

how do you treat helicobacter

A

Very little knowledge of pathogenicityTreatment will be based off the presence of species and clinical signs.Some animals don’t experience long term eradication of infection

378
Q

describe the eye

A

Eye: Many specialized structuresWith the CNS converts light to visual images

379
Q

what happens with inappropriate function of the eye

A

Inappropriate function:Loss of sightPain

380
Q

what can cause ocular disease

A

Ocular disease:CongenitalImmune mediatedSecondary to systemic diseaseTraumaticInflammatory

381
Q

what can cause inflammation of the conjunctiva

A

IrritantAllergic, ocular trauma, foreign body, fur, eyelash irritationInfection:Bacterial, systemic disease (distemper)

382
Q

what are the clinical signs of conjunctivitis

A

Red, inflamed conjunctivaChemosis: swelling (edema)Discharge:Serous to mucopurulentCrusting

383
Q

what are the signs of pain caused by conjunctivitis

A

Protruding nictitant membraneSquintingBlepharospasm

384
Q

how do you diagnose conjunctivitis

A

Signs, historyNeed to (try to) identify initiating cause:Complete ocular examBacterial cultureTesting for systemic diseaseAllergy testing

385
Q

how do you treat conjunctivitis

A

Depends on causeAntibiotic+/- steroids (when not?)

386
Q

when do you not give steroids for conjunctivitis

A

if there is an ulcer

387
Q

what is epiphora

A

Abnormal overflow of tearsObstructed nasolacrimal ductOverproduction of tears

388
Q

what causes epiphora

A

Congenital obstructionInfection/inflammationTraumaForeign bodyTumors

389
Q

what are the clinical signs of epiphora

A

Clinical signs:Excessive watery dischargeIrritation of underlying skinEye rubbing

390
Q

how do you diagnose epiphora

A

History – Eye examFluorescein (why?), schirmerDiagnostic imaging, surgical exploration

391
Q

how do you treat epiphora

A

Depends on underlying causeFlushingStentingSurgeryRemoval of irritantCorrection of deformity

392
Q

what is the most common complication of treating epiphora

A

re-occurance

393
Q

what is cherry eye

A

Prolapse of nictitating membraneWith inflammation & hypertrophy

394
Q

which animals are pre-disposed to cherry eye

A

Cocker spaniels, English bulldogs, Boston terriers, BeaglesRare in cats

395
Q

what causes cherry eye

A

Causes:Genetic predispositionOcular infection/irritationSun damage

396
Q

what are the clinical signs of cherry eye

A

Red mass in medial canthusMucopurulent dischargeIrritation:ConjunctivitisTearingSquintingUnilateral or Bilateral

397
Q

how do you treat cherry eye

A

Surgical correction (not removal)Important for tear production, can predispose to KCS

398
Q

what is entropion

A

Entropion:Most common seenInversion of eyelidVery painfulCreates eye damage

399
Q

what is entropion/ectropion

A

Conformational abnormalities of the eyelid

400
Q

what is ectropion

A

EVersionDroopy eyesExposed conjunctiva:Bacterial infection, irritant exposure

401
Q

what are the clinical signs of ectropion/entropion

A

BlepharospasmSquintingEpiphoraCorneal ulceration  change in corneal color

402
Q

how do you treat entropion/ectropion

A

surgical correction

403
Q

what is a corneal ulcer

A

Defect in the corneal epitheliumFrequent if dogs and cats

404
Q

what causes corneal ulcers

A

InfectionTraumaForeign bodyEntropionKCS

405
Q

what are the clinical signs of corneal ulcers

A

Pain: squinting, epiphora, prominent thrid eyelid, pawing at eyeVisual defect in corneaClouding of the eyeConjunctivitis

406
Q

how do you diagnose corneal ulcers

A

History & Eye examFluorescein eye stain

407
Q

how do you treat corneal ulcers

A

Removal of causeControl of inflammationPain reductionAntibioticsE-CollarSerumCorneal graft

408
Q

what is chronic superficial keratitis (pannus)

A

Progressive, bilateral, inflammatory condition of the cornea

409
Q

what causes pannus (CSK)

A

Genetic predisposition(German shepherdsLabradors retrieversBorder colliesGreyhounds)Probably immune-mediatedUV radiationsAltitude

410
Q

What are the clinical signs of pannus (CSK)

A

White, pink or brown pigmentation, vascularization & opacificationStarting at OUTSIDE edge of cornea and working inwardsWill affect signtUsually causes discomfort

411
Q

how do you diagnose pannus (CSK)

A

DiagnosisHistory & clinical signs

412
Q

how do you treat pannus (CSK)

A

Earlier treatment = better prognosisNo cure, can be managed medicallyCorticosteroids (topical, injections)LifelongReduce exposure to UV

413
Q

what is KCS

A

Tear (aqueous) deficiencyMost common cause of conjunctivitis in dogs, rare in cats

