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BOD 2 > GI, Liver, Pancreas, Gallblader Diseases > Flashcards

GI, Liver, Pancreas, Gallblader Diseases Flashcards

1
Q

Palatoschisis

A

cleft palate resulting in starvation (cant make negative pressure while nursing) or aspiration pneumonia
genetic (brachycephalic) or toxic (steroids, antifungals, antiseizures, Veratrum, lupine,) viral (canine distemper intrauterine infection or nutritional (excessive vitamin A or D)
occurs in dogs, horses, and cows

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2
Q

Cheiloschisis

A

cleft lip/ hair lip

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3
Q

What time frame does Veratrum californicum ingestion result in palatoschisis

A

on day 14 of gestation

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4
Q

What time frame of gestation does Lupine ingestion result in palatoschisis?

A

between days 40-50 of gestation

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5
Q

What is the cause of cleft palate (palatoschisis)

A

-Genetic (brachycephalic)
-Nutritional (excessive vit A or D)
-Drugs (Steroids, antifungals, antiseizure medications)
-Viruses (intrauterine infection of canine distemper)
-Toxic plants (Veratrum californicum- d14 or lupine d40-50)

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6
Q

Prognathism

A

developmental anomaly where extension or bulging out (protrusion) of the lower jaw (mandible). It occurs when the teeth are not properly aligned due to the shape of the face bones

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7
Q

Brachygnathia inferior

A

developmental anomaly where abnormal shortening of the mandible occurs

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8
Q

Agnathia

A

developmental anomaly where there is an absence of the mandible

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9
Q

Stomatitis

A

inflammation of the oral cavity

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10
Q

gingivitis

A

inflammation of the gingiva

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11
Q

glossitis

A

inflammation of the tongue

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12
Q

Pulpitis

A

inflammation of the tooth

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13
Q

Cheilitis

A

inflammation of the lip

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14
Q

pharyngitis

A

inflammation of the pharynx

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15
Q

What are the three infectious agents resulting in vesicular stomatitides?

A

1) Foot and Mouth Disease (picornavirus)
2) Vesicular stomatitis (Rhabdovirus)
3) Vesicular exanthema (Calicivirus)

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16
Q

What are the five infectious agents resulting in erosive/ulcerative stomatitides?

A
  1. Bovine viral diarrhea (pestivirus)
  2. Rinderpest (morbillivirus)
  3. Malignant catarrhal fever (herpes)
  4. Feline calicivirus
  5. Bluetongue (orbivirus)
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17
Q

Vesicular stomatitides

A

caused by virus-induced epithelial cytolysis leading to vesicles/bullae that rupture and erode leading to an ulcer/scab in the oral cavity

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18
Q

How do we sample oral lesions

A

-Punch/Wedge biopsies

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19
Q

What species is not susceptible to foot and mouth disease?
-Pigs
-Horses
-Cows
-Sheep

A

Horses

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20
Q

Can horses get foot and mouth disease?

A

No

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21
Q

What are causes of bacterial stomatitis?

A

-Actinomycosis: “Lumpy jaw”
-Actinobacillosis: “Wooden tongue”
-Necrobacillosis: ‘Calf diphtheria”
-Infectious stomatitis “mouth rot in reptiles’

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22
Q

What causes lumpy jaw

A

Actinomyces bovis

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23
Q

Lumpy Jaw

A

caused by actinomyces bovis
deep stomatitis and disfigured mandible
Pathogenesis: normal oral bacteria, invade through penetrating wounds, destroy bone (pyogranulomatous osteomyelitis)

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24
Q

What causes wooden tongue

A

Actinobacillus lingnieressi

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25
Q

Wooden Tongue

A

Caused by Actinobacillus lingnieressi
Tongue is very firm
Yellow granules exude from the ulcerated tongue surface (sulfur granules)

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26
Q

Necrobacillosis

A

focal or multifocial areas of oral necrosis
caused by fusobacerium necrophorum
Pathogenesis:
Trauma to oral cavity via mechanical trauma or primary viral infection leading colonization of F. necrophorum and coagulative necrosis

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27
Q

Mouth Rot

A

Infectious stomatitis of lizards, snakes, and turtles caused by stress leading to immunosuppression and normal bacterial overgrowth

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28
Q

Feline Lymphocytic Plasmacytic Stomatitis

A

Chronic gingivostomatitis with severe lymphoplasmacytic inflammation
affecting premolar/molar teeth (caudal oral mucosa lateral to palatoglossal folds
idiopathic (antigenic overstimulation +/- calicivirus)
tx: teeth extraction

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29
Q

How do you treat Feline Lymphocytic Plasmacytic Stomatitis

A

teeth extraction

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30
Q

What is the cause of Feline Lymphocytic Plasmacytic Stomatitis

A

idiopathic (antigenic overstimulation overstimulation +/- calicivirus)

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31
Q

Eosinophilic Stomatitis

A

Oral granulomas “rodent ulcers”
common in cats
occurs on lips, anywhere in the mouth
grouped into the eosinophilic granulomas complex
idiopathic, autoimmune cause

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32
Q

Neoplasms of the oral cavity in the dog

A

Melanoma (most common)
squamous cell carcinoma
fibrosarcoma
papilloma

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33
Q

Neoplasms of the oral cavity in the cat

A

Squamous cell carcinoma (most common)
fibrosarcoma
lymphoma
melanoma

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34
Q

Canine papilloma

A

generally papilloma virus induced
most common in younger dogs
may regress spontaneously
can look similar to papillary squamous cell carcinoma but would have evidence of histologic and/or radiographic evidence of invasion

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35
Q

Peripheral odontogenic fibroma

A

a neoplastic-like lesion of odontogenic mesenchyme
common in dogs and infrequent in cats
benign
Local excision is curative

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36
Q

Acanthomatous Ameloblastoma

A

a neoplastic like lesion
tumor of periodontal ligament
occurs in dogs
locally invasive- aggressive
Wide surgical excision is needed as recurrence is common
Does not metastasize

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37
Q

Gingival hyperplasia

A

very common in dogs, especially brachycephalic breeds
benign lesion
caused by trauma and irritation

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38
Q

Causes of trauma to the oral cavity

A

Physical (chewing, carrying heavy items, or trauma such as hit by vehicle or blunt force trauma)

Chemical (acid or alkali chemical burns)

Traumatic (electrocution)

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39
Q

Hypsodont teeth

A

teeth that continuously grow
horses, cheek teeth of ruminants, tusks of boars

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40
Q

Brachydont teeth

A

teeth that do not grow after eruption

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41
Q

Is enamel capable of regeneration and repair?

A

NO

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42
Q

Anodontia

A

a primary dysplasia where failure of development / agenesis of the teeth

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43
Q

Oligodontia

A

a primary dysplasia where too few teeth

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44
Q

Polyodontia

A

a primary dysplasia where supernumerary teeth

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45
Q

Enamel hypoplasia

A

a secondary dysplasia where the enamel is underdeveloped typically due to bovine viral diarrhea virus intrauterine infection, puppies of canine distemper virus, malnutrition, and vitamin/mineral deficits (Calcium, Vit A, C, D, phosphorus)

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46
Q

What can result due to abnormal wearing of the teeth

A

1) Wave mouth
2) Infection, loss, damage
3) Dental fractures
4) Surrounding soft tissue damage

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47
Q

What can result in the teeth being yellow?

A

Tetracyclines

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48
Q

What can result in the teeth being orange red

A

Porphyrins (heme components)

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49
Q

What can result in the teeth being brown

A

Fluorosis

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50
Q

Periodontal disease

A

common in dogs and sheep
Damage of gingiva and periodontal disease
Dental plaque (bacterial mass mixed with organic matrix and food)
Dental calculi or tarter - mineralized bacterial mass

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51
Q

Mineralized bacterial mass of periodontal disease

A

Dental calculi or tartar

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52
Q

Bacterial mass mixed with organic matrix and food

A

dental plaque

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53
Q

What is the result of periodontal disease?

A

-Tooth loss due to destruction of periodontal ligament
-Pulpitis
-Tooth root abscess
-Bacteremia leading to heart disease (endocarditis)

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54
Q

Ranula

A

a salivary gland disease where there is mucus extravasation
cyst involving the sublingual or submaxillary gland

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55
Q

Salivary cyst

A

distention of the salivary duct

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56
Q

Mucocele

A

pseudocyst in the glandular tissue (mucus extravasation)

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57
Q

Sialadenitis

A

inflammation of the salivary glands

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58
Q

Infectious causes of sialadenitis

A

1) Rabies
2) Canine distemper virus
3) Sialodacryoadenitis virus (Rats)
4) Salmonella typhisuis leading to suppurative parotid sialoadenitis (pigs)

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59
Q

Diseases of Salivary Glands

A

1) Sialadenitis due to infection or foreign body (grass awn)
2) Infarction
3) Sialolithiasis
4) Neoplasia
5) Mucocele

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60
Q

Sialolithiasis

A

when hardened mineral deposits formed in the salivary glands.

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61
Q

What are common neoplasms of a salivary gland?

A

-Adenoma
-Adenocarcinoma
-Mixed tumor

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62
Q

Lethal glossopharyngeal defect

A

“bird tongue”
congenital defect where the tongue is not as wide and rostral half of the tongue is folded medially where the papilla margins are

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63
Q

Choristoma of the tongue

A

a developmental tumor-like growth of microscopically normal tissue in an abnormal location.
hair on the tongue

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64
Q

Thrush

A

Candidiasis of the tongue
caused by canidida albicans

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65
Q

Infectious causes of glossitis

A

1) Candidiasis
2) Wooden Tongue (Actinobacillus linguieresii)

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66
Q

Uremic glossitis of carnivores

A

High Blood BUN (uremia) causes vascular damage/vasculitis leading to thrombosis and infarction +/- the caustic effect from ammonia due to urease-producing bacteria

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67
Q

Uremic glossitis of herbivores

A

High blood and salivary urea leading to GI bacteria split urea and ammonia causing local caustic effect

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68
Q

What is the most common cause of neoplasia of the tongue?

A

Squamous cell carcinoma

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69
Q

What type of cells make up the carnivore esophagus?

A

nonkeratinizing stratified squamous epithelium

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70
Q

What type of cells make up the ruminant, pig, and horse esophagus?

A

keratinizing stratified squamous epithelium

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71
Q

What species have an esophagus with nonkeratinizing stratified squamous epithelium

A

Carnivores

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72
Q

What animals have striated muscle in their esophagus?

A

Dogs and ruminants

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73
Q

What part of the esophagus has serosa?

A

only the abdominal portion

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74
Q

What portion of the horse esophagus is smooth muscle

A

aborad third distal 2/3
horses cannot vomit

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75
Q

Megaesophagus

A

primarily dogs and can be either
-Congenital: Persistent right 4th aortic arch (vascular ring) or idiopathic denervation
-Acquired: Neuromuscular (Myasthenia gravis or polymyositis), Chagas disease, Hypothyroidism, or lead poisoning

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76
Q

Chagas disease

A

a parasitic disease that can lead to acquired megaesophagus

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77
Q

Choke

A

esophageal obstruction
commonly over larynx, thoracic inlet, base of heart, and diaphragmatic hiatus
more common in large animals
Leads to: Perforation leading to pneumonia/pleuritis, cellulitis, stenosis, periesophageal adhesions

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78
Q

What are the 4 common sites for choke

A

-Over the larynx
-Thoracic inlet
-Base of heart
-Diaphragmatic hiatus

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79
Q

Bloat

A

increased intraabdominal pressure
prevents blood from returning to the heart
cervical part of esophagus becomes congested while the caudal part becomes blanched by blood being driven away
leading to a bloat line

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80
Q

Bloat line

A

a line in the esophagus caused by the cervical part becoming congested with blood from blood being prevented from returning to the heart and the caudal part having blood driven away (blanched)

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81
Q

Ulcerative esophagitis

A

full thickness mucosa destruction that can result in perforation
caused by:
1. Reflux (monogastric animals- aborad third linear ulcers)
2. Toxins (Cantharidin- blister beetles and spanish flies) or chemical burns
3. Viruses: papular stomatitis, BVDV, MCF
4. Trauma (foreign body or iatrogenic)
5. Parasitic: Gongylonema (ruminants and primates w intermediate host of cockroaches and dung beetles) or Gastrophilus nasalis (equids) or Spirocerca lupi (canids, intermediate host of dung beetles)

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82
Q

Spirocerca lupi

A

a parasite of dogs and canids that has an intermediate host of dung beetles
Produce nodules in the distal esophagus that then penetrate the aorta leading to rupture
granulomatous inflammation and fibrosis leading to neoplasia (fibrosarcoma and osteosarcoma)
Rarely hypertrophic osteopathy

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83
Q

What can cause esophageal sarcoma?

A

Spirocerca lupi

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84
Q

What can cause esophageal papilloma

A

bovine papilloma virus

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85
Q

What can cause esophageal squamous cell carcinoma

A

cows consuming bracken fern
cows with papilloma virus

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86
Q

Forestomach vs Stomachs

A

Forestomachs: House digestive flora for breaking down cellulose

Abomasum/C3/Stomach: Enzymatic and hydrolytic digestion of food. Non-glandular stomach- horses

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87
Q

Ruminal tympany

A

Bloat of the forestomach due to over-distention of the rumen due to accumulation of fermentation gases
Can be primary (frothy) or secondary (gaseous bloat)

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88
Q

Primary Ruminal tympany

A

Frothy bloat due to a change in diet to some types of legumes (alfalfa or grain concentrate) leading to a lower rumen pH and stable foam that mixes with rumen contents to block the cardia and failure to eructate and bloat

distended left paralumbar fossa
bloat line

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89
Q

Secondary Ruminal tympany

A

Bloat that is gaseous due to physical or functional obstruction (hairballs, plant fiber balls, lead substances, or sharp metal)
Stenosis of the esophagus
*Gases cant escape

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90
Q

Trichobezoar

A

a ruminal foreign body of hair (hairballs)

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91
Q

Phytobezoars

A

a ruminal foreign body of plant fiber balls

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92
Q

How can lead substances lead to secondary ruminal tympany

A

lead poisoning interferes with motility

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93
Q

What can lead to inflammation of the forestomachs?

A

1) Grain overload, rumen overload, lactic acidosis (Chemical rumenitis)
2) Sudden feed change
*Sequella of bacterial ruminitis (Fusobacteria necrophorum and Trueperella pyogenes) and mycotic ruminitis

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94
Q

What bacteria result in ruminitis after grain overload. lactic acidosis, or a sudden feed change?

A

Fusobacteria necrophroum
Trueperella pyogenes

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95
Q

Ruminitis-Liver Abscess

A

Result from rapidly fermentable grain leading to acidosis (low pH) and subsequent damage to mucosa from Fusobacterium necrophorum overgrowth leading to rumen wall abscess
Bacteria access and travel to the liver via the portal vein, causing liver abscesses

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96
Q

Result of Ruminitis-Liver Abscess complex

A

-Rumen wall abscess
-Multifocal hepatic abscesses
-Caudal vena caval pyemia (fatal septic embolism)
-Pulmonary embolic pneumonia and hemorrhage (rupture of pulmonary artery)
-Vegetative valvular endocarditis (tricuspid valve)
-Jugular thrombosis

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97
Q

Hemoptysis

A

coughing up blood, a result of rupture of the pulmonary artery due to septic embolism of ruminitis-liver abscess complex

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98
Q

What are the causative agents of mycotic ruminits

A

Aspergillus and Zygomyecetes (mucor)

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99
Q

Mycotic Ruminitis

A

caused by lactic acidosis, mechanical injury, or antibiotics (calves)
can be angioinvasive, resulting in infarction of the vessels
presents as circular well delineated lesions on the stomach wall
caused by aspergillus and Zygomycetes (mucor)

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100
Q

Vagal indigestion

A

function outflow problem from the forestomaches due to vagus nerve damage
Clinical signs: ruminoreticular distention
Can be type I-IV
I: lesions around vagus nerve (failure of eructation)
II: anatomical conditions resulting in failure of omasal transport
III: physical impaction of abomasum
IV: pregnancy related shifting of abomasum and partial forestomach obstruction

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101
Q

Type I vagal indigestion

A

lesions around the vagus nerve resulting in failure of eructation

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102
Q

Type II vagal indigestion

A

functional or anatomic conditions that result in failure of omasal transport

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103
Q

Type III vagal indigestion

A

Physical impaction of the abomasum leading to function outflow problem

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104
Q

Type IV vagal indigestion

A

Pregnancy related shifting of the abomasum and partial forestomach obstruction leading to a functional outflow problem of the forestomachs

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105
Q

Gastric Dilation and Volvulus

A

occur in large “barrel” chested dogs, rarely pigs, and guinea pigs
Causes: large means, postprandial exercise, hereditary
The dilated stomach and displacement (twisted) compresses on the diaphragm, vena cava and portal vein leading to decreased venous return and decreased cardiac output leading to shock

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106
Q

What causes gastric dilation and volvulus

A

Idiopathic but potentially large meals, postprandial exercise, hereditary

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107
Q

Gastric Dilation and Rupture

A

Horses with fermentable carbohydrates, lush pasture, excessive water intake
Aborad impaction (closer to stomach)
Grass sickness/dysautonomia
horses dropping really fast
Antemortem: hemorrhage, fibrin
PostMortem: clean tear

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108
Q

What species is gastric dilation and rupture common in?

A

Horses

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109
Q

How can you tell a gastric rupture in a horse is antemortem vs postmortem?

A

hemorrhage and fibrin in antemortem while clean tear in postmortem

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110
Q

LDA

A

Left displaced abomasum
mostly in dairy cows- seldom fatal but requires surgery, older high producers, post-calving period
leads to abomasal ulcers and fibrous adhesions due to HCl secretion from obstructions

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111
Q

How does LDA occur

A

left displaced abomasum occurs when animal is on a high grain diet and hypocalcemia leads to fermentation, atony, and production of gas, recent parturition, and displacement of abomasum to the cranial left abdomen leading to obstruction, HCl secretion, chloride sequestration, hypochloremia and metabolic alkalosis

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112
Q

What is a result of LDA?

A

abomasal ulcers and fibrous adhesions to the abdominal wall
short termL hypochloremia and metabolic alkalosis

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113
Q

What side of the body is the abomasum normally on?

A

the caudad right side

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114
Q

What is RDA

A

Right Displacement of the abomasum
Displaced to the right and dorsal with rotation (20% have volvulus) leading to vagus nerve trauma and vagal indgiestion
can be fatal

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115
Q

Is LDA or RDA more fatal?

A

RDA

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116
Q

What can result in gastric/abomasal impaction?

A

1) Low quality roughage - low water intake, poor mastication
2) Vagal nerve damage (vagal indigestion, pyloric stenosis)
3) Hypochloremia, hypokalemia, metabolic alkalosis
4) Abomasal empyting defect of Suffolk Sheep

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117
Q

Gastric ulcers

A

mucosal defect (partial thickness damage is erosion)
caused by foreign body, chemical, drugs (steroids or NSAIDS), stress, hepatic disease, vasculitis, gastritis, gastrinomas, mast cell tumors, Addison’s disease, equine ulceration syndrome, finely ground feed (pigs), idiopathic

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118
Q

Projectile vomiting

A

vomiting that is not accompanied by retching movements

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119
Q

True vomiting

A

accompanied with retching movements like contraction of abdominal wall and neck muscles and extension of the neck

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120
Q

What are the two main infectious causes of abomasitis in ruminants?

A

1) Clostridium septicum (Braxy) -hemorrhagic
2) Clostridium perfringens type A - ulcerative emphysematous

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121
Q

How does gastritis in pigs typically occur

A

hemorrhagic gastritis secondary to sepsis

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122
Q

What is the likely cause of hemorrhagic abomasitis and death due to endotoxemia

A

Clostridium septicum (Braxy)

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123
Q

What is the likely cause of ulcerative emphysematous abomasitis?

A

Clostridium perfingens type A

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124
Q

What oral tumor would have positive IHC labeling for melan A and PNL2?

A

melanoma

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125
Q

What three syndromes make up feline triaditis?

A

Inflammatory bowel disease (enteritis)
Cholangiohepatitis
Pancreatitis

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126
Q

Which hepatotoxic agent classically causes megalocytosis?

A

Pyrrolizidine alkaloid

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127
Q

What clostridial disease is associated with foci of necrosis, surrounding neutrophils and intrahepatic bacilli?

A

Clostridium piliforme

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128
Q

With cirrhosis of the liver what changes do you expect?

A

Parenchymal loss with fibrosis and nodular regeneration

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129
Q

Ruminant Haemonchosis

A

Caused by haemonchus contortus (sheep and goats) and haemonchus placei (cattle)
leading to blood loss
in heavy burden and lead to protein losing gastropathy leading to anemia and bottle jaw (submandibular edema)

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130
Q

Ruminant Ostertagiosis

A

Caused by O. Ostertagi (cattle) and teladorsagia circumcincta (sheep and goats)
*Lead to mucosal metaplasia/hyperplasia
Type I and II
Clinical signs: achlorhydria, diarrhea, hypoproteinemia, wasting

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131
Q

Type I Ostertagiosis

A

during July-September, typically in calves in their first grazing season
ingested larvae develop with arresting

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132
Q

Type II Ostertagiosis

A

during March to May, from the emergence of L4 stages ingested the previous autumn. from gastric glands within the abomasum
occurs months after larval ingestion

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133
Q

What gastric bot lives in the squamous portion of the horses gastric mucosa?

A

Gasterophilus intestinalis

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134
Q

What gastric bot lives in the glandular portion of the equine stomach and esophagus?

A

Gasterophilus nasalis

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135
Q

Draschia megastoma

A

equine stomach nematode that causes tumor like nodules and ulcers in the glandular mucosa

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136
Q

What can cause equine parasitic gastritis?

A
  1. gastric bots (gasterophilus intestinalus and nasalis)
  2. Draschia megastoma
  3. Trichostrongylosis
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137
Q

What neoplasms of the stomach are benign

A

Adenoma and Leiomyomas

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138
Q

What neoplasms do horses typically get in the stomach and are malignant?

A

Squamous cell carcinoma

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139
Q

What neoplasms do dogs typically get in the stomach and are malignant?

A

Adenocarcinomas

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140
Q

What neoplasms of the stomach are malignant?

A
  1. Squamous cell carcinoma (horses)
  2. Adenocarcinoma (Canine)
  3. Leiomyosarcoma
  4. Lymphoma (Abomasum)
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141
Q

Clinical signs of intestinal disease

A
  1. Anorexia
  2. Weight loss
  3. Poor hair coat
  4. Vomiting
  5. Belching/Flatulence
  6. Abdominal pain
  7. Changes in stool color and consistency (diarrhea)
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142
Q

Patterns of intestinal disease

A

-Normal
-Diffuse
-Regionally/locally extensive
-Multifocal
-Multifocal to coalescing
-Disseminated

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143
Q

Diarrhea

A

Secretion of abnormally fluid feces accompanied by an increased volume of feces and an increased frequency of defecation
can be inflammatory or non-inflammatory
1. Induce intestinal secretion
2. Induce inflammation
3. Invasion

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144
Q

Maldigestive/Malabsorptive Diarrhea

A

defective digestion/absorption leading to stools with increased osmolarity
-Dysfunction of intestinal loops, bacterial overgrowth, reduced gastric acidity

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145
Q

Osmotic diarrhea

A

Diarrhea exerted by luminal solutes such as undigested carbohydrates and proteins

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146
Q

Hypersecretive Diarrhea

A

Diarrhea where excessive intestinal fluid secretion induced by enterotoxins

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147
Q

Exudative Diarrhea

A

diarrhea from increased capillary or epithelial permeability

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148
Q

Deranged motility diarrhea

A

Diarrhea from either:
1) intestinal hypermotility leading to decreased intestinal transit time and malabsorption.
2) Decreased motility leading to increased intestinal transit time and subsequent bacterial overgrowth and malabsorption

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149
Q

Invasive and cytotoxin Mediated Diarrhea

A

diarrhea where bacteria ingestion results in cytotoxin release and acute inflammation results in diarrhea

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150
Q

Small Bowel Diarrhea

A

-Normal to mildly increased defecation frequency
-fecal volume is normal to increased
-no fecal mucus
-Melena present
-No tenesmus
-No urgency
-no dyschezia (difficulty pooping)
-Vomitting may be present
-Steatorrhea may be present (fat excretion)

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151
Q

Hematochezia

A

fresh blood passed in stool, often seen in large bowel diarrhea

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152
Q

What type of diarrhea had melena present

A

Small bowel diarrhea

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153
Q

What type of diarrhea often has mucus present?

A

Large bowel diarrhea

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154
Q

What type of diarrhea has a markedly increased frequency of defecation

A

Large bowel diarrhea

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155
Q

What type of diarrhea has a decreased fecal volume

A

large bowel diarrhea

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156
Q

Result of intestinal disease

A

1) Dehydration leading to hypoperfusion and shock
2) Metabolic acidosis
3) electrolyte imbalance
4) Hypoproteinemia leading to ascites

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157
Q

Broad causes of enteritis

A

1) Viruses- common in very young animals
2) Bacteria- primary or secondary to viral infections
3) Parasites - heavy burden
4) Dietary toxins (accidental or iatrogenic)
5) Allergies (food hypersensitivity)
6) Idiopathic (unknown causes)

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158
Q

7 Agents of bacterial enteritis

A

1) Clostridium
2) Mycobacterium avium spp. Paratuberculosis
3) Lawsonia intracellularis
4) Brachyspira hyodysenteriae
5) E Coli
6) Salmonella spp
7) Rhodococcus equi

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159
Q

What Clostridium enteritis results in enterotoxemia

A

Clostridium perfringens

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160
Q

What agent causes sudden death in well-nourished animals by necrotizing/hemorragic enterocolitis and toxemia. Growth favored by sudden feed changes, antibiotics, and fermentable feeds

A

Clostridium perfringes

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161
Q

What factors favor clostridial growth in the intestines?

A

Sudden feed changes, antibiotic, and fermentable feeds

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162
Q

C. perfringens type A

A

alpha toxin that causes necrohemorrhagic enteritis and abomasitis, hemorrhagic bowel syndrome
also antibiotic enteritis (horse and rabbits) and colitis X in horses

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163
Q

What causes antibiotic enteritis in horses and rabbits

A

Clostridium perfringens Type A

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164
Q

What is a cause of colitis X in horses

A

Clostridium perfringens Type A

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165
Q

What causes lamb dysentery?

A

Clostridium perfringens Type B (a, B, e toxins)

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166
Q

What does Clostridium perfringes Type C cause?

A

bloody diarrhea in neonates (esp piglets)

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167
Q

What can cause pulpy kidney disease and encephalomalacia in lambs?

A

Clostridium perfringes Type D (a, e toxins)

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168
Q

What Clostridium perfringens exotoxins can cause enteritis in lagomorphs and enterotoxemia in ruminants?

A

Clostridium perfringes Type E (a, l toxins)

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169
Q

How does pulp kidney (overeating) disease occur (type D)?

A

Rapid Diet Change (high in CHO)
Favors rapid growth of clostridial organisms massive toxin production
angiotoxin leads to endothelial damage
hemorrhages, encephalomalacia (symmetrical necrosis and hemorrhage and nephrosis
rapid death and decomposition of kidneys at a faster rate than that of the rest of the carcass

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170
Q

What is Clostridium difficile associated with

A

oral antibiotic use leading to colitis in horse (mucosal edema, congestion and hemorrhage)

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171
Q

What disease is caused by Clostridium piliforme

A

Tyzzer’s disease

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172
Q

What clostridium species causes enterocolitis and hepatitis in rodents, foals, dogs, and cats typically less than 1 month of age

A

Clostridium piliforme (Tyzzer’s disease)

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173
Q

What bacteria has a criss-crossed/haystack appearance and causes enterocolitis and hepatitis?

A

Clostridium piliforme (Tyzzer’s Disease)

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174
Q

What is a common agent that causes mycobacterial enteritis?

A

Mycobacterium avium spp. Paratuberculosis (Johne’s Disease)

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175
Q

How is Mycobacterium avium spp. Paratuberculosis transmitted

A

oral and transplacentally

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176
Q

What does Mycobacterium avium spp. Paratuberculosis infection lead to?

A

Johne’s Disease characterized by chronic wasting disease, diarrhea. malabsorption and cytokine effects
diffuse granulmatous enteritis with prominent mucosal folds due to expansion of lamina propria by macrophages
Granulomatous lymphangitis and lymphadenitis

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177
Q

How does Mycobacterium avium spp. Paratuberculosis infection differ in sheep/goats versus cows

A

Diarrhea may not occur in sheep/goats. Hepatitis is much more likely and caseating granulmomas of the tuberculoate form and lymphangitis

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178
Q

What are the histological findings of Mycobacterium avium spp. Paratuberculosis infection

A

1) thickening of lamina propria by macrophages and multinucleated giant cells
2) acid-fast bacilli (Mycobacterium) within macrophages
3) Granulomatous inflammation can lead to mineralization of tissue, such as the aorta

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179
Q

Goat/Sheep Johne’s

A

typically isn’t diarrhea but have caseating granulomas and lymphangitis and granulomatous hepatitis

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180
Q

What is the mechanism of diarrhea in Johne’s disease

A

inflammatory, malabsorption

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181
Q

What causes proliferative ileitis in pigs?

A

Lawsonia intracellularis

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182
Q

proliferative ileitis in pigs

A

Caused by lawsonia intracellularis
affects pigs >4weeks
ileium is affected
Proliferative hemorrhagic enteropathy (large hemorrhagic cast in the lumen of thickened ileum with corrugated serosal surface
gross lesions of ileum: markedly thickened intestinal wall with cobblestone or cerebriform appearance

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183
Q

Is lawsonia intracellular more likely to affect pigs greater of less than 4 weeks

A

Greater than 4 weeks

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184
Q

What pathogen gives the gross lesion of cobblestone or cerebriform appearance in the intestinal wall of ileum due to mucosa being covered bt fibrinonecrotic (diphthertic) pseumembrane or cast

A

Lawsonia intracellularis

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185
Q

What part of the intestine does Lawsonia intracellularis typically affect in the pig?

A

Ileum

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186
Q

Lawsonia intracellularis histologic lesions

A

hyperplasia of crypt epithelium (tortuous) with crypt necrosis and hyperplasia

Silver stain highlights intracellular curved or slight spiral organisms in the apical cyotplasm of enterocyte

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187
Q

What is cause of intracellular curved or slight spiral organisms in the apical cytoplas of enterocytes causing hyperplasia and necrosis of crypt epithelium

A

Lawsonia intracellularis

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188
Q

What is the cause of swine dysentery

A

Brachyspira hyodysenteriae

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189
Q

Where part of the intestine does Brachyspira hyodysenteriae typically affect in pigs

A

Colon

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190
Q

Swine dysentery

A

Cause: Brachyspira hyodysenteriae
Pigs 8-14 weeks old
Colon affected
Gross lesions: bloody diarrhea, fibrinonecrotic pseudomembranes
Histolesions: Luminal spirochetes (silverstain)

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191
Q

E. Coli (Colibacillosis)

A

Neonatal pigs and calves most affected
Stress, overcrowding, infection with other pathogens
Types: ETEC, EHEC, Edema disease (enterotoxemic), Septicemic (EIEC), Enterpathogenic (EPEC,AAEC)

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192
Q

Edema disease (enterotoxemic colibacillosis)

A

Pigs 6 to 14 weeks old
E coli infection that produces an enterotoxin (verotoxin)
toxin produced in the small intestine then spreads hematogenously
Clinical signs neurologic signs, edema

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193
Q

What species is most affected by Salmonellosis

A

Horses
Cats and dogs on a raw diet

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194
Q

Salmonellosis

A

Acute, chronic, carrier
All species but esp horses or cats/dogs on raw diet
Small and large intestine
Gallblader
Mesenteric lymph nodes

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195
Q

What is the best tissue to culture Salmonellosis

A

Mesenteric lymph nodes

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196
Q

What animals are most affeced by peracute Salmonella septicemia

A

Young animal
acute necrosis of the blood vessels

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197
Q

What causes acute fibrinous cholecystitis in calves

A

Salmonella dublin

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198
Q

Acute Enteric Salmonellosis

A

Catarrhal enteritis with diffuse fibrinonecrotic ileotyphlocolitis
Mesenteric lymphadenopathy
fibrinous cholecystitis in calves with Salmonella dublin

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199
Q

What makes you highly suspicious of Salmonella Dublin

A

Fibrinous cholecystitis

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200
Q

Chronic enteric salmonellosis

A

lesion of pigs after chronic infection
button ulcers on the colon
Rectral strictures that can cause obstruction

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201
Q

What can cause rectal strictures that can lead to obstruction in pigs

A

chronic enteric salmonellosis

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202
Q

What is a likely result of cats on raw diets

A

Salmonella septicemia

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203
Q

Can nondiarrhea cats still shed salmonella

A

yes

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204
Q

Rhodococcus entercolitis in foals

A

Caused by Rhodococcus equi
Suppurative bronchopneumonia
Ulcerative colitis and pyogranulomatous lymphadenitis

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205
Q

What causes ulcerative colitis and pyogranulomatous lymphadenitis as well as suppurative bronchopneumonia is foals

A

Rhodococcus equi

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206
Q

What group pathogens are common in young animals and can compromise the GI mucosa resulting in secondary infection?

A

Viral enteritis

207
Q

T/F some viruses can cause immunesuppression

A

True

208
Q

What is the tropism for Parvovirus

A

Mitotically active cells suchs as
1) Crypts (immature secretory crypt epithelium)
2) Peyer’s patches (destruction of secondary lymphoid tissue)

209
Q

What is the tropism for enteric Coronavirus

A

1) Tips and middle of villi resulting in fusion
2) Crypt epithelium leading to hyperplasia
3) Both small and large intestines

210
Q

What is the tropism for Rotavirus

A

1) Upper two thirds of intestinal villi
2) Only small intestine
3) Vacuoliation of enterocytes

211
Q

What portion of intestine does Rotavirus affect

A

Only the small intestine at the upper two thirds of the intestinal villi leading to vacuolation of enterocytes

212
Q

Rotavirus enteritis pathogenesis

A

1)Fecal-oral route transmission
2) Viral replication in mature enterocytes
3) Necrosis and sloughing of absorptive cells
4)Villous atrophy
5) Maldigested/malabsorptive diarrhea
*Young animals

213
Q

What diarrhea does Rotavirus lead to

A

Maldigested/malabsorptive diarrhea due to necrosis of absorptive cells

214
Q

Rotavirus lesions

A

Possible only diarrhea grossly (hemorrhages, serosal glass appearance)
Histologically: villus blunting as rate of enterocyte loss exceeds replacement

215
Q

What species does coronavirus enteritis typically affect

A

primarily a cat and pig disease

216
Q

How is coronavirus enteritis spread

A

Fecal/oral spread through environmental contamination and fomites

217
Q

Coronavirus enteritis pathogenesis

A

1)Ingestion
2) 1 to 4 day incubation
3) 2 days post-infection, virus enters and colonizes enterocytes of the upper duodenum
4) Spreads caudally through the small intestine and colon
5) Villus blunting and crypt hyperplasia

218
Q

What part of the intestine does coronavirus affect?

A

Both the large and small intestine
villus blunting and crypt hyperplasia

219
Q

Porcine coronavirus enteritis

A

Transmissible gastroenteritis (TGE)
highly contagious with high mortality in pigs less than 1 day
Gross: thin, gas or fluid filled intestine
Histology: severe villous atrophy

220
Q

Feline coronavirus enteritis

A

generally mild and self-limiting disease of neonates ages 2 to 7 months
rarely fatal
repeat infection and long term shedders
Mutated virus and abnormal immune response can result in feline infectious peritonitis virus (FIP)

221
Q

What is the gold standard diagnosis for Feline coronavirus enteritis

A

Immunohistochemistry

222
Q

What is your #1 differential for a calf enteritis under 5 days old

A

Acute enterotoxigenic colibacillosis (ETEC)

223
Q

Does Parvovirus 1 or 2 cause parvovirus enteritis

A

Canine parvovirus enteritis (CPV-2)

224
Q

Canine parvovirus-2

A

a strain of feline panleukopenis virus (FPV) that infects dogs
virus receptor binding determines host susceptibility to parvovirus (transferrin receptor)
intersititial myocarditis in puppies is rare

225
Q

Clinical signs of Canine parvovirus-2

A

Vomiting, diarrhea, sudden death from infection of intestinal crypts
Myocardial necrosis to puppies born to unvaccinated bitches and infected up to 8 weeks of age
Bone marrow and lymphoid depletion leading to immune suppression

226
Q

How might you get myocardial necrosis of puppies with CPV-2

A

Puppies are born to unvaccinated bitches (no maternal antibodies)
Infected up to 8 weeks of age where the myocytes are still undergoing cell division

227
Q

Lesions of CPV-2 infection

A

1) Serosal hemorrhage
2) Mucosal hemorrhage
3) Crypt necrosis
4) Immunohistochemical staining of parvovirus antigen in crypt epithelium
5) Myocardial necrosis

228
Q

What affects on the host do nematodes have with intestinal infection

A

-Indirect undernourishment (Competition for nutrients)
-Local irritation (enterocolitis)
-Obstruction of gut lumen (if large burden)
-Loss of blood (anemia)
-Migration to other vital sites

229
Q

Death due to Parascaris equorum infection is often due to:
A) Diarrhea and dehydration
B) Impaction and perforation
C) Salmonella spp
D) Poor doing and weight loss

A

Impaction and perforation

230
Q

What ascarid commonly infects pigs

A

Ascaris suum

231
Q

What is a sequela of Ascaris suum and Toxocara canis

A

Intestinal impaction +/- perforation

232
Q

3 ways Ascarids are transmitted

A

1) Intrauterine
2) Through milk
3) ova - fecal - oral
*Larvae then penetrate the intestine and migrate to the liver

233
Q

Ocular toxocariasis or neural larva migrans

A

a risk of zoonotic nematodes

234
Q

What are the sequela of Ancylostoma caninum (hookworm) infection

A

hemorrhagic enteritis, anemia

235
Q

Small strongyles in equine

A

cyathostomin parasites where larva emerge from the large intestinal walls (cecum and colon)
Large emegence of L4 can result in typhocolitis

236
Q

What can result in typhocolitis of the horse?

A

Small strongyles/Cyathostomin parasites from the large emergence of L4 larva

237
Q

Strongylus vulgarus in the horse can result in:

A

1) Verminous arteritis
2) Eosinophilic endarteritis with aneurysm
3) Non-strangulating intestinal infraction

238
Q

What can cause verminous arteritis in the horse

A

Strongylus vulgarus

239
Q

Larval Cyathostomosis

A

Synchronous development of arrested larvae and amergence of L4s leading to catarrhal or hemorrhagic enteritis and protein losing enteropathy

240
Q

What are the sequela of Anoplocephala perfoliate infection in the horse

A

intussuception, impaction or rupture of the ileo-cecal valve

241
Q

Coccidiosis

A

typically affect poultry, ruminants, and pigs
age: young
lesion: proliferative, hemorrhagic or necrotic lesions
Clinical signs: Poor doing associated with diarrhea

242
Q

T/F coccidious can cause hemorrhagic enteritis

A

T

243
Q

T/F enterocytes rupture in all stages on the coccidiosis life cycle

A

T

244
Q

What is the pathogenic species of Eimeria in camelids

A

Eimeria macusaniensis

245
Q

Eimeria macusaniensis

A

Pathogenic species of Eimeria in camelids
Usually young animals
Clinical signs: colic, protein losