Pathology Exam Ii Additional Cards Due To Cram.com F-Up

Front 1

Renal parasites

Back 1

-require urinary tract for perpetuation
-Stephanurus dentatus (in pigs)
-Dioctophyma renale (dogs, humans)
-Klossiella (horses, guinea pigs, mice)
-Encephalitozoan cuniculi (rabbits, dogs)
-Toxocara canis (dogs)
-Capillaria plica (dogs)

Front 2

Primary Renal Neoplasia

Back 2

-Adenoma
-Carcinoma
-Nephroblastoma
-Transitional Cell Carcinoma

Kidney is usually the recipient of neoplasms, rarely the primary site

Front 3

Neoplasms that metastasize to Kidneys

Back 3

-Lymphosarcoma
--infiltrative, expansile, tan masses
--Most common neoplasm in the kidney
-Mast cell tumor
-Hemangiosarcoma
-Malignant melanoma

Kidney is usually the recipient of neoplasms, rarely the primary site

Front 4

Renal adenoma

Back 4

-Spherical mass of renal tubule epithelium cells

Front 5

Renal carcinoma

Back 5

-AKA clear cell carcinoma
-Malignant
-Most commonly reported in dog an ox
-Neoplastic tubule epithelium
-Papillary, tubular, or acinar patterns
-Metastases go to lungs
-Histologically have cuboidal cells that do not stain heavily

Front 6

Nephroblastoma

Back 6

-AKA embryonal nephroma
-Most common in pigs
-Not usually malignant
-Also seen in dog, chicken, rabbit
-Bulbous, encapsulated, firm mass
-Grossly similar to lymphosarcoma
-Complex mixture of connective tissue and primitive nephrons
-Neoplasm tries to replicate the entire nephron, not just one cell type

Front 7

Transitional Cell Carcinoma

Back 7

-Neoplastic transformation of the pelvic urothelium
-More commonly occurs in lower urinary tract

Front 8

Acute Renal Failure

Back 8

-Acute Tubular Necrosis is most common cause for Acute renal failure
-Patients are weak and depressed
--due to altered metabolism
-Anuria or oliguria are common presenting signs
--due to reduced renal blood flow or obstructive casts in tubules
-Prerenal: due to decreased blood flow
-Intrarenal: due to infarct
-Postrenal: due to obstruction in urine outflow

Front 9

Acute renal failure chemical chemistry

Back 9

-Azotemia
-High blood-urea nitrogen
-High creatinine due to decreased filtration

Front 10

Chronic Renal Failure

Back 10

-Usually insidious, progressive, and lethal
-Sometimes preceded by acute renal failure episode
-Most nephrons are physiologically impaired and microscopically abnormal
-Some fully functional nephrons are present, but few and far between
--too few for homeostasis
-

Front 11

Uremia

Back 11

-Clinicopathologic syndrome due to prolonged azotemia
-Signs due to prolonged azotemia
-Extra-renal clinical effects of renal failure
-Depressed, nauseated, uncomfortable patients

Front 12

Azotemia

Back 12

-Elevated urea nitrogen
-BUN
-NOT the same thing as uremia

Front 13

Clinical Hallmarks of Chronic Kidney disease/Chronic Renal Failure/ End-stage Renal Disease

Back 13

-PU/PD
-Isosthenuria, inability to concentrate urine
-Azotemia and hyperphosphatemia
-Nephrotic syndrome
-Uremia

Front 14

Gross appearance of end-stage kidney

Back 14

-Wrinkled, granular surface texture
-Slightly shrunken and firm
-Pallor and firmness due to generalized fibrosis
-Minute cysts in cortical parenchyma
-Reduction in cortical mass
-Adhesion of cortex to capsule

Front 15

Histological appearance of end-stage kidney

Back 15

-Atrophic and ectatic tubules
-Regenerating tubule epithelium
-Cystic bowman's capsules
-Sclerotic glomeruli
-Periglomerular and intertubular fibrosis
-Casts
-Lymphocyte and pasmocyte inflammatory cell infiltrate
-Tubule mineralization

Front 16

Systemic effects of Uremia

Back 16

-Anemia
-Alimentary tract erosion and ulcers
-Secondary hyperparathyroidism
--elevated P
--bound Ca
--PTH stimulation
--Demineralization of bones
-Dystrophic mineralization
-Atrial endocardial mineralization
-Pleural "frosting"
-Arteriolar necrosis
-Severe edema in lungs and intestines
-Emaciation
-Encephalopathy

Front 17

Alimentary tract ulceration due to Uremia

Back 17

-Ulcerative glossitis near areas of tooth contact
-Halitosis
-Gingivitis
-Erosive to ulcerative gastritis

Front 18

Feline Renal Transplantation Post-op complications

Back 18

-Hypertension
-Hypoperfusion
-Fibrosis
-Hydronephrosis
-Transplant rejection
-increased incidence of lymphosarcoma

Front 19

Lower Urinary Tract

Back 19

-Ureters
-Bladder
-Urethra

Front 20

Ureters

Back 20

-Part of lower urinary tract
-Propel urine from kidneys to bladder
-Lined by urothelium (transitional epithelium)
-Ureteral peristalsis due to circumferential and longitudinal smooth muscle
-Enter bladder at trigone
-Oblique angle of entry prevents retrograde flow with bladder distention

Front 21

Bladder

Back 21

-Lower urinary tract
-Sole purpose is to hold urine
-HUGE distendability
-Intraluminal pressure does not increase until quite enlarged
-Smooth muscle wall and transitional epithelium (urothelium) are thick when bladder is empty

Front 22

Urothelium

Back 22

-Transitional epithelium
-Resists leakage and absorption of urine
-Highly stretchable
-Uroplakins in umbrella cells increase surface area

Front 23

Round ligaments

Back 23

-Remnants of umbilical arteries

Front 24

Urethral Crest

Back 24

-Zone between bladder and beginning of the urethra

Front 25

Ureteral Lesions due to Trauma

Back 25

-Mistake from surgery, errant ligation
-Necrosis due to urolith formation
-Blunt trauma, hit by car
--rupture does not occur when bladder is empty
-Ruptured bladder of foals due to parturition
-Bladder eversion due to severe dystocia

Front 26

Persistent urachus

Back 26

-Common in puppies and foals
-Urine dribbles at umbilicus
-Easy route for ascending infection

Front 27

Urachal remnant

Back 27

-Nipple-like or saccular pouch at the tip of the bladder
-Results in incomplete emptying of the bladder urine
-Nidus for infections and/or urolith formation

Front 28

Ectopic Ureters

Back 28

-Ureters enter at an abnormal spot, NOT at bladder
-abnormal distal ureter insertion site
-predisposes animal to ascending infections
-Usually recognized by dribbling urine

Front 29

Ureteritis

Back 29

-Extension of cystitis and pyelonephritis

Front 30

Bacterial Cystitis

Back 30

-Bacteria is normally inhibited by urine flow and mucosal IgA
-Leukocytes cannot function in urine
-Signs: pollakiuria, stranguria, hematuria, inappropriate voiding
-Bacteria can spawn uroliths
-Bacterial urease creates ammonium ions, increases pH, alkalinizes the urine
-Will get struvite precipitates

Front 31

Bacteria Cystitis pathogens

Back 31

-Staphylococcus
-Enterococcus
-Klebsiella
-Proteus
-Streprococcus
-E. coli is extremely common
-Fimbral adhesion factors attach to urothelium
--adhesion virulence factor is essential, otherwise bacteria would be flushed away

Front 32

Struvite

Back 32

-Magnesium ammonium phosphate crystals
--normal constituent of urine
-May precipitate in bladder due to cystitis
-Most common form of urolith
-Prisms
-Caused by diet and/or infection, associated with bacterial infection
-Common in dogs, cattle, cats

Front 33

Bladder Neoplasia

Back 33

-Transitional Cell Carcinoma
--often is advanced before recognized
-Squamous Cell carcinoma
-Leiomyoma

Front 34

Features of Cystitis

Back 34

-Hyperemia
-Edema
-Hemorrhage
-Ulceration
-Exudate
-Small numbers of lymphocytes and plasma cells are normal, inflammation increases leukocyte component
-Chronic inflammation causes proliferative changes
-Ammonia odor due to bacterial ureases liberating ammonia ions

Front 35

Cytological evidence for Cystitis from urine sediment smear

Back 35

-Neutrophils (pyuria)
-Bacteria
-Sloughed dysplastic epithelium
-RBCs
-Aggregates of crystals

Front 36

Urolith

Back 36

-Visible concretion found anywhere in the urinary tract
-Formed by the precipitation of crystalline mineral on organic matrix
-Free-floating crystals are NOT uroliths
-Can form anywhere from renal pelvis to urethra
-Accrete on necrotic tissue and by layering of crystals
-Gross identification is unreliable, need mineral analysis
-Morphology varies with incorporation of different pigments, textures, and sizes
-Formation is due to diet, water intake, urine pH, and secreted cofactors

Front 37

Consequences of Urolith Formation

Back 37

-Bladder necrosis
-Bladder rupture
-Hydroureter
-Hydronephrosis
-Cystitis
-Injury and inflammation to mucosa
-Obstruction
-Pain
-Death

Front 38

Urolith formation

Back 38

-Related to diet
-Need a nidus to get crystals to start growing
--Anything can become a focus
-Crystals grow in layers
-Can grow into obstructive plugs
-Can form anywhere along the urinary tract

Front 39

Urolith Etiology

Back 39

-Usually an infection or nutritional issue
-Inborn errors in metabolism
-Abnormal mineral intake
-Decreased water intake
-Altered urine pH
-bacterial cystitis

Front 40

Struvite formation and Bacteria

Back 40

-Bacterial ureaases create excess ammonium ions
-Increases pH of urine, more alkaline
-Solubility of struvite changes due to increased pH
-Crystals can form

Front 41

Sterile Struvite Uroliths

Back 41

-Due to calculogenic diets
-High grain rations for ruminants
-High ash diets for carnivores

Front 42

Feline Urologic Syndromes

Back 42

-Most common in male neutered cats
-Diets with high magnesium and ash
-Uroliths lodge in urethra
-Mucoprotein matrix with struvite gravel
-forms rubbery plug that can be dislodged

Front 43

Feline Lower Urinary Tract Disease
FLUTD

Back 43

-Bacterial or stone/mineral disease
-Half are struvite based
-Can also be due to calcium oxalate, bacterial cystitis, and interstitial cystitis

Front 44

Calcium Oxalate Uroliths

Back 44

-NOT the result of infections
-Due to increased Ca and oxalate excretion in urine
-Incidence of Calcium Oxalate uroliths is about the same as Struvite/MAP uroliths

Front 45

Calcium Carbonate uroliths

Back 45

-Clay-like sludge accumulates when bladder cannot empty completely
-Common cause of urolithiases in sheep and goats
--smooth, bronze colored BBs
--SEVERE problem for males due to urethra and sigmoid flexure
--caused by diets rich in alfalfa and grain
-Common in pet pigs

Front 46

Uric Acid uroliths

Back 46

-Common in Dalmatians due to autosomal recessive defect
-Gout: extracellular deposition of uric acid
--Related to diet and metabolism
--causes ATN and nephritis

Front 47

Allopurinol

Back 47

-Used to treat uric acid stones in dogs
-Inhibits Xanthine oxidase activity, prevents formation of uric acid
-Causes increased excretion of xanthine
--xanthine uroliths are possible as a consequence

Front 48

Silicate uroliths

Back 48

-Common in herbivores grazing plants with high silica content
-Occurs in conjunction with limited water intake
-Silicic acid from plants exceeds saturation point and precipitates

Front 49

Bladder papilloma

Back 49

-Benign
-Fibrous projections covered by normal-appearing urothelium
-Do not confuse with polyps (caused by inflammation

Front 50

Transitional Cell Carcinoma

Back 50

-Common aggressive tumor of urothelium
-Most likely initiated by chemical exposure
-Can arise anywhere from pelvis to urethra
-Signs: pollakiuria, stranguria, hematuria
-Can metastasize into abdominal cavity and spread to lungs and retroperitoneum
-Half of cases metastasize before diagnosis
-Need to do surgical biopsy for confirmation

Front 51

Tumors of Bladder Muscular Tunic

Back 51

-Leiomyoma
-Firm white masses of well-differentiated smooth muscle
-Bladder emptying may be impaired

Front 52

Upper Alimentary System

Back 52

-Extends from lips to the distal esophagus
-Includes salivary glands
-Mucus membranes of the lips, buccal cavity, and oropharynx
-Craniofacial bones
--mandibles, maxillae, palatine, nasoincisive bones
-Teeth and gingiva
-Tonsils

Front 53

Oral cavity components

Back 53

-Gingiva, may have melanin pigmentation
-Papillae on tongue
-Hard palate
-Teeth
-Mucocutaneous junctions of the lips

Front 54

Palatoschisis

Back 54

-Clef palate
-Incomplete fusion of the lateral palatine processes
-Direct communication between oropharynx and nasopharynx
-Results in ineffective swallowing/suckling
-Entrapment of food and fluids in nasal cavity
-increases liklihood of developing aspiration pneumonia
-Can be idiopathic, heritable mutation, or due to teratogens (poisinous plants, viruses)

Front 55

Brachygnathia

Back 55

-Shortness of the mandible or maxilla
-Superior brachygnathia= underbite, maxilla is short
-Brachygnathia inferior= overbite, mandible is short
--horses
-Results in difficult prehension or mastication

Front 56

Epitheliogenesis imperfecta

Back 56

-Defect in formation of epithelium
-Leads to clefts, bullae, ulcers
-May affect haired skin and/or mucosa
-Autosomal recessive mode of inheritance in cattle, horses, and dogs

Front 57

Diseases of the Teeth

Back 57

-Very common in animals
-Dental anatomy is complex
-Dental development is also complex
-Many inductive interactions exist
--ectodermal, neural crest, mesenchymal elements
-Developmental mishaps lead to permanent lesions that predispose animal to periodontal disease

Front 58

Developmental dental anomalies

Back 58

-Adontia: no teeth
-Oligodontia: fewer teeth than normal
-Pseudo-oligodontia: failure of a tooth to erupt, delayed eruption
-Polydontia: Supernumerary teeth, too many teeth
-Pseudopolyodontia: retained deciduous teeth
-Heterotropic polyodontia: extra teeth outside dental arcade
--results from misplaced or displaced tooth germ

Front 59

Malocclusion

Back 59

-Developmental dental anomaly
-Makes prehension and mastication difficult
-Common in animals whose teeth continue to grow (rodents)
-If untreated, can lead to penetration and abscessation of facial structures

Front 60

Tetracyclines and Ameloblasts

Back 60

-Tetracyclines can be toxic to ameloblasts
-will lead to enamel hypoplasia and yellow discoloration

-Incorporated into all mineralizing tissues
--used in labeling expriments

Front 61

Congenital Erythropoietic porphyria

Back 61

-Genetic enzyme deficiency in cats, cattle, swine, and humans
-Leads to tooth discoloration, hemolysis, and renal disease
-Stains teeth brown

Front 62

Odontodystrophies

Back 62

-Diseases during tooth development
-Can lead to permanent defects in hard tissues of the teeth and eventual decay
-Enamel, dentin are affected
-Bovine fluoride toxicity is an example
--enamel defects with pitting of the teeth and advanced tooth decay

Front 63

Nutritional causes of Odontodystrophies

Back 63

-Diseases during tooth development
-Bovine fluoride toxicity
-caused by vitamin A or calcium deficiency
-Can also be due to malnutrition
-Enamel defects with pitting of the teeth and advanced tooth decay

Front 64

Infectious causes of Odontodystrophies

Back 64

-Canine Distemper Virus
-Bovine Diarrhea Virus
-Viruses are toxic to ameloblasts (enamel forming cells)

Front 65

Dental Attrition

Back 65

-Loss of a tooth surface by mechanical wear
-WEAR
-Wave mouth: dental arcade with teeth that wear at different rates
-Shear mouth: development of sharp points that are not worn by normal masticatory grinding
-Severe versions can be prevented by floating teeth
-If untreated, can result in malnutrition

Front 66

Dental plaque

Back 66

-Bacterial biofilm
-Adheres to enamel surface
-Resistant to removal by salivary flow
-Usually gram+ aerobes or gram- anaerobes
-Plaque eventually becomes tarter
-Invisible on gross examination
-Can pack into the gingival sulcus
-Often involved in the pathogenesis of dental cavities and gingivitis

Front 67

Dental calculus

Back 67

-Tarter
-Mineralized dental plaque
-Amalgam of mineralized salivary secretions
-Calcium carbonate and dead bacteria, may also contain food particles and cell debris
-Firmly attached to tooth surface

Front 68

Dental Caries

Back 68

-Cavities
-Demineralization with enzymatic degradation of the tooth
-Erosions in hard tissues of the teeth
-Very common in humans
-Occurs in sheep, horses, rare in dogs and cats
-Organic acids produced by plaque bacteria initiate demineralization process
-Enzymatic demineralization by organic acids

Front 69

Gingivitis

Back 69

-Periodontal disease
-Inflammation with blunting of the free gingival margin
-Impaction of food and foreign material in the gingival sulcus
-Buildup of calculus and bacterial colonization initiates gingivitis
-Can progress to periodontitis

Front 70

Periodontitis

Back 70

-Inflammation of the periodontal membrane
--connective tissue layer connecting teeth to alveolar bone
-Occurs most commonly as an extension of gingivitis

Front 71

Chronic gingivitis and periodontitis

Back 71

-Blunting and recession of the free gingival margin
-Alveolar bone resorption
--Loosening and loss of teeth
-Periodontitis and tooth rot abscesses result
-May extend into the pulp cavity
-May result in osteomyelitis
-Secondary fibrogingival hyperplasia will occur
-In end-stage, tooth roots will be exposed

Front 72

Histology of Periodontitis

Back 72

-Bacterial plug forms between tooth and gingiva
-With progression, can see erosion and sloughing og epithelial surface of gingiva
-Will see erosion of pink cementum adjacent to tooth

Front 73

Feline Odontoclastic Resorptive Lesions

Back 73

-Idiopathic syndrome of cats
-Affects subgingival neck or upper tooth rooths of cheek teeth
-Red and swollen gingiva with periodontitis
-Odontoclast resorption of cementum and dentin
-Bone and tooth is eroded by activated osteoclasts
-Have to remove teeth to treat

Front 74

Equine Infundibular Necrosis

Back 74

-Food gets packed into infundibular occlusal surfaces of maxillary M1
-Can progress to pulp of the tooth and lead to tooth rot and abscesses
-Tooth root fracture may occur, causes sinusitits
-Bad smelling nasal discharge may be present
--bacteria gets into maxillary sinus from tooth root

Front 75

Pulpitis histology

Back 75

-Pulp cavity shows inflammation and osteocementum (reactive bone)
-On X-ray can see lysis and bone proliferation

Front 76

Upper Alimentary System Types of Inflammation

Back 76

-Stomatitis: in oral cavity
-Cheilitis: lips
-Glossitis: tongue
-Pharyngitis: pharynx
-Catarrhal: mucous
-Proliferative: thickened epithelial layer, hyperplastic
-Fibronecrotic: diphtheritic membrane, pseudomembranous colitis

Front 77

Causes of Inflammatory disease of the Oral Mucosa

Back 77

-Infectious agents (viral, fungal, bacterial)
-Trauma and foreign bodies
-Chemical or electrical injury
-Intoxication
-Immune-mediated disease
-Systemic disease
-Unknown etiologies

Front 78

Clinical signs of upper alimentary inflammation

Back 78

-Anorexia
-Weight loss due to painful mastication
-Hypersalvation
-Papules: small elevated lesions
-Vesicles and bullae
-Erosions
-Ulcers
-Diphtheritic membranes and necrotic foci

Front 79

Oral erosions

Back 79

-Circumscribed areas of epithelial cell denudation
-Denudation down to the basement membrane but not below
-Stops at basement membrane

Front 80

Oral Ulcers

Back 80

-Focal defects in mucosa
-Extend below the basement membrane

Front 81

Candidiasis

Back 81

-Superficial stomatitis
-Thrush
-Fungal yeast
-Common in dogs, pigs, foals
-Parakeratotic lingual epithelium has embedded Candida yeast
-Squamous mucosa of the tongue proliferates and mixes with fungal yeast
-Will have altered epithelial turnover and oral microfloral populations
-May be result of prior antibiotic use or immunosuppression

Front 82

Vesicular diseases of oral mucosa

Back 82

-Occur in most domestic animals
-Accumulations of serous fluid between epidermis and lamina propria
-basement membrane remains intact
-Usually no bleeding
-Mechanical disruption can lead to erosions
-Regeneration and re-epithelialization can occur if no other complications

Front 83

Foot and Mouth Disease

Back 83

-Viruses causing of Vesicular Disease
-Aphthovirus
-Affects cloven hoofed animals
-Cattle, sheep, goats, pigs
-Will have ulcers on the tongue, teats, and coronary bands
-Hypersalivation
-High morbidity with low mortality
-Animal disease with HUGE economic impacts

Front 84

Foot and Mouth Disease Pathogenesis

Back 84

-Respiratory epithelium infection becomes viremic
-Will have ballooning degradation, desmosome stretching and acantholysis
-Vesicles form with neutrophil infiltrates
-Vesicles coalesce to bullae
-Bullae rupture in 12-24 hours
-Ulceration leads to re-epithelialization or secondary infection

Front 85

Foot and Mouth Disease lesions

Back 85

-Nose
-Mouth
-Feet
-Udder
-Coronary Band

Front 86

Feline Calicivirus

Back 86

-Oral vesicular disease, part of Feline Upper Respiratory Disease Complex
-Lingual and oropharyngeal vesicles lead to ulcers
Histologically will see foci of pyknotic/necrotic cells in stratum corneum
-Virus is often isolated from cats with chronic stomatitis and gingivitis
-Cat will be anorexic and hypersalivating

Front 87

Erosive and Ulcerative Disease

Back 87

-Characterized by erosions and ulcers that are NOT preceded by vesicles or bullae
-BVD
-Malignant Catarrhal Fever
-Bluetongue Virus
-Can be caused by chronic renal disease or chemical/electrical urns

Front 88

Bovine Viral Diarrhea

Back 88

-Caused by bovine pestivirus
-Has world-wide distribution
-Usually low mortality

Front 89

BVD Pathogenesis

Back 89

-Epithelial cell necrosis along entire alimentary tract
-Lymphoid necrosis
-Leads to alimentary erosions and ulcers
-Will have bloody or non-bloody diarrhea with enteritis
-Early embryonic death, fetal malformations, abortions
-Immunosuppression results from lymphoid depletion

Front 90

Malignant Catarrhal Fever

Back 90

-"Snot Sickness"
-Occurs in cattle, wild ruminants, goats
-Caused by lymphotrophic Gammaherpes viruses
-Causes severe systemic disease
-T-cell mediated graft vs. host type reaction
-Lymphoproliferation
-Multi-organ necrotizing vasculitis
--petechia and ischemic necrosis of overlying epithelium
--Corneal edema
-Erosive-ulcerative mucosal and cutaneous lesions

Front 91

Bluetongue Virus

Back 91

-Caused by an Orbivirus
-Transmitted by Culicoides gnats
-Causes severe systemic disease
-Infection and necrosis of vascular endothelium
-Lymphoproliferation
-Multi-organ necrotizing vasculitis
-Erosive mucosal and cutaneous lesions
-Petechia and ischemic necrosis of underlying epithelium
-Corenal edema

Front 92

Feline Rhinotracheitis

Back 92

-Herpesvirus
-Directly attacks and kills epithelial cells
-Mostly in oral cavity, on skin, and other sites
-Causes erosions and ulcers on tongue and lip
-Necrotizing tracheitis and bronchitis lead to secondary bacterial infection

Front 93

Infectious Bovine Rhinotracheitis

Back 93

-Herpesvirus
-Directly attacks and kills epithelial cells
-Causes erosions and ulcers of tongue and lip
-Necrotizing tracheitis and bronchitis that lead to secondary bacterial infections
-Causes late-term abortions in horses and cattle

Front 94

Uremic Ulcers

Back 94

-Common in cats and dogs with renal failure
-Bilaterally symmetrical
-On ventral and lateral surface of the tongue
-Usually secondary to a vasculopathy

Front 95

Parapoxviruses

Back 95

-Bovine papular stomatitis
-Contagious ecthyma
-Causes necrosis
-Virus attacks epithelial cells, induces epithelial proliferation with viral inclusion bodies
-Epithelial degeneration and formation of pustules occurs, leads to ulcers
-Most often at musculocutaneous junctions

Front 96

Oral Necrotizing Diseases

Back 96

-Heterogenous diseases
-Characterized by necrosis of the oral epithelium and underlying tissue
-Often accompanied by inflammation
-Can be due to foreign bodies or trauma
-Oral necrobacillosis
-Actinomycosis (lumpy jaw)
-Actinobacillosis (wooden tongue)

Front 97

Oral necrobacillosis

Back 97

-Acute necrotizing and ulcerative lesion
-Affects oral cavity, pharynx, maybe esophagus, tracheal, larynx
-Organisms produce endotoxins and exotoxins
--leads to extensive mucosal coagulation necrosis
-Gross lesion is a necrotic grey plaque surrounded by a zone of hyperemia
-Can occur secondary to trauma, viral stomatitis, or tooth eruption
-Tend to see in younger animals
-Facultative anaerobes, smell BAD

Front 98

Actinobacillosis

Back 98

-Wooden Tongue Disease
-Caused by actinobacillus lignieresi
--Gram- coccobacillus, normal component of oral microflora
-Lesion is a deep pyogranulomatous glossitis with clumps of organisms that form sulfur granules
-Leads to fibrosis of the tongue
-Tongue becomes enlarged and very firm

Front 99

Actinomyces bovis

Back 99

-"Lumpy Jaw"
-Caused by Actinomyces bovis
--gram+ filamentous bacteria
-Causes pyogranulomatous cellulitis and osteomyelitis
-Extensive bone lysis and proliferation
-Extends into the bone of the jaw

Front 100

Tumors and Tumor-like lesions of the Oral Cavity

Back 100

-Neoplasms and proliferative lesions are common in the oral cavity
-Diagnose based on history, physical exam, radiology, and biopsy
-May cause bleeding, pain, halitosis, difficulty holding and chewing food, swelling, excessive salivation

Front 101

Fibrogingival hyperplasia

Back 101

-Proliferative, non-neoplastic lesion in the oral cavity
-Common in dogs and cats
-Mostly due to chronic inflammation associated with gingival disease
-Most cases seen in older dogs
-Lesions may be diffuse, multifocal, or solitary
-Edema, cell infiltration, fibrovascular tissue proliferation cause bulk of mass

Front 102

Eosinophilic Granulomas

Back 102

-Occur in oral cavity of cats and arctic breed dogs
-Gross lesions are solitary ulcerated masses and plaques
-Can arise anywhere in the oropharynx
-histologically lesions are eosinophilic granulomatous inflammation with multifocal flame figures

Front 103

Plasmacytic Stomatitis

Back 103

-Unique to cats
-Focal to multi-focal raised hyperemic gingival plaques
-Histologically looks like severe submucosal plasmacytic inflammation
-May have underlying viral association
-Inflammation of plasma cells in oral cavity
-Cat will be anorexic and hypersalivating

Front 104

Calcinosis Circumscripta

Back 104

-Occurs in large-breed dogs on tongue
-Mineralized granulomatous foci
-Metastatic ossification may occur over time
--osseous metaplasia
-Round, raised granulomas surrounding mineralized foci
-Benign

Front 105

Epulis

Back 105

-Benign proliferation of gingiva in the oral cavity

Front 106

Epulides

Back 106

-Tumors of periodontal ligament origin
-Frequently seen in dogs, less often in cats
-Fibromatous Epulides are benign
-Acanthomatous Epulides are bad news
--ameloblast origin, AMELOBLASTOMA
-Vary in microscopic appearance and clinical behavior

Front 107

Fibromatous Epulis

Back 107

-Of Periodontal Ligament Origin
-Benign masses arising near the teeth
-Can be single or multiple

Front 108

Fibromatous Epulis of Periodontal Ligament Origin

Back 108

-Benign masses near teeth
-Can be single or multiple, multi-focal to coalescing
-Firm, epithelium covered lesions
-May interfere with mastication
-Can cut out with surgery
-Looks like fibrogingival hyperplasia or acanthomatous epulis
-Histologically have dense cellular stroma of spindle cells and dense collagen
--May also ave osseous, dentinous elements
--remnants of tooth development go crazy

Front 109

Oral Viral Papilloma

Back 109

-Benign oral growths in dogs, cattle, horses
-Occurs mostly in young animals
-May be congenital
-Can arise anywhere in the mouth
-May be focal or multifocal
-Interfere with mastication
-Pedunculated with distinctive roughened irregular surface
-Histologially look very pink with viral inclusion bodies

Front 110

Benign oral neoplasms

Back 110

-Histiocytoma
-Plasmocytoma
-Fibroma
-Ossifying Fibroma
-Granular cell tumor
-Transmissible Venereal Tumor

Front 111

Primary Dental Tumors

Back 111

-Ameloblastoma
--will come back with surgical excision
-Ameloblastic fibro-adenoma
--from enamel, dentin, osseo-cementous material
-Complexor compound odontoma
--hamartomatous malformations with "denticles"

Front 112

Acanthomatous Ameloblastoma

Back 112

-Acanthomatous epulis
-Locally aggressive neoplasms
-Grossly may resemble benign stromal proliferations
-Frequently infiltrate bone and cause local tissue destruction
-Do not metastasize
-Characterized by cords and solid sheets of ameloblastic epithelial cells

Front 113

Malignant Oral Neoplasms

Back 113

-Common in dogs and cats
-Rare in large domestic animals
-Accurate diagnosis is needed for prognosis and treatment
-Malignant melanoma and squamous cell carcinoma are most common
-Can also be a fibrosarcoma or a lymphosarcoma

Front 114

Oral Malignant Melanoma

Back 114

-Most common canine oral malignancy
-40% of all tumors in the oral cavity of dogs
-Less common in cats
-Arise anywhere in the mouth or upper lip
-Usually in older dogs
-Malignant behavior
--local tissue destruction
--Rapid metastasis via lymphatics to regional lymph nodes, lungs, r other viscera
-Need to biopsy for ddiagnosis

Front 115

Oral Squamous Cell Carcinoma

Back 115

-Much more common in dogs and cats than in horses and cattle
-In dogs, go to tonsils and gingiva
-In cats, go to sublingual mucosa and gingiva
-Older animals are at greater risk
-Malignant behavior with poor prognosis
--locally aggressive and infiltrative
-Metastasize to regional lymph nodes is most common
-Looks like large, ulcerated tumor with extensive surface necrosis
-Highly infiltrative, will destroy local tissue and bone
-Usually slow to metastasize, except for tonsillar squamous cell tumors in dogs

Front 116

Oral Fibrosarcoma

Back 116

-Relatively common in dogs and cats
-Usually older animals
-Malignant, locally aggressive but seldom metastasize
--stick to mandibles and maxilla
-Usually complete surgical removal is impossible, recurrences are common

Front 117

Diseases of Salivary Glands

Back 117

-Dilation and rupture of the duct system
-Can be a ranula or Mucocele
-Occur after damage to salivary gland or duct
-Saliva leaks out to form cysts or tunnels along the path of least resistance in the tissue
-Lesions may be painful or obstructuve

Front 118

Ranula

Back 118

-Cystic distension of a salivary duct in the floor of the mouth

Front 119

Mucocele

Back 119

-Collection of salivary gland mucus in a nonepithelial-lined cyst
-Can be due to ranula rupture
-Not a true cyst, no epithelial lining

Front 120

Diseases of the Esophagus

Back 120

-Congenital and acquired anomalies are rare
-Can have segmented aplasia or stenosis
-Esophago-respiratory fistulae
-Diverticula

Front 121

Esophagitis

Back 121

-Inflammation of the Esophagus
-Can be chemical, physical, or infectious causes

Front 122

Chemical cause of Esophagitis

Back 122

-Caustic
-Commonly occurs secondary to reflux of gastric acid into the distal esophagus
-Also occurs in foals
-REFLUX
-Mucosa will be thickened and have plaques

Front 123

Physical causes of Esophagitis

Back 123

-Equine choke
-Esophageal foreign body
-Pressure necrosis of the esophageal mucosa

Front 124

Infectious agents as cause of Esophagitis

Back 124

-Systemic diseases (BVD, MCF, BPS, IBR)
-Candida albicans (extends from tongue to esophagus)
-Spirocerca lupi in dogs
--leads to large inflammatory nodules, dysplasia, and neoplasia

Front 125

Esophageal Obstruction and Necrosis

Back 125

-Physical cause of esophagitis
-Can be impaction of ingesta, foreign body, neoplasia, inflammation that reduces lumen diameter, scarring, external compression due to space-occupying mass, persistent right aortic arch
-Idiopathic Muscular hypertrophy
-Pressure necrosis of esophageal wall may result in perforation and cellulitis
-Secondary aspiration pneumonia
-Esophagus is hard to repair, damage leads to euthanization

Front 126

Dysphagia

Back 126

-Swallowing Disorders
-Can be Oral, Pharyngea, crico-esophageal, or esophageal
-can result from pain from inflammation or neoplasia
-Nerve deficits can cause dysphagia
-Primary muscle disease (myasthenia gravis)

Front 127

Megaesophagus

Back 127

-Big esophagus
-Can be congenital or acquired
-hereditary in GSHD, MSCH, GDAN, Wire-haired fox terriers
-Can be acquired due to prior esophagitis or impaction with distal stricture and proximal dilation
--occurs secondary to obstruction or stricture

Front 128

Intestine Physiology

Back 128

-Digests ingesta
-Absorbs nutrients, electrolytes, and water
-Herbivore intestines are longer and more complex
-Has mucosa of epithelial cells and supporting mesenchyme
--lamina propria and mmuscularis mucosa
-Submucosa has blood vessels and lymphatics
-Outer muscularis muscles and serosa

Front 129

Intestinal Mucosa

Back 129

-Has absorptive enterocytes
-Crypt epithelium
-Goblet cells to secrete mucus
-Paneth cells for immune cells
-Enterochromaffin cells for neuroendocrine cells
-M-cells: specialized epithelium for immune function
-Inflammatory cells

Front 130

Innate antimicrobial defense systems in Intestine

Back 130

-INflammatory cells
-intestinal secretions
-Extraintestinal secretions (gastric acid, bile, pancreatic enzymes)
-Non-pathogenic competing microflora
-High rates of epithelial turnover
-Peristalsis

Front 131

Small intestine Anatomy

Back 131

-Slender villi lined by epithelial cells with microvilli
-Microvillus border or enterocytes increases absorptive surface
--also contains digestive enzymes
-More mature cells out towards edges, top of crypts
-Crypts are regenerative epithelium
-GALT
-Leaky intercellular junctions

Front 132

Large intestine Anatomy

Back 132

-Crypts: deep invaginations into glands
-No villi
-Tight intercellular junctions
-Very efficient at absorbing water and electrolytes
-Goblet cells produce mucus

Front 133

Diarrhea

Back 133

-Secretion of abnormally fluid feces
-Accompanied by increased volume of feces
-Increased frequency of defecation

Front 134

Diarrhea mechanisms

Back 134

1. Hypersecretion
2. Exudation/Effusion
3. Deranged intestinal motility
4. Malabsorption/maldigestion

Front 135

Hypersecretion as a mechanism of Diarrhea

Back 135

-Functional derangement
-Active process
-Hypersecretion by structurally intact mucosa
-Mucosa is totally normal, just secreting TONS of fluid
--NO LESIONS
-Can be due to pathogens secreting toxins
-Results in net efflux of fluid and electrolytes

Front 136

Malabsorption/Maldigestion as a mechanism of diarrhea

Back 136

-Passive process, due to osmosis
--osmotic draw of fluids into the lumen
-Can be intestinal or non-intestinal causes
-Intestinal acute loss or impaired function of villous epithelial cells or brush border enzymes
--Villus atrophy
-Intestinal Acute loss of crypt epithelial cells and villus atrophy
-intestinal Chronic high turnover rate of epithelial cells, will have immature enterocytes on the surface
--cannot function as well as mature enterocytes
-Exocrine pancreatic insufficiency
-Chronic liver disease, esp. with biliary obstruction
-Chronic gastritis

Front 137

intestinal microvillus damage

Back 137

-Glycocalyx is removed
-Malabsorptive/maldigestive cause of diarrhea

Front 138

Villus Epithelial Necrosis

Back 138

-Cells at the top of the villi die and disappear
-Maldigestive/malabsorptive cause of diarrhea

Front 139

Villus Epithelial regeneration

Back 139

-Villus may contract and lose surface area
-Cells are immature, do not absorb as well
-Cause of maldigestive/malabsorptive diarrhea

Front 140

Intestinal Crypt necrosis

Back 140

-No crypts, no regenerative tissue to replace enterocytes on villus surface
-No enterocytes, no digestion
-Cause of malabsorptive/maldigestive diarrhea

Front 141

Early Crypt regeneration

Back 141

-Immature epithelium on villi
-Cannot fully digest or absorb nutrients

Front 142

Exudative/Effusive mechanism of Diarrhea

Back 142

-Passive pricess
-Caused by increased capillary or epithelial permeability
-Can be due to hemorrhage, erosion/ulceration, or necrosis
-Lymphatic obstruction can lead to protein-losing enteropathy
--will get fluid in the lumen
-Villus epithelial and lamina propria damage with necrosis
--hemmorhage, fibrin, necrotic debris, inflammatory cells, diphtheritic membrane
-Infiltrative disease, proteins will be lost

Front 143

Deranged intestinal Motility as a cause of Diarrhea

Back 143

-Hypermotility: leads to decreased contact time with mucosa
-Hypomotility: can lead to bacterial overgrowth and production of toxic substances or reduced fermentation
--leads to osmotic or secretory diarrhea
-Abnormal motility can be caused by acute inflammation of the bowel or peritoneum
--functional ileus or GI stasis
-Physical obstruction/strictures, intussusception, foreign body, neoplasm can change motility

Front 144

Enteritis

Back 144

Inflammation of the small intestine

Front 145

Colitis

Back 145

Inflammation of the colon

Front 146

Typhlitis

Back 146

inflammation of the cecum

Front 147

Gastroenteritis

Back 147

inflammation of the stomach and small itestines

Front 148

Enterocolitis

Back 148

Inflammation of small intestine and colon

Front 149

Typhlocolitis

Back 149

Inflammation of cecum and colon

Front 150

Enterotyphlocolitis

Back 150

Inflammation of small intestine, cecum, and colon

Front 151

Proctitis

Back 151

Inflammation of the Rectum

Front 152

Mucoid Exudate

Back 152

-intestinal acute reaction to injury
-Non-specific form of mild enteritis
-Increased mucin production
-increased rates of mature enterocyte sloughing
-Commonly seen with nematode parasitism
--Ostertagia, Hemonchus, Trichostrongylus)

Front 153

Hemorrhagic enteritis

Back 153

-Acute intestinal reaction to injury
-Destruction of the villi
-Can be caused by bacteria (Salmonella) or bacterial toxins (Clostridium perfringens)
-Will have loss of RBCs and plasma proteins
-Can see manifestations of shock due to vasodilation and pooling of blood i the GI tract
-if loosing 1-2ml of blood per villus can be A LOT of blood!

Front 154

Diphtheritic Membranes

Back 154

-Acute intestinal reaction to injury
-Pseudomembranous colitis or enteritis, sits on the surface
-Results from necrosis of the mucosa
-Composed of necrotic cells, fibrin, and neutrophils
-In horses, cattle, and swine caused by Salmonella
-In dogs and cats caused by parvovirus

Front 155

Villus Contraction or Blunting

Back 155

-Acute intestinal reaction to injury
-Smooth muscle contraction within the villus leads to reduction of digestive/absorptive surface area
-Increased rates of enterocyte loss from villus tips (Rotavirus)
-Decreased rates of crypt cell replication (Parvovirus, BVD)
-Histologically looks like villi are shorter and tips are lined by immature/less differentiated enterocytes

Front 156

Villus Atrophy

Back 156

-Subacute to chronic response of intestine to injury
-Vilus contracts initially
-Results from chronic enteric disease and increased enterocyte turnover
-Common with nematode and protozoal parasitism, granulomatous disease (Johne's disease), and viruses

Front 157

Villus Fusion

Back 157

-Chronic intestinal reaction to Injury
-"Clubbing"
-Unknown cause, occurs with chronic disease
-Results in reduction of absorptive surface area

Front 158

Crypt Abscesses

Back 158

-Chronic intestinal reaction to injury
-Dilation of the crypts
-Intraluminal accumulation of necrotic inflammatory cells and sloughed enterocytes
-May result from villus blunting
-Unknown significance

Front 159

Decreased mucous production by enterocytes

Back 159

-Will occur as a reaction to chronic intestinal injury
-Mature mucous cells are replaced with poorly differentiated cells, will have decreased mucus production

Front 160

Lymphangiectasia

Back 160

-Chronic reaction to intestinal injury
-Dilation of lacteals or larger lymphatic vessels
-Result of increased hydrostatic pressure or increased lymphatic drainage
-Fibrosis of the bowel wall leads to imparied motility
-Mesenteric lymph node pathology (fibrosis, neoplastic, or inflamamtory disease)
-Chronic hepatitis with portal hypertension
-Constrictive pericarditis or congestive heart failure with passive congestion
-Inflammation of lymphatic ducts
-Protein or lipids are lost to lumen

Front 161

Granulomatous inflammation

Back 161

-Type IV hypersensitivity reaction
-Activated macrophages become epithelioid macrophages and multinucleate giant cells
-Lamina propria is infiltrated
-Rhodococcus and Johne's disease

Front 162

intestinal fibrosis

Back 162

-Results in impaired peristalsis
-Lymphangiectasia
-Abnormal microflora proliferation
-Bowel contracture/stenosis
-Decreased absorption

Front 163

Inflammatory Bowel Disease

Back 163

-Chronic response to injury due to hypersensitivity reaction
-Gastroenteritis of unknown cause
-Increased numbers of inflammatory cells in lamina propria with chronic villus and crypt changes
-Eosinophilic enteritis can result in segmental thickening of the muscular wall
--muscularis hypertrophy along affected segment
-Can be caused by predisposing conditions including food allergy, hypersensitivity to parasites or other ingested substances, pre-lymphoma

Front 164

Syndromes associated with Inflammatory Bowel Disease

Back 164

-Lymphoplasmacytic gastroenteritis
-Eosinophilic gastroentertitis
-Granulomatous enteritis in horses

Front 165

Equine lymphoplasmacytic Enterocolitis histology

Back 165

-TONS of inflammatory cells in lamina propria
-Loss of crypts
-Villi look consolidated

Front 166

Secretory Diarrheal Diseases

Back 166

-Will have normal small intestine, no morphological changes in gut
-Recovery will be rapid with removal of the inciting cause

Front 167

Secretory Diarrheal Disease Mechanisms

Back 167

-Bacteria colonize the brush border of villous epithelial cells
-bacterial protein "enterotoxin" binds to enterocyte membrane receptors and change cell metabolism
-Will get increased fluid secretion due to increase in cAMP or cGMP
-Common bacteria:
--E. coli (mostly)
--Salmonella
--Shigella

Front 168

Enterotoxigenic E. coli

Back 168

-Causes secretory diarrheal diseases
-Most common in neonates and post-weaned pigs
-Dehydration
-Homogenous fluid-distended small intestine
-Chyle is present in lacteals
-E. coli colonizes the surface of apical villous enterocytes
-Will have normal histological epithelial cell morphology

Front 169

Pathogens of Differentiated Enterocytes: mechanism

Back 169

-Microorganisms replicate in or on villous enterocytes
-Results in Hydropic degeneration, cell death, cell sloughing, villus atrophy
-Repair is rapid and complete
-Tropism of microorganism determines degree of villi atrophy

Front 170

Attaching and Effacing E. Coli

Back 170

-Pathogen of Differentiated Enterocytes
-Intimin bacterial virulence factor causes enterocyte attachment and pedestal formation
-Disrupts microvillus
-Causes malabsorption and maldigestion

Front 171

Cryptosporidium

Back 171

-Pathogen of differentiated enterocytes
-Protozoal organism
-Attaches to absorptive enterocytes and displaces microvilli
-Causes malabsorption and maldigestion
-Dehydration and watery or bloody diarrhea
-Histologically will get villus blunting leading to atrophy and villus fusion
--lymphoplasmacytic enteritis with small intracellular protozoal organisms on enterocyte surface
-On SEM can see cryptosporidia displacing microvilli of venterocytes
--"big butts" squishing microvilli

Front 172

Destruction and Acute loss of Enterocytes

Back 172

1. Coronavirus
2. Rotavirus
3. Coccidiosis

-Epithelial sloughing of villus tips leads to villus blunting and villus fusion
-Malabsorption and maldigestion follows, with osmotic diarrhea

Front 173

Pathogens of Differentiated Enterocytes

Back 173

-Coronavirus
-Rotavirus
-Salmonella

Front 174

Coronavirus/Rotavirus Gross lesions

Back 174

-Fluid filled intestines
-Villous atrophy
-Chyle is absent from lacteals
--cannot digest or absorb nutrients
-Thin-walled appearance to intestines
-Catarrhal or fibrinonecrotic exudate

Front 175

Coronavirus/Rotavirus Histologic Lesions

Back 175

-Degeneration and sloughing of villous enterocytes
-Villus atrophy
-Attenuation of remaining enterocytes
-Lateral fusion of villi

Front 176

Salmonella

Back 176

-Pathogen of differentiated enterocytes that also damages structures in the lamina propria
-Very important pathogen
-Has many different virulence factors
-Enterocyte invasion and necrosis leads to malabsorption
-Also causes exudative diarrhea
-Causes fibrinonecrotic/hemorrhagic/ulcerative entercolitis with diphtheritic membranes
-Septicemia is also common, can invade into blood vessels

Front 177

Salmonella Virulence Factors

Back 177

-Flagella for motility
-Fimbrae for enterocyte adhesion
-LPS endotoxin for invasiveness and to avoid phagocytosis

Front 178

Species affected by Salmonella

Back 178

-Horses: fibrinous and necrotizing typhlocolitis
-Swine: necrotizing and ulcerative colitis or proctitis with vascular fibrin thrombi
--can cause segmental infarction and rectal strictures
-Swine: Enterocolitis and septicemia
-Humans
-Cattle

Front 179

Pathogens of Replicating epithelium (crypts)

Back 179

-Parvoviruses
--Canine Parvovirus
--Feline Panleukopenia
-Cause significant enteric disease in dogs and cats
-Radiomimetic viruses attack replicating cells
--mimic radiation

Front 180

Feline Panleukopenia

Back 180

-Pathogenesis of replicating epithelium (Crypts)
-Attack replicating bone marrow and lymphoid cells
--Lymphoid and granulocytic stem cell depletion
-Secondary viremia with depression and fever
-Viral invasion and replication within crypt cells
--crypt cell necrosis with denudation of villus tips
-Mature enterocytes cannot replace denuded tips, leads to malabsorption and maldigestion
-Villus blunting and fusion can lead to loss of mucosal barrier and septicemia

Front 181

Feline Panleukopenia Clinical signs

Back 181

-Vomiting
-Diarrhea
-Dehydration
-Depsis

Front 182

Feline Panleukopenia Gross characteristics

Back 182

-Necrotizing or necrohemorrhagic enteritis
-Blood in intestinal contents
-Submucosa and mural edema
-Congested serosa with granular appearance
--early signs of peritonitis
-GALT necrosis, looks like "punched out peyer's patches"
-Bone marrow depletion and thymic atrophy
-Cerebellar hypoplasia in kittens

Front 183

Feline Panleukopenia Histology

Back 183

-Crypt necrosis
-Villus blunting and fusion
-Secondary bacterial infection with erosions, ulcers, and possibly peritonitis
-Lymphoid necrosis
--GALT, lymph nodes, and thymus affected
--Peyer's patches are depleted or collapsed
-Bone marrow depletion
-Necrotizing enteritis with crypt epithelial necrosis, villous atrophy and fusion, and submucosal edema

Front 184

BVD

Back 184

-Pathogen of replicating epithelium (crypts)
-Attacks replicating cells
-Causes mucosal crypt cell necrosis
--necrosis leads to erosions and ulcers
-Occurs throughout the entire GI tract, including oral cavity
-Ulcerative enterocolitis, stomatitis, esophagitis, abomasitis
-Lymphoid depletion with immunosuppression

Front 185

pathogens that affect Lamina Propria

Back 185

-Invade system via macrophages
-Cause Granulomatous inflammation
-Johne's disease (ruminants)
-Rhodococcus equi (young horses)
-Mycobacterium avium (horses, primates)
-Histoplasma capsulatum (dogs)
-Idiopathic granulomatous enteritis/colitis

Front 186

Johne's disease

Back 186

-Mycobacterium paratuberculosis
-Pathogen that affects Lamina Propria
-Facultative intracellular bacillus
-Endemic in cattle herds
-Significant cause of chronic diarrhea and emaciation in cattle

Front 187

Johne's disease gross lesions

Back 187

-Granular appearing muscosal surface, sometimes ulcerated
-Thickened, "corrugated" mucosa
-Enlarged mesenteric lymph nodes
-Diffuse granulomatous ileitis
-Mesenteric lymphadenitis
-Villus blunting, atrophy, and fusion
-Protein-losing enteropathy with hypoproteinemia
-Leads to emaciation
-Can see acid-fast bacilli in epithelioid macrophages

Front 188

Pathogens that Cause Proliferative and Hyperplastic Lesions

Back 188

-Cause inflammation or stimulate mucosa to proliferate
-Thickened, granular appearing mucosa
-Thick mucosal folds that appear corrugated
-May have fibrinonecrotic mucosal exudate
-Enlarged mesenteric lymph nodes

Front 189

Lawsonia Intracellularis

Back 189

-Proliferative enteritis in swine and horses
-Replicates in apical cytoplasm of crypt/villous epithelial cells
-Hyperplasia and necrosis of epithelial cells without cell maturation
-Mucosal thickening within immature cells
-Mucosa is thickened by proliferative branched and dilated crypts
-Rod-shaped bacteria in apical portions of cells
-Lack goblet cells
-Foci of necrosis and hemorrhage

Front 190

Forestomach Anatomy

Back 190

-"Distal esophageal dilations"
-Lined by stratified squamous non-glandular mucosa
-In ruminants: rumen, reticulum, and omasum
-In horses: up to margo-plicatus
-Esophageal region has stratified squamous epithelium
-Cardia secretes mucin
-Fundus/body secretes pepsinogen and HCl
-Pylorus secretes mucin and contains G-cells, secrete gastrin

Front 191

Rumen

Back 191

-"Fermentation vat"
-Ingesta is metabolized to volatile fatty acids by microorganisms
-Aglandular mucosa with stratified squamous epithelium
-Saliva is key for digestion

Front 192

Reticulum

Back 192

-Honeycomb pattern of mucosal folds
-Stratified Squamous epithelium with muscularis mucosae

Front 193

Omasum

Back 193

-Stratified squamous epithelium
-more than 100 longitudinal folds with conical papillae
-Absorbs water from ingesta
-Particulate digesta accumulates between the folds

Front 194

Ruminal Tympany

Back 194

-"Bloat"
1. Primary bloat: due to feed types
--diet associated with high protein
--Can be caused by an abrupt change in diet
--Slimy foam traps gas, obstructs cardia and prevents eructation
2. Secondary Bloat: Due to physical or functional failure of eructation
--traps free fluid or gas in rumen

Front 195

Primary Bloat types

Back 195

1. Pasture bloat:
--due to succulent forages high in proteins (alfalfa, clover)
--Proteins stabilize foam and decrease saliva production
--Shifts in microflora produce slime
2. Feedlot Bloat:
--high concentrate diets that reduce saliva production
--Promotes bacterial growth, stabilizes foam and promotes acidosis
--Acidosis leads to ruminal atony, no rumen activity

Front 196

Secondary Bloat

Back 196

-Physical failure
-Esophageal obstruction
-Foreign body
-Stricture
-Extraluminal mass
-Vagal nerve damage
-"Rumen Drinkers" in young calves
-Poor quality diet

Front 197

Rumen Drinkers

Back 197

-Young calves that are bucket fed with open esophageal groove
-Milk gets into rumen too early
-Milk putrefies and ferments, leads to acidosis and rumen atony

Front 198

Gross lesions associated with Ruminal Tympany

Back 198

-Rumen distension leads to overall abdominal distension, mostly on the left side
-Other structures are compressed
-Intraluminal slimy foam or free gas
-Esophageal bloat line, segmental congestion of the mucosa
-Congestion and edema of the tissues of the neck
-Pulmonary atelectasis

Front 199

Hardware Disease

Back 199

-Traumatic Reticuloperitonitis and Reticulopericarditis
-Cow ingests some sharp foreign body, which falls into the reticulum
-Transmural perforation of the reticulum
--diaphragm
--pericardial sac and pleura
-Ruminal contents and flora can leak into pericardial or peritoneal space
-Will cause septic peritonitis or pericarditis
-Cow can wall off infection
-Can lead to adhesions or heart failure

Front 200

Rumen Acidosis

Back 200

-"Chemical Rumenitis," grain overload, lactic acidosis
-Often leads to secondary bacterial or fungal infections
-Ulcerative and inflammatory condition
-Caused by ingestion of too much concentrated feed rich in starch, overload of carbohydrate
-Can affect the rumen, retiulum, and omasum

Front 201

Rumen Acidosis Pathogenesis

Back 201

1. Rapid fermentation of Carbohydrate leads to excess production of volatile fatty acids
2. Microflora shifts, changes to microbes of lower pH
3. pH of rumen drops
4. Rumen stops moving, Rumen Atony
-Osmotic pressure increases and fluid flows into the rumen, leads to fluid bloat
-Systemic hemocontraction leads to hypovolemic shock
5. Metabolic acidosis: Causes further shift in microflora, start to produce acid and further lower pH
6. Chemical burn effect leads to erosions and ulcers
7. secondary bacterial or fungal infection
8. Septic invasion of blood vessels
9. Septic emboli go right to liver or to vena cava and heart, then lungs

Front 202

Gross lesions associated with Rumen Acidosis

Back 202

-Dehydration
-Sunken eyes
-Intraluminal grain and abundant fluid in the rumen
-Acid smell of rumen juices
-Mucosa of forestomach will be reddened, may have adherent fibrin and debris
-Ruminal papillae will be blunt
-Erosions/ulcers/infarcts may be present

Front 203

Necrotizing Ulcerative Rumenitis

Back 203

-Consequence of rumen acidosis
-Rumen papilla look detached
-Fibrin and neutrophils can cover ulcer
-May have intravascular fibrin thrombus

Front 204

Ruminal Acidosis Sequelae

Back 204

-Laminitis and sole ulcers
-Rumenitis and ulcers that can become very large
--Heal into star-shaped scars (contraction of myofibroblasts)
-Invasion of opportunistic microbes
-Septic vasculitis
--dissemination via portal vein, leads to liver abscesses
--Dissemination via vena cava to heart and lung

Front 205

Fungal Omasitis
Mucormycosis

Back 205

-Fungal hyphae
-Necrosis with ulcers and fibrino-supprative inflammation
-Fibrin thrombi
-Fungal embolus with fungal hyphae

Front 206

Stomach Mucosa

Back 206

-Organized into folds (Rugae)
-Glands are composed of parietal cells, chief cells, and neuroendocrine cells
-Luminal surface has mucous-secreting cells that develop from mucous neck region
-Mucus cells are on the surface, acid cells are in crypts

Front 207

Components of gastic Mucosal barrier

Back 207

-gastric mucous cell secretions
--prevent back-diffusion of HCl and self digestion
--Mucus lubricates and protects stomach from self-digestion
--Bicarbonate ions act as an acid buffer and neutralize HCl
-Cells are replaced every 3-5 days, have high turnover
--need adequate blood flow for replacement

Front 208

Prostaglandins and Stomach gsatric mucosal barrier

Back 208

-Gastric secretions and cell turnover are under Prostaglandin control
-Control blood flow, secretions, and cell turnover

Front 209

Gastric Digestive Enzyme Secretion

Back 209

-ACh
-Gastrin from G-cells
-Histamine, stimulates acid production
-Has receptors on basolateral membrane
-Pepsinogen secretion from Chief cells
--requires HCl cleavage to activate pepsin

Front 210

Ulcer

Back 210

-Mucosal defect in which entire epithelial thickness has been lost
-Down to or through submucosa
-Craterform lesion with reddened base
-May or may not have fibrin and blood

Front 211

Gastric Ulcer Clinical Signs

Back 211

-Dogs and Cats: vomiting, inappetance, abdominal pain, anemia, melena
-Cattle: partial or complete anorexia, decreased milk production, melena, discomfort
-Horses: anorexia, poor performance, bruxism (grinding teeth)

Front 212

NSAIDS and gastric ulcers

Back 212

-Interfere with prostaglandin synthesis
-Inhibits COX enzymes, leads to decreased prostaglandin synthesis
-Increases secretion by parietal cells
-Decreases bicarbonate secretion by mucus cells
-Decreases blood supply with reduced numbers of replacement mucus cells
-Decreases mucus production

Front 213

Specific causes of Gastric ulcers in dogs and cats

Back 213

1. Direct trauma to mucosal epithelium
-bile reflux from duodenum
-Ingestion of caustic substances
-Penetrating foreign bodies
2. Mast Cell Tumors
-pyloric/anterior duodenal ulcers due to excess circulating histamine, stimulates basolateral membrane cells
3. Gastric Adenocarconimas
4. "Stress" due to epi/norepi release
-increased vasoconstriction with decreased perfusion of gastric wall, can cause regional infarction and small areas of coagulation necrosis

Front 214

Specific causes of gastric ulcers in Dogs and Cats

Back 214

1. Chronic liver disease, decreases gastrin breakdown and increases acid production
2. Corticosteroids, inhibit COX enzyme activation
3. Gastrin-producing tumors

Front 215

Causes of gastric ulcers in Cattle

Back 215

1. Dietary change
2. Heavy grain feeding
3. DA
4. BVD
5. gastric lymphosarcoma

Front 216

Bovine gastric Lymphosarcoma

Back 216

-Leads to ulcers
-Ulcers on thickened abomasal wall
-Manifestation of Bovine Leukemia Virus
-Abomasum is the major predilection site, can also see ulcers in eye, cardiac atria, uterus, and spinal cord

Front 217

Gastric Ulcers in Swine

Back 217

-Pars esophageal predilection site, stratified squamous epithelium
-Ulceration can result in exsanguination, leads to acute death
-No definitive cause has been identified
-Risk factors include gender (castrated males), genotype, season, small particle size of feed, anorexia, high carbohydrate diet, and bacteria presence

Front 218

Gastric Ulcers in Horses

Back 218

-Horses produce acid constantly, need to eat constantly
-Changes in feeding will disrupt normal gastric function
-Margo plicatus predilection site in adults
-Pylorus/proximal duodenum predilection site in foals
-NSAIDS can contribute
-Stress can contribue
-irregular feeding intervals, high grain diets, frequent transport

Front 219

Gross lesions of Gastric Ulcers

Back 219

-Red/brown mucosal depression
-Crater-like lesion
-Older lesions will have raised edges
-Might have fresh or digested blood in the lumen of the stomach or distal intestines

Front 220

Sequelae of Gastric Ulcers

Back 220

-Bleeding, melena, anemia, exsanguination
-Perforation lead to peritonitis
-Can have a secondary infection due to bacteria or fungi
-Healing will lead to fibrosis and a scar

Front 221

Histology of an equine acute gastric ulcer

Back 221

Will have neutrophils, inflammation, fibrin, and granulation tissue
-Can see area with stratified squamous epithelium

Front 222

Acute gastric dilation

Back 222

-Caused by rapid overconsumption of food
-Can be exacerbated by exercise or aerophagia
-Obstruction of the pylorus or cardia can cause issues
-Clostridium perfringens
-Abnormal gastric motility

Front 223

Acute gastric dilation lesions

Back 223

-Stomach is filled with food, fluid, and gas
-Stomach has thin wall
-Pulmonary atelectasis
-Can cause peracute death
--compresses vena cava
--ischemic necrosis of the stomach wall that leads to sepsis

Front 224

Acute gastric Dilation in Horses

Back 224

-Dilation leads to rupture
-Horses cannot vomit
-Increased gastric tension will result in transmural tear along greater curvature
-Hemorrhage and fibrinous peritonitis will follow
-Usually a small rupture

Front 225

Acute gastric Dilation sequelae in dogs, sows, monkeys

Back 225

-Ischemia of the gastric wall
-Leads to compression of the lungs and the posterior vena cava
-Respiratory distress, hypovolemic shock, and cardiac arrythmias can follow
-Death can occur but rarely a rupture

Front 226

DAs

Back 226

-Mostly occur post-calving
-Hypocalcemia (Milk fever) leads to lactic acidosis and atony
-No rumen movement or incomplete filling leads to abomasal displacement
-85% are to left
-15% to right, right can twist and lead to infarct
-Chronic displacements can lead to peritoneal adhesions or abomasal ulcers

Front 227

Gastric impaction

Back 227

-Occurs in horses, cattle, sheep
-Stomach gets distended by roughage
-Caused by poor quality fibrous roughage
--inadequate water intake
--inadequate mastication, may be due to poor teeth
-Can have vagal nerve damage
-Pyloric stenosis
-Abomasal emptying defect
-Usually is a combination of factors

Front 228

Gastritis or Abomasitis

Back 228

-Inflammation of the stomach
-Due to viral, bacterial, fungal, protozoal, parasitic causes
-Can be a manifestation of a hypersensitivity reaction

Front 229

Hemorrhagic gastritis

Back 229

-Typically caused by Clostridium bacteria
-Anaerobic bacteria produces potent exotoxins
--Clostridium perfringens
-Causes abomasal bloat with mucosal necrosis, hemorrhage, and mural emphysema
-In dogs is caused by clostridium perfringens

Front 230

Abomasal Hemorrhage

Back 230

-Caused by haemonchus contortus
-No infection, just severe wasting with anemia and hypoproteinemia
-Loss of blood and proteins

Front 231

Inflammatory Bowel Disease

Back 231

-Eosinophilic gastritis/gastroenteritis
-Seen in dogs, cats, horses
-Type of hypersensitivity reaction
-Can have dietary component
-Eosinophils infiltrate the lamina propria, along with lymphocytes and plasma cells
-Eventual loss of gastric glands and mucosal fibrosis
-Cells crowd into the lamina propria and crowd out everything else
-Subtle mucosal thickening
-Animal will have vomiting and diarrhea

Front 232

Parasitic gastritis

Back 232

-Inflammation
-Hyperplasia of the gastric glands
-Hyperplasia of mucosal lymphoid follicles
-Excess mucus production
--catarrhal exudate
-Mucoid cells go crazy
-Will have "moroccan leather" texture
-Ostertagia in ruminants, leads to proliferative gastritis
-Trichostrongylus in ruminants and horses
-Hyostrongylus rubidus in swine

Front 233

Gastric Neoplasia

Back 233

1. Tumors of mucosa cells:
--squamous cell carcinoma
--Adenocarcinoma (glandular cells)
2. Tumors of the cell wall
--leiomyoma/leiomyosarcoma
--Gastrointestinal stromal tumor (GIST)
3. Tumors from somewhere else
--lymphosarcoma
--Mast cell tumors

Front 234

Oral squamous cell carcinoma

Back 234

-Common in older horses
-Cauliflower-like and ulcerative, expansile
-Fibrous reaction is common
-DEsmoplasia: proliferative response fibrosis
-Carcinomatosis is common
-Secondary ulceration with surface bacterial infection and accumulation of fibrinonecrotic debris

Front 235

Gastric Adenocarcinoma

Back 235

-Most common in the dog
-Infiltrative, ulcerative lesion
-Frequent transmural invasion with desmoplasia and carcinomatosis
-Poor prognosis

Front 236

gastric Lymphosarcoma

Back 236

-Expansion and infiltration of the wall by homogenous, soft, bulging, pale tan tissue
-May or may not have ulceration of the overlying mucosa
-Bovine Leukemia Virus can cause

Front 237

Bovine Leukemia Virus

Back 237

-Retrovirus
-Causes enzootic leukemia in cattle
-Results in multi-organ lymphosarcoma
--GI tract, heart, uterus, spinal cord
-Can see in other species
--dogs, cats, horses
-May be related to FeLV in cats in some cases
-Expansion and infiltration of the wall by homogenous, soft, bulging, pale tan tissue

Front 238

Functional obstructions of the Intestine

Back 238

-Functional intestinal stasis from lack of effective innervation
--leads to reduced peristalsis
-BIG issue in horses
-Caused by:
--surgery
--Peritonitis
--Chronic distention
--Congenital or idiopathic
-Distended, thin-walled, often impacted bowel

Front 239

Congenital Intestinal Stenosis

Back 239

-Nerve issue in large colon
-Predominant in white foals born to "overo-spotted" parents
-Caused by segmental absence of submucosa or myenteric plexus
-Neural crest cells failed to migrate
-Segmental stenosis of the small colon
-Distension of the large/small colon proximal to the stenosis

Front 240

Mechanical obstructions in Intestine

Back 240

-Most common type of obstruction
-Foreign bodies
-Intussusception
-Volvulus/torsion
-Stenosis
-Incarcerations
-Can result in distension and filling with gas
-Bacterial overgrowth with toxins
-Electrolyte imbalance and hypovolemia
-Segmental intestinal ischemia with perforation and septic peritonitis
-Shock and death

Front 241

Causes of intraluminal intestinal obstructions

Back 241

-Foreign bodies
-Enteroliths
-Trichobezoars (hair balls)
-Parasites
-Fecal impactions
-Sand/forage impactions

Front 242

Intussusception

Back 242

-Telescoping of proximal segment of bowel into distal segment
-More common in younger animals
-Causes irritability, hypermobility, dysmotility
-Can be associated with parasitism
--foals: prascaris equorum or anoplocephala perfoliata
--Puppies: toxocara canis, ancylostoma caninum
-Can be due to inflammation, foreign body, or intramural lesion
-Usually the proximal segment goes into the distal segment
-Will have venous infarction, sloughing of inner necrotic portion and healing

Front 243

Gastric Volvulus and torsion

Back 243

-Torsion: rotation of a tubular organ along its long axis
-Volvulus: twisting of the stomach or intestine around its mesenteric axis
-Common in horses, cattle, and swine
-Less common in dogs and rare in cats
-Animal will become shocky, toxemic
-Can lead to peritonitis or perforation

Front 244

Hernia

Back 244

-Displacement of a portion o the intestine through a normal or pathogenic foramen
-Umbilical hernia
-Inguinal/scrotal hernia
-Diaphragmatic hernia
-Epiploic foramen entrapment
-Will have entrapment, strangulation of the blood supply, infarction, and death

Front 245

External hernia

Back 245

-hernia beyond the abdominal cavity

Front 246

Umbilical hernia

Back 246

-Congenital or secondary to omphalitis
-Peritoneum forms sac
-happens most often in calves

Front 247

Inguinal Hernia

Back 247

-Congenital or inherited
-Can be acquired
-Vaginal tunic forms the sac

Front 248

Perineal hernia

Back 248

-Paritoneum forms sac lateral to the rectum
-Occurs in old male dogs with prostatic disease

Front 249

Strangulating Lipomas

Back 249

-Blobs of fat grow in mesentary and wrap around bowel, cut off blood supply
-Common in older horses
-Lipomas on mesenteric stalk
-Segmental infarction and ischemia
-Bacterial translocation with septic peritonitis

Front 250

Intestinal Stenosis or Stricture

Back 250

-Can be due to scarring
-Surgery
-intestinal neoplasm that narrows lumen
-Necrotizing enteritis
--leaves thick, scarred wall with narrow lumen and dilated proximal bowel
-Can have congenital stenosis

Front 251

Equine Verminous arteritis

Back 251

-Strongylus vulgaris
-4th stage larvae enter the intima of small arteries or small intestine and large intestine
-Migrate to anterior mesenteric artery
-Cause thrombosis and thromboemboli, leading to arterial infarction

Front 252

Alimentary Lymphosarcoma

Back 252

-Arises from lymphoid tissue in gut
-Does not involve peripheral lymph nodes
-Can be diffuse infiltrates or discrete solid masses
-Occur in many species
--cats more often than dogs
--horses
--cattle
--sheep, goats, camelids

Front 253

Alimentary lymphosarcoma in the Cat

Back 253

-Most common neoplasm in GI for cats
-Mostly in jejunum or ileum, maybe in liver and kidney
-Causes vomiting, diarrhea, or constipation
-Poor prognosis
-Can be associated with FeLV
-Can be spontaneous

Front 254

Alimentary lymphosarcoma in the cow

Back 254

-Most common neoplasia
-Often associated with Bovine Leukemia Virus infection
-Will have tan, bulging tissue
-HUGE number of lymphocytes and lymphoblasts in tissue

Front 255

GI Adenocarcinoma

Back 255

-Most common GI neoplasia in the dog
-2nd most common GI neoplasia in the cat
-40% are in colon and rectum
-Invasive neoplasms with desmoplasia
-White, firm lesions with stenosis ("napkin ring" lesions)
-Metastasize to regional lymph nodes
-Carcinomatosis is common
-Clinical signs:
--pain on defecation, straining, constipation, blood in feces, pencil-like feces passed

Front 256

Mast Cell Tumors in Intestine

Back 256

-Found within the intestines of cats and dogs
-Associated with gastric and proximal duodenal ulcers
-Due to production of histamine and stimulation of gastric parietal cells to secrete acid

Front 257

Liver embryology

Back 257

-Liver, biliary system, and pancreas all originate from endodermal epithelium of duodenum

Front 258

Liver Anatomy

Back 258

-Made up of many lobes
-Usually a red color

Front 259

Species without gallbladder

Back 259

-Rat and Horse

Front 260

Gallbladder

Back 260

-Cystic duct
--obstruction is no big deal
-Series of hepatic ducts
-Common bile duct
--obstruction is a big problem

Front 261

Liver Blood Supply

Back 261

-Portal vein and hepatic artery supply blood to the liver
-Hepatic artery procides 30% of blood flow to liver, all oxygenated
-Portal vein drains intestinal tract, spleen, pancreas, stomach
--provides 60-70% of afferent blood flow to the liver
--Blood is "used," has low O2 content
--High nutrient content
-Hepatic vein drains the liver, joins the caudal vena cava at the diaphragm
-Liver has discontinuous capillaries, plasma cells bathe the hepatocytes

Front 262

Liver Histology

Back 262

-Liver is divided into lobules
--"lobule" does not really exist
-Central vein bordered by portal triads in corners
-Blood enters liver at hepatic arteriole, travels through liver sinusoids, and collects in central vein
--Central vein enters vena cava from hepatic vein
-Hepatocytes surround sinusoids

Front 263

Portal Triad in Liver

Back 263

-Hepatic arteriole
-Bile duct
-Portal venule

Front 264

Portal Acinus

Back 264

-Branch of the portal triad in the center

Front 265

Hepatocytes

Back 265

-Surround liver sinusoids
-Functional cells of the liver
-Are bathed in blood by discontinuous capillaries
-Oxygenated blood flows from venter to periphery through sinusoids

Front 266

Bile canaliculi

Back 266

-Little canals
-Part of the hepatocyte cell membrane
-Structures between hepatocytes
-Join small biliary ducts that end up in bile ducts
-Bile flows between hepatocytes, from periphery to center in canaliculi

Front 267

Stellate cell

Back 267

-Lives in space of Disse
-Involved in vitamin A metabolism
-Normally contain Fat
-Accumulate in older animals
-Can be transformed into a myofibroblast by cytokine and growth factor stimulation
--leads to fibrosis in the liver

Front 268

Kupffer cells

Back 268

-Fixed macropahges in the liver
-Phagocytic for bacterial and particulate material
-Deals with infectious agents, toxins
-Degrades bacterial endotoxins
-Involved in liver metabolism
-Contain iron from phagocytosed RBCs and lipofuscin/veroid from lipid metabolism
-Collects pigments
-May be necrotic in sepsis and toxemia
-Apoptotic cells may be phagocytosed leading to eosinophilic cytoplasmic inclusions
-Iron will stain with prussian blue

Front 269

Zone 1 of the Liver

Back 269

-Closest to the protal area, periportal
-Highest concentration of oxygenated blood from hepatic artery
-highest concentration of blood nutrients
-Also highest concentration of direct toxins from GI tract (via portal vein)
-Usually more resistant to toxic and anoxic injury or nutritional deficiency
-Higher mitotic activity
-Hepatocytes in this area are most capable of regeneration

Front 270

Zone 2 of the Liver

Back 270

-Intermediate zone between zones 1 and 3
-"Mid-zonal"

Front 271

Zone 3 in the Liver

Back 271

-Closest to the central vein, "centrilobular"
-Lowest in O2 and nutrient supply
-Usually most susceptible to anoxic or toxic injury and nutritional deficiency
-has highest level of P450 enzymes
-Bile canalicular system is farthest from the bile ducts
--most common site for bile casts in intrahepatic cholestasis
-Site of earliest and most persistent fat storage and glycogen synthesis

Front 272

Function of the Liver

Back 272

-Protein synthesis
--albumin, fibrinogen, clotting factors, globulins
-Bile production, metabolism and transport
-Conversion of NH3 to NH2
-Conversion of amines and other toxic compounds of GI origin

Front 273

Albumin

Back 273

-Produced in the Liver
-Main oncotic force in blood
-Pulls fluid back into vessels from interstitium
-If imbalanced or low, can cause edema or ascities

Front 274

Fibrinogen

Back 274

-Major protein for clotting
-Produced in the liver
-Absence can lead to coagulopathies

Front 275

Bile production

Back 275

-Occurs in the Liver
-Hb breakdown is broken down into unconjugated bilirubin, carried to liver by albumin
-Liver takes up biliribun, metabolizes, and exports as conjugated
-Liver produced chlesterol and bile acids

Front 276

Metabolic properties of the Liver

Back 276

-Makes a lot of proteins
--globulins, albumin, fibrinogen, clotting factors
-Metabolizes drugs, endogenous and exogenous steroids
-Metabolizes products from GI tract

Front 277

Ways to Damage the Liver

Back 277

-Drugs
-Toxins
-Inflammatory diseases
-Bacteria, protozoa

Front 278

Pathogenesis of Jaundice

Back 278

-Hyperbilirubinemia
-Indicative of Late-stage liver disease
-Can occur due to:
1. increased breakdown of RBCs (pre-hepatic)
2. Something wrong with the liver (hepatic)
3. Bile duct obstruction (post-hepatic)
-All tissues in the body will turn yellow

Front 279

Hypoalbuminemia

Back 279

-Low serum albumin
-No return of fluid to vessels
--edema and ascites
-

Front 280

What happens when liver is ill

Back 280

1. hyperbilirubinemia
2. Coagulopathies
3. Hypoalbuminenia, leading to ascites or edema
4. Drug toxicities and drug overdoses due to deranged metabolism
5. Hyperammonimea
6. Hepatoencephalopathy

Front 281

Treatment for Primary Liver Disease

Back 281

-Not sure if any of the actually work
-Don't seem to do much harm

Front 282

Reactions to Liver Injury

Back 282

1. Hydropic or Vacuolar degeneration
2. Glycogen accumulation
3. Fatty Liver Change
4. Storage Disorders
5. Necrosis
6. Inflammation
7. Bile Stasis
8. Regeneration
9. Fibrosis
10. Bile Duct Hyperplasia

Front 283

Hydropic or Vacuolar Degeneration
Cell Swelling

Back 283

-Can be a sign of early liver disease
-Something interferes with Na/K ATPase
--anything that affects ATP production
--membrane damage
-Reversible injury
-Excess water enters liver due to inactivation of Na/K ATPase
-

Front 284

Glycogen Accumulation

Back 284

-Common response to changes in the liver
-50% of biopsies from sick liver has glycogen accumulation
-Glycogen accumulates in the cytoplasm
-Can be due to corticosteroids
-Any disease process can lead to glycogen accumulation
-Rarely associated with necrosis
-Will have a large, swollen liver and hepatocytes
-Can be due to hypoadrenocorticism

Front 285

Fatty change/ Hepatic Lipidosis/ Steatosis

Back 285

-Happens in all animals
-Can have many underlying causes, need to figure out real cause
-Accumulation of fat in vacuoles
-Reversible change
-Frequently leads to necrosis
-Liver will be fatty, enalrged, swollen, yellow, friable
-Really severe livers will float on autopsy
-Histologically will look like clear vacuoles filled with fat

Front 286

Causes of fatty liver

Back 286

-Excessive ingestion of fats
-Excessive mobilization of fat
-Excessive fatty acid synthesis and triglyceride formation
--due to CHO intake
-Decreased oxidation of fatty acids due to hepatocyte dysfunction
-Decreased apoprotein synthesis
-Impaired secretion of lipoprotein

Front 287

Storage Disorders

Back 287

-Common in liver, but hard to recognize
-Inherited disorders
-Accumulation of specific compounds in the liver due to excessive ingestion or inherited storage diseases
-Usually compounds accumulate in kupffer cells or hepatocytes
-Need to identify storage product, enzyme deficiency, or defective gene
-Clear, brown, yellow vacuoles or cytoplasmic material, depends on stored material
-May lead to necrosis or dysfunction

Front 288

Necrosis

Back 288

-Cell death
-Individual cells shrink with nuclear fragmentation
-Cell swelling with nuclear pyknosis and cytoplasmic eosinophilia
-Complete dissolution of the cell
-Pattern of necrosis helps in determining the cause of hepatic necrosis

Front 289

Patterns of Necrosis

Back 289

-Help determine cause of hepatic necrosis
-Helps predict prognosis and therapy
-Multifocal random (infectious agents)
--disease spots all around the liver
--almost always infectious
-Massive (toxic and nutritional causes)
--large portions of liver affected
-Zonal (hypoxia or toxins)
--based on different hepatic zones

Front 290

Centrilobular hepatic necrosis

Back 290

-Indicative of ischemia, toxins, metabolic, issue, or vascular issue
-Necrosis will be right around the central lobule
-Most vulnerable zone, furthest from arteries
-Centrilobular area has the highest concentration of P450 enzyme
--indirect toxin is made into a toxic compoun

Front 291

Inflammation of the Liver
Hepatitis, cholangitis, cholangiohepatitis

Back 291

-Very common in the liver
-Rarely occurs without an infection

Front 292

Hepatic Copper Storage Disorders

Back 292

-Progressive process with necrosis and inflammation
-Accumulation of Cu in hepatocytes
-Associated with liver necrosis or inflammation
-Can chelate copper, animals get better
-Availability of copper in dogfood has changed, has increased in last few years
-Inherited predisposition

Front 293

Bridging Hepatic Necrosis

Back 293

-Bridges between two different areas

Front 294

Coagulative necrosis

Back 294

-Can still see outline of the cell
-Due to ischemia, toxins, metabolic diseases
-

Front 295

-

Back 295

-

Front 296

-

Back 296

-

Front 297

Hepatitis

Back 297

-Inflammation of the liver
-Most commonly idiopathic in dogs
-Can be due to bacteria, viruses, protozoa, nematodes, cestodes
-May be primary and lead to necrosis
-May be secondary to necrosis
-Can contribute to ongoing necrosis, fibrosis, and bile duct hyperplasia
-Really difficult to treat, don't really know tht

Front 298

-

Back 298

-

Front 299

-

Back 299

-Inflammation of bile ducts and hepatocytes

Front 300

Bile st

Back 300

-Usually associated with toxins or obstructions
-May also be seen with inflammatory disease
-Occurs in all animals
-Bile is collecting in canaliculi or bile ducts
-Too much bile is metabolized
--intense RBC destruction
-Disease in liver prevents bile from moving
-Duct obstruction backs up bile duct
-Animals are icterus/jaundice
-Can accumulate as yellow-green casts in canaliculi between hepatocytes or intrahepatic bile ducts

Front 301

-

Back 301

-

Front 302

Sequelae of Necrosis and Inflammation in the Liver

Back 302

-Liver is EXTREMELY good at regenerating
-Can remove most of the liver and it will regenerate
-Depends on severity and extent of damage
-Minor liver injuries can regenerate
-Will not regrow the entire liver, but if cut off liver in a small zone it can regenerate
-Periportal hepatocytes and oval cells in biliary epithelium are really good at regenerating
-Possible Sequelae:
1. Regeneration
2. Fibrosis/cirrhosis
3. Bile duct hyperplasia

Front 303

Oval Cell

Back 303

-In Biliary epithelium
-"theoretical cells"
-Can make bile duct epithelium
-Pleuripotential cells, can become hepatocytes or bile duct epithelium
-Start to proliferate with damage
-Will get nodules of hepatocytes divided by collagen
-Non-specific stimulation also leads to bile duct hyperplasia

Front 304

Liver regeneration

Back 304

-Post-necrotic response
-Liver has tremendous reserve and regeneration capacity
-Regeneration depends on severity and extent
-Severity of a toxin can be dose-dependent
-75% of liver can be removed before dysfunction occurs
-Liver can regenerate 80% of its mass and will function if connective tissue framework stays intact
-Chronic, repeated, high toxin dose, lots of infectious agent will lead to more severe problems

Front 305

Multifocal random destruction of the liver

Back 305

-Leads to liquefactive necrosis with neutrophils
-Most likely a bacterial infection

Front 306

Zonal destruction of the liver

Back 306

-All cells in a certain zone are destroyed
-Liver can respond and regenerate completely
--everything can go back to normal
-TOXIN

Front 307

Hepatocyte response to injury

Back 307

1. Damaged Hepatocytes release growth factors
2. Kupffer cells produce transforming growth factor beta
3. Stellate cells are induced to become myofibroblasts, lay down collagen in space of Disse
-Collagen between hepatocytes and sinusoids prevents hepatocytes from being bathed in blood
-Blood is shunted through the liver (BAD)
-Can get fibrosis in the portal area
4. Liver is not functioning, but does not look bad
5. If insult continues, lose normal connective tissue framework of the liver

Front 308

Myofibroblasts

Back 308

-Fibroblast that produces collagen
-Also has actin filaments that allow contraction
-Lay down collagen

Front 309

Chronic response to liver injury

Back 309

-Liver necrosis continues for a long time
-Fibrosis occurs
-Liver may become nodular and less functional
-Can be due to chronic, repeated, high-toxin dose, or lots of an infectious agent
-Results in loss of normal connective tissue framework of the liver
--Basement membrane is lost, cannot regenerate hepatocytes

Front 310

Bile duct hyperplasia and Liver Necrosis

Back 310

-Occurs in every liver that is chronically injured
-With every liver injury and regeneration, will also get bile duct hyperplasia
-Oval cells proliferate non-specifically, produce new hepatocytes AND Bile ducts
-Proliferation of bile duct epithelium in portal areas
-May be associated with necrosis, inflammation, toxins, or blockage of bile ducts
-Non-specific reaction to injury

Front 311

Stages of Liver Fibrosis

Back 311

1. Lining up of collagen along sinusoids
2. bridging fibrosis
--portal-portal
--portal-central
--central-central
3. Diffuse fibrosis with nodules of hepatocytes and bile duct hyperplasia
-Loss of normal connective tissue framework of the liver
-No basement membrane, no regeneration

Stages are a continuum, not a set process

Front 312

Liver fibrosis Steps

Back 312

1. Injury, inflammation, hypoxia with hepatocyte necrosis
2. Proliferation of fibroblasts and myofibroblasts from stellate cells
3. Stellate cells produce collagen in space of Disse
4. Fenestrations in hepatic endothelial cells are closed, blood is shunted from portal vein through the liver and into hepatic vein
--Blood functionally bypasses the liver hepatocytes

Front 313

Liver fibrosis

Back 313

-Post-necrotic and post-inflammatory response
-Almost always occurs in conjunction with hepatocyte regeneration and bile duct hyperplasia
-Hepatocyte regeneration leads to nodules of hepatocytes divided by collagen (Cirrhosis)

Front 314

Transformation of Stellate cells

Back 314

-Stellate cells are normally lipocytes in the liver
-Can be induced to change into myofibroblasts and fibroblasts to produce collagen in response to liver injury
-Jupffer cells produce TGF-b to cause transformation

Front 315

Cirrhosis

Back 315

-Diffuse fibrosis with bridging of the lobular architecture and formation of abnormal vascular anastomoses
-Lots of bridging fibrosis
-Nodules of hepatocytes divided by collagen
-End-stage liver fibrosis, results in liver failure
-Point where liver cannot be fixed, loss of basement membrane
-Liver is non-functional

Front 316

Cat liver fibrosis

Back 316

-Usually do not end up with nodules of regeneration
-Primary disease is cholangitis and cholangiohepatitis
--fibrosis stops at bridging stage

Front 317

Hepatocyte Regeneration

Back 317

-Can regenerate from periportal hepatocytes
-Can regenerate from oval cells

Front 318

Increased vascular pressure due to liver cirrhosis

Back 318

-Portal vein pressure increases due to contraction of the liver parenchyma
-Leads to ascites
-Also leads to portal shunts from portal vein to vena cava
-Decreases osmotic pressure

Front 319

Main points of Cirrhosis

Back 319

1. Diffuse fibrosis
2. Nodular regeneration
3. Bile duct hyperplasia

-May have variable amounts of inflammation or necrosis
-May have bile stasis
-hepatocytes are filled with lipid

Front 320

Gross cirrhotic liver

Back 320

-Tan, brown
-Clear nodules

Front 321

Ascites due to liver cirrhosis

Back 321

-Due to contraction and decreased function
-Portal vein shunt, decreases osmotic pressure
--Multiple shunts of portal vein
--toxins that liver normally filters leads to hepatoencephalopathy
-Portal hypertension
-Hypoalbuminemia due to decreased liver function, decreased oncotic pressure

Front 322

Categories of Liver Disease

Back 322

1. Congenital/inherited
2. Traumatic
3. Circulatory
4. Inflammatory
5. Toxic
6. Hyperplastic and Neoplastic diseases

Front 323

Hereditary hyperbilirubinemia

Back 323

-Animal has inability to conjugate bile
-Exceptionally rare

Front 324

Congenital/Inherited liver diseases

Back 324

-Hereditary hyperbilirubnemia
-Storage diseases
-Diaphragmatic pericardial hernias
-Vascular shunts
-Biliary abnormalities

Front 325

Liver trauma

Back 325

-Liver can be displaced through hernias
-Can be ruptured
--blunt or sharp trauma
-Hemoperitoneum
-Predisposing factors:
--hepatitis
--neoplastic liver
--Fatty liver
--Amyloidosis
-Trauma is not the issue, but what happens because of the trauma (hematoperitoneum)

Front 326

Amyloidosis

Back 326

-Result of Chronic inflammatory diseases
-Can predispose animals to trauma rupture of liver

Front 327

Circulatory diseases of the Liver

Back 327

-Congestion due to right heart failure or obstruction of the caudal vena cava
--can be acute or chronic
-Infarction (rare due to dual blood supply)
-Porto-systemic or porto-caval shunts
-Portal thrombi (uncommon)
-Peliosis hepatis

Front 328

Portp-systemic or porto-hepatic shunts

Back 328

-Relatively common
-Vascular connection between portal vein and caudal vena cava or azygous vein
-Blood bypasses the liver
-May be congenital or acquired
--acquired secondary to portal hypertension from cirrhosis/fibrosis
--Will have multiple shunts
-Can be extrahepatic (larger, small dogs) or intrahepatic (short, large dogs)

Front 329

Chronic passive congestion of the liver

Back 329

-Usually due to heart disease
-Liver is swollen, filled with blood
-Fibrin on the surface of the liver due to getting pushed out from increased pressure in the liver
-Variegated pattern of the liver, looks like nugmeg
-Histologically looks like congestion, esp. in central lobular areas
-May have atrophy or loss of hepatocytes

Front 330

Portal vein thrombi

Back 330

-Can lead to infartcs of the gut
-Cause ascites

Front 331

Portal vein hypoplasia

Back 331

-Microvascular dysplasia and non-cirrhotic portal hypertension
-Common in dogs with abnormal portal vein development
-May have no clinical signs (only elevated bile acids)
-May have severe signs (ascites)

Front 332

Peliosis hepatis

Back 332

-Dilations of sinusoids in the liver
-Usually in old cats, cattle, and humans

Front 333

Inflammatory diseases of the Liver

Back 333

-Viral
-bacterial
-Fungal
-Parasitic
-Idiopathic

Front 334

Viral inflammatory liver diseases

Back 334

-Most are species specific
-Mostly necrosis with neutrophils or lymphocytic
-Canine adenovirus
-Rift valley fever in ruminants
-Herpesviruses (cows, horses, dogs, fish)
--all species have a herpesvirus with liver necrosis
-Coronaviruses (FIP in cats)
-Woodchuck hepatitis virus
-Hepatitis A, B, C, D, E, G

Front 335

Bacterial inflammatory liver diseases

Back 335

-Usually necrosis with neutrophils
-Most common in large animals
-Often spread from the gut, bacterial infection starts out in GI and spreads to the liver

Front 336

Clostridial organisms in the liver

Back 336

-Associated with liver flukes
-Multifocal random abscesses or acute supprative hepatitis
-Organisms live within cells
-Affect every species

Front 337

Mycobacterium in the liver

Back 337

-Most common in birds and fish
-Common problem in zoos
-Livers are diffusely swollen, filled with mycobacteria
-Form granulomas
-Acid-fast positive
-All are transmissible to immunocompromised individulas

Front 338

Fungal hepititis

Back 338

-not as common in domestic animals
-Granulomatous or pyogranulomatous inflammation

Front 339

Protozoal liver infection

Back 339

-Toxoplasma gondii
-Causes multifocal random liver necrosis in many species

Front 340

Parasitic issues with liver

Back 340

-Ascaris suum: causes milk spots
-Fluke infestations (mostly large animals)
-Causes transient necrosis in young animals
-leads to multiple fibrous scars
-Can bring in other bacteria

Front 341

Idiopathic inflammatory diseases in Liver

Back 341

-Chronic active hepatitis in the dog
-Cholangitis in cats
-Serum hepatitis in the horse

Front 342

Chronic-active Hepatitis in the Dog

Back 342

-EXTREMELY common
-Unknown cause or prognosis, don't know how to treat
-Chronic inflammation of the liver
-Mild GI or liver signs
-individual cell necrosis leads to bridging portal fibrosis, bile duct hyperplaisa, and nodular regeneration
-Begins centrilobular and spreads to portal areas
-May be associated with copper accumulation

Front 343

Lobular dissecting hepatitis

Back 343

-Hepatitis in dogs
-leads to cirrhosis

Front 344

Chronic cholangitis in cats

Back 344

-Cats die of this! Most common inflammatory disease in cat liver
-Suspected ascending bacterial infection or obstruction of extrahepatic bile ducts
-Severe inflammation in bile ducts and surrounding portal area
-May be associated with IBD
-Lymphocytic inflammation, can look like lymphosarcomas
-Tx: antibiotics or corticosteroids

Front 345

Serum hepatitis in the Horse

Back 345

-Associated with injection of biological serum of equine origin
-Dish-rag livers, small and flabby
-Extensive loss of hepatocytes
-Prolonged incubation period
-Leads to icterus and hepatoencephalopathy
-Small, friable liver
-Severe centrolobular necrosis

Front 346

Toxins in the Liver

Back 346

-Liver's job is to detoxify, leads it to be a common site of toxic injury
-Receives blood from the portal system, ingested toxins reach liver first
-Biotransformation site, transforms endogenous and exogenous substances
--makes toxins out of non-toxic compounds

Front 347

Predictable Liver Toxins

Back 347

-Effects are based on group and dose
-Know what is going to happen
-Toxic plants, etc.

Front 348

Idiosyncratic liver toxicity

Back 348

-Dangerous!
-Do not know how much is going to cause what kinds of responses
-not dose or breed dependent
-Ex: rimadyl and hepatotoxicity, not dose-dependednt

Front 349

Manifestations of Liver Toxicity

Back 349

-No changes
-Hepatocellular swelling
-Lipidosis
-Necrosis, usually in a specific pattern
-Inflammation (usually secondary)
-Fibrosis
-Bile duct hyperplasia

Front 350

Direct vs. indirect liver toxicity

Back 350

-Direct: Drug arrives in liver and is toxic to the liver
-Indirect: drug needs to be metabolized
--cytochrome p450 system in centrolobular area
--Most common

Front 351

Toxic Liver Injury

Back 351

-Pattern of necrosis depends on many factors
-Identity of the toxin cannot be determined based on morphologic grounds alone
--should be verified by toxicological testing
-Patterned necrosis of the liver can be caused by vascular disease or hypoxia

Front 352

Benzodazepines in cats

Back 352

-Animals present in liver failure
--hepatoencephalopathy, hemorrhages, edema, acites, bleeding disorders
-Small, flabby livers
-Liver enzymes are greatly elevated
-Extensive loss of central hepatocytes, severe necrosis
-Bile duct hyperplasia
-Due to vallium or vallium-related compounds
-Idiosyncratic, not dosage dependent

Front 353

Acute copper toxicity in sheep

Back 353

-Chelate copper, when copper is released it causes hemolytic anemia
-Hemolysis leads to severe anemia, centrolobular hepatic necrosis
-Not a direct liver toxin, but ends up killing hepatocytes
-Different from Cu accumulation in dogs

Front 354

Phenobarbital cirrhosis in dogs

Back 354

-Phenobarbital is used for seizures
-Small number of dogs can develop liver issues
-Diffuse hepatic fibrosis, nodular regeneration, and bile duct hyperplasia
-Phenobarbital is metabolized in the liver
-Now people monitor liver enzymes when dog is on phenobarbital

Front 355

Cirrhosis in large animals

Back 355

-Exposure to long-term toxic plant?

Front 356

Pattern of Necrosis due to Liver toxin depends on....

Back 356

1. Site of metabolism
2. Exposure to other drugs and toxins
3. Diet, age, genetics, sex

Front 357

CCL4 patterned necrosis due to toxins

Back 357

-Drug metabolized by cytochrome P450 enzyme
-Causes liver necrosis near central vein, where P450 enzyme is concentrated
-indirect, predictable toxin
-With small dose and no damage to framework, liver can regenerate
-With large dose, and damage to framework, liver does not regenerate and leads to fibrosis and cirrhosis
-Changing level of P450 concentration can expand or shrink zone of necrosis
--certain drugs or diets will change concentrations
--Shifts location and severity of toxicity

Front 358

Allyl Alcohol in the Liver

Back 358

-Metabolized by alcohol dehydrogenase
-Highest concentration of alcohol dehydrogenase is in periportal area of liver
-Most necrosis occurs in periportal area
-Can alter sites of necrosis with certain diets

Front 359

Chronic Exposure to Toxins

Back 359

-Leads to fibrosis, nodular regeneration, and bile duct hyperplasia

Front 360

Hyperplastic Liver

Back 360

-Common in the gallbladder and liver
-Cystic hyperplasia of the gall bladder
-Nodular hyperplasia in the liver

Front 361

Nodular hyperplasia in the liver

Back 361

-All dogs over 10 have nodular hyperplasia in the liver
--can see on ultrasound
-Often mistaken for neoplasia
-Can be all sorts of different colors

Front 362

Neoplastic disease in the Liver

Back 362

1. Adenomas : benign neoplasia
2. Carcinomas
3. Metastatic tumors

Front 363

Hepatic adenomas

Back 363

-Benign
-Hepatocellular: uncommon
-Cholangiocellular: also uncommon
-Cystadenomas
-Cholangiocellular cystadenoma

Front 364

Hepatocellular carcinomas

Back 364

-Rare
-Associated with hepatitis B in humans and woodchucks

Front 365

Bile duct carcinomas

Back 365

-Cholangiocellular carcinomas
-more common than hepatocellular carcinomas
-Common in asian sloth bears, associated with asian liver fluke

Front 366

Metastatic disease

Back 366

-Lymphosarcoma
-Hemangiosarcoma (dogs)
-Pancreatic adenocarcinoma
-Pancretic islet cell tumor
-Leukemias
-Histiocytic sarcoma
-Mast cell tumor
-GI adenocarcinomas
-Splenic carcinomas
-Adrenal carcnimoas

Front 367

Hepatic lymphosarcoma

Back 367

-Can look like ANYTHING
-Do cytology

Front 368

Gallbladder Lesions

Back 368

1. Mucocele
2. Infarcts
3. Stones

None are common

Front 369

Mucocele

Back 369

-Enlarged gallbladder
-Accumulation of inspissated bile or mucin in gall bladder
-New finding

Front 370

Gallbladder Infarcts

Back 370

-leads to necrosis of the gallbladder
-Often leads to rupture and secondary peritonitis

Front 371

Choleliths

Back 371

-Gall stones
-Rare, but present

Front 372

Pancreas Pathology

Back 372

-pretty simple organ
-Few things go wrong with it
-When things go wrong, they go VERY wrong
-Can be easy to fix

Front 373

Pancreatic Anatomy

Back 373

-Lies along the stomach and duodenum
-Has right and left lobes
-Tan/red tissue
-Histologically has acinar cells (zymogen granules)
--interlobar cells make bicarbonate buffer
-Minimal regeneration ability

Front 374

Pancreatic Function

Back 374

-Involved in digestion
-Produces bicarbonate
--LOTS produced
-Makes enzymes
--proteases
--lipase
--amylase
--Elastase
--Ribonuclease

Front 375

Decreased enzyme production in the Pancreas

Exocrine Pancreatic Insufficiency

Back 375

-Just give pancreatic enzymes in food
-Will see polyphagia, weight loss, diarrhea
-Mostly an inherited condition
--T-cell apoptosis causes pancreatic exocrine cells to disappear

Front 376

Acute Pancreatic Necrosis
(Acute necrotizing pancreatitis)

Back 376

-Severe problem in dogs, cats, humans
-10-20% of cases die, animals are extremely ill and in shock
-Most common and devastating form of necrosis in pancreas
-Very rapid progression, 12-14 hours
-Anti-inflammatory drugs will not work
-No definitive cause or treatment
-When chronic, leads to fibrosis
--fibrosis in pancreas and in fat around the pancreas
--will have adhesions

Front 377

Pancreatic Reaction to Injury

Back 377

1. Atrophy
2. Necrosis
3. Inflammation
4. Fibrosis

Front 378

Pancreatic Atrophy

Back 378

-Mostly inherited condition
-Pancreas is destroyed early in life by apoptotic T-cell mediated process
-Exocrine cells are lost
--Ducts ans islets are all that are left
-Results in Pancreatic Exocrine Insufficiency
-Zymogen granules are reduced or absent
-Grossly looks like just a series of ducts

Front 379

Pancreatic necrosis

Back 379

-Common response to injury
-pathogenesis is not totally understood
-Could be due to duct obstruction
-Can be due to direct acinar injury

Front 380

Cause of Acute Pancreatic Necrosis

Back 380

-Do not know what causes it
-Diet, toxins, hormonal imbalance?

Front 381

Pathogenesis of Pacreatic necrosis

Back 381

1. Insult (unknown cause)
2. Zymogen granules are not secreted, stay in acinar cells
--no enzyme secretion
3. Zymogen granules fuse with lysosomes, causes trypsinogen activation (becomes trypsin)
4. Trypsin activates digestion enzymes in the pancreas
5. Digestion enzymes start to digest pancreas, leads to necrosis
--starts coagulative and ends liquefactive
6. necrosis acts on local blood vessels, leads to thrombosis and further ischemia
7. Necrosis attracts inflammatory cells, neutrophils and macrophages
--release enzymes and cause more necrosis
8. Fat surrounding pancreas is metabolized, causes fat necrosis
--get saponification of fat
9. Release of enzymes activates kinin, coagulation, fibrinolysis, and complement
--leads to further inflammation, shock, circulatory collapse

Front 382

Trypsinogen in pancreas

Back 382

-Trypsinogen is converted into active trypsin
-Usually only activated in the duodenum
-When activated in the pancreas can cause major issue
-Other enzymes are activated
--DNAase, lipase, proteases, elastases, RNAases
--Digestion enzymes, digest stuff
-When in pancreas, digestion enzymes digest the pancreas itself

Front 383

Digestion enzymes

Back 383

-Proteases
-DNAases
-Lipases
-Elastases
-RNAases

Front 384

Acute Pancreatic necrosis signs

Back 384

-PAINFUL process!
-Animals are hypocalcemic due to Ca deposition for saponification
-Animals are EXTREMELY ill
-Enzymes will be circulating in blood

Front 385

Acute Pancreatic necrosis and circulating enzymes

Back 385

-Pancreatic enzymes start to circulate in the blood
-Can test for enzymes
-Enzymes activate kinin system, coagulation system, fibrinolytic system, and complement system
--leads to further inflammation

Front 386

Systemic Inflammatory Reaction Syndrome
SIRS

Back 386

-Occurs when all systems are activated
-Kinin system
-Coagulation system
-Fibrinolytic system
-Complement system
-Occurs with Acute Pancreatic necrosis
-Leads to Acute Respiratory Distress Syndrome
-Multi-organ Dysfunction Syndrome
-DIC

Front 387

Acute Necrotizing Pancreatitis Gross Lesion

Back 387

-Swollen, firm, hemorrhagic, necrotic pancreas
-Peripancreatic fat necrosis (saponification)
-Thrombi in vessels
-Serosanguineous peritoneal effusion with fat droplets
-Peritonitis with adhesions
-Friable necrosis and adhesions

Front 388

Systemic Effects of Pancreatic Necrosis

Back 388

-Circulating trypsin and other proteases bind plasma protease inhibitors and deplete them
-All other proteases in blood are activated
-Activation of:
--kinin system
--Coagulation system
--fibrinolytic system
--complement system
-Leads to shock, DIC, SIRS, death

Front 389

Acute Pancreatic necrosis histology

Back 389

-Coagulation and liquefactive necrosis of parenchyma and fat
-Influx of neutrophils following necrosis
-Edema
-Hemorrhage
-Mineralization in fat
-Vascular necrosis and Thrombi

Front 390

Pancreatic Inflammation

Back 390

-Rarely a primary event
-Acute: in response to necrosis or associated with an ascending infection
-Chronic: lymphocytes and plasma cells
--can be with or without fibrosis
-Chronic active: acute necrosis on top of chronic necrosis
-Uncommonly due to an ascending infection

Front 391

Pancreatic Fibrosis

Back 391

-Result of inflammation and necrosis
-Interstitial accumulation of fibroblasts and collagen
-Rarely be associated with exocrine pancreatic insufficiency, not often
-Pancreas will appear "wooden"
-Usually incidental finding

Front 392

Categories of Exocrine Pancreatic Disease

Back 392

1. Congenital
2. Necrosis and inflammation
3. Neoplasia and Hyperplasia

Front 393

Congenital and Inherited Pancreatic Disease

Back 393

-Hypoplasia of the exocrine pancreas, RARE
-Atrophy of exocrine pancreas
--associated with Exocrine pancreatic insufficiency
--Common in collies, herman shepherds

Front 394

Ectopic Pancreatic Tissue

Back 394

-Pancreatic tissue in one ormore abdominal sites
-Occasionally seen as incidental finding in dogs and cats

Front 395

pancreatic necrosis and Inflammation

Back 395

-Common cause of illness and death in dogs
-Less common in cats
-Seen in horses, swine, birds
-Cause is not usually known, does have associated factors
-Pathogenesis is thought to be autodigestion of pancreas due to inappropriate activation of pancreatic enzymes

Front 396

Factors associated with Pancreatic necrosis and Inflammation

Back 396

-Obesity
-Alcohol
-Drugs
-Organophosphate compounds
-Biliary tract disease
-high fat diet
-Hyperlipidemia
-Trauma
-Ischemia
-Hypercalcemia
-Specific breeds (yorkies, miniature schnauzers)
-Diabetes mellitus

Front 397

Pancreatic Nodular Hyperplasia

Back 397

-Nodular acinar or ductular hyperplasia
-Common in dogs, cats, and cattle
-NORMAL finding!
-Biopsy before doing anything!
-incidental finding unless mistaken for neoplasia

Front 398

Pancreatic adenomas

Back 398

-Rare

Front 399

Pancreatic Carcinomas and Adenocarcinomas

Back 399

-Very nasty tumors
-Usually acinar, ductal, or islet cells
-Often metastasize to the lymph nodes and liver before being detected
-May spread to other tissues of the peritoneal cavity (carciinomatosis)
-Devastating cancers, only survive if found early as incidental finding
-Commonly spread to the liver

Front 400

Islet cell tumors

Back 400

-Usually rare
-At the end of panreatic lobes
-Can spread to the liver