414
Q

what causes KCS

A

Causes:AutoimmuneDrug therapyDistemperGenetic

415
Q

what are the clinical signs of KCS

A

Clinical signs:ConjunctivitisChronic muco-purulent dischargeCorneal ulcerationScarringPain/discomfort (rubbing)Depends on severity of disease (amount of tears produced)

416
Q

how do you diagnose KCS

A

History and Eye examSchirmer tear testNormal: 18-24 mmKCS

417
Q

how do you treat KCS

A

TreatmentEye lubrificationImmune suppressive drugsNeed to verify the presence of corneal ulcer before treatment

418
Q

what is anterior uveitis

A

Inflammation of the anterior chamber of the eyeIrisCiliary bodyCommon in dogs and cats

419
Q

what causes anterior uveitis

A

Systemic diseasesTraumaIrritantsCataractNeoplasiaIdiopathic

420
Q

what are the clinical signs of anterior uveitis

A

Eye appears cloudyIncrease in proteins in anterior chamberInflammation of corneaPainfulMiosisDecrease IOP (intra-ocular pressure)PhotophobiaBlepharospasm

421
Q

how do you diagnose anterior uveitis

A

History, Signs, Eye examOphthalmoscope examIOP measurement (very important why?)Fluorescein

422
Q

how do you treat anterior uveitis

A

Fast and aggressive treatment is crucial!prevent glaucoma, scarring of the uveal structures, and possibly blindnessClose monitoring of treatmentRemove initiating causeReduce inflammation (NSAIDS, Steroids)+/- antibioticsAtropine Dilates the pupil and helps prevent scarring of the irisReduces pain***Contraindicated if glaucomaPrognosis depends on causeTreatment can be life-long

423
Q

what is cataracts

A

Opacity of the lens that causes blurry visionMost common in dogsCan be young or adult onset

424
Q

what causes cataracts

A

Causes:AgeGeneticsRadiationTraumaInflammationSystemic disease (DM)

425
Q

describe nuclear sclerosis

A

Affects the lensNormal changeMild vision impairmentCan see retina

426
Q

describe cataracts

A

Affects the lensAbnormal changeMore severe impairmentCannot see to retina

427
Q

how do you diagnose cataracts

A

Diagnosis:HistoryRapid onset in young dogsOphthalmic examMay require dilation (what to check before?)

428
Q

how do you treat cataracts

A

Surgical removalSteroids if inflammationAtropine

429
Q

what is progressive retinal atrophy

A

Genetic disorder in which the retina atrophies and the animal goes blindAffects cats and dogsBilateral conditionNon-painfulEarly onset, progressive

430
Q

what are the clinical signs of progressive retinal atrophy

A

Dilated pupils (glow or shine of the eye)Night blindness at first, then complete blindnessOwners may notice more since quicker onset than old dogsDisorientationFear of dark roomsGetting lostCataract formation common in later stages

431
Q

how do you diagnose progressive retinal atrophy

A

Needs exam by ophthalmologistChange in retina blood vessel pattern, optic nerve, etc

432
Q

how do you treat progressive retinal atrophy

A

NoneClient education! Not painful!

433
Q

what causes bone fractures

A

TraumaNutrient deficienciesNeoplasmHormonal imbalanceInfection

434
Q

how do you classify bone fractures

A

Open vs closedComplete vs incomplete

435
Q

describe a linear fracture

A

Linear: incomplete, parallele to bone

436
Q

describe a greenstick fracture

A

incomplete, bent

437
Q

describe a comminuted fracture

A

multiple bone fragments

438
Q

describe a compression fracture

A

collapse of vertebra

439
Q

describe an avulsion fracture

A

loss of section of bone due to muscle contraction

440
Q

how do you diagnose a bone fracture

A

History, signs: severe lameness, pain, crepitus on palpationRadiographs

441
Q

what can bone fractures be associated with

A

If the result of trauma  Can be associated with more severe damage!Shock, internal organ damage, internal bleeding

442
Q

how do you initially manage a bone fracture

A

Initial management: immobilizationReduces painReduces trauma to soft tissueClosed fractures (2-4 days), open (8h; 24-48h)

443
Q

how do you repair a bone fracture

A

External coaptation: splint or castExternal fixationInternal fixation: plates, screws, nails, pins, wires

444
Q

what factors are to be considered when treating a bone fracture

A

FracturePatientEnvironment

445
Q

what is important to remember about a splint or cast repair

A

Splints need frequent evaluations and changescomplications may result in a longer overall healing periodwhereas some fixation methods improve the chance of successful outcomes without demanding post-operative care.

446
Q

what is panosteitis

A

Acute, self-limiting condition in quickly growing animalsPain & inflammationIn long bonesMost common in large and giant dog breeds

447
Q

what causes panosteitis

A

Unknown (idiopathic)GeneticStressAutoimmune factors

448
Q

what are the clinical signs of panosteitis

A

Acute lameness in young animalsOften shifting lameness, intermittentMay be associated with muscle atrophyFever, anorexia, lethargy

449
Q

how do you diagnose panosteitis

A

History, signs, PERadiographs (may be NSF if acute)Rule out more serious causes

450
Q

how do you treat panosteitis

A

PalliativePain reliefReview dietExcessive development contributes to this disorder

451
Q

what is degenerative joint disease

A

Progressive, long-term deterioration of the joint cartilage, causing damageFrequent in dogs and cats

452
Q

what causes degenerative joint disease

A

AgeInfectionTraumaDevelopmental dystrophiesObesityAutoimmune conditions

453
Q

what are the clinical signs of degenerative joint disease

A

LamenessWorst with exercise, weather changes, inactivityMuscle atrophyJoint inflammation and crepitusDecrease in activity, gait change

454
Q

how do you diagnose degenerative joint disease

A

history and PE radiographs

455
Q

describe degenerative joint disease

A

Narrowed joint spaceBone sclerosisOsteophytesJoint effusionNon-inflammatorySeverity of lesion not indicative of pain

456
Q

how do you treat degenerative joint disease

A

PalliativeWeight lossPain management (monitoring)Low impact exerciseSpecialized dietsPhysical therapySurgeryJoint replacement or excision

457
Q

what is hip dysplasia

A

Very common ☹Abnormal development of coxofemoral jointJoint laxityLeads to DJDMost common in large breeds

458
Q

what causes hip dysplasia

A

GeneticExtra nutrients in diet

459
Q

what are the clinical signs of hip dysplasia

A

VariableLameness, bunny hopReduced range of motionMuscle atrophy

460
Q

how do you diagnose hip dysplasia

A

History & PESubluxation testRadiographsSpecial protocols: OFA, PennHIP

461
Q

how do you treat hip dysplasia

A

Medical managementSurgical optionsTPO (triple pelvis osteotomy)THR (total hip replacement)FHO (femoral head osteotomy)

462
Q

what is osteochondritis dissecans

A

Results from abnormal bone formation from cartilage precursors.Leads to retention of excessive cartilage in the jointForms flaps and breaks off in joint spaceDebris can lead to synovitis and osteoarthritis

463
Q

what are the most common sites of osteochondritis dissecans

A

ShoulderElbowStifleTarsal jointMost common in large and giant breeds

464
Q

what are the clinical signs of osteochondritis dissecans

A

4-8 mo oldLamenessInflammation, joint effusionMuscle atrophy

465
Q

how do you diagnose osteochondritis dissecans

A

Signs and history, PERadiographsCytology to rule out infectiousArthroscopy

466
Q

how do you treat osteochondritis dissecans

A

Removal of joint debris + curette to stimulate new formation of cartilageNSAIDSWeight controlPrognosis depends on joint (+: shoulder, stifle; -: elbow, tarsus) and degree of damageLikely genetic so stop breeding

467
Q

what is patellar luxation

A

Patella no longer stays confined to femoral grooveMedial or lateral movementCan be uni or bilateralCan lead to osteoarthritisToy and small breedsMostly genetics

468
Q

what are the clinical signs of patellar luxation

A

Can develop very earlySkipping lamenessAbnormal leg position: bow legged or knock-kneedRarely painful

469
Q

how do you diagnose patellar luxation

A

History, Signs, PEOrthopedic examRadiographs to evaluate changes

470
Q

when do you do surgery for patellar luxation

A

If animal symptomaticConsidered for grade 2 and overReconstruction of soft tissue and groove (mostly)

471
Q

what is a cranial cruciate ligament rupture

A

Most common causes of hindlimb lamenessTear or rupture of stifle stabilisation ligament

472
Q

what causes CCL

A

TraumaAutoimmune diseaseConformational deformity (genetic)40-60% of dogs that have CCL in one knee will, at some future time, develop a similar problem in the other knee.

473
Q

what are the clinical signs for CCL

A

Lameness, non-weight bearingPainJoint effusionMuscle atrophyDrawer sign: Radiographs

474
Q

how do you treat CCL

A

MedicalWeight loss, Physical therapyNSAID, analgesics, joint supplementsSurgicalBest treatment optionDone to restore stability, not repairOsteotomy or suture technique

475
Q

what is intervertebral disk disease

A

Degeneration and protrusion of the disk located between the vertrebraPuts pressure on spinal cord, causing CNS signs

476
Q

which animals are genetically pre-disposed to intervertebral disk disease

A

Genetic predisposition in chondrodystrophic dogsDachshunds, Shih Tzus, Lhasa Apsos, Basset, Corgis, Beagles, Cocker

477
Q

what are the clinical signs of IVDD

A

Neck and back painMuscle spasm (stiff, round back)Ataxia, paraplegia, toe knuckling

478
Q

how do you diagnose IVDD

A

History, signs and PENeurological examRadiographs/CT

479
Q

how do you treat IVDD

A

Conservative treatment with cage rest, confinement, and pain medicationsfirst episode and the neurologic deficits are mildSurgeryMore severe casesLoss of deep sensation requires emergency surgeryPrognosis is variable

Vet Nursing (27 decks)

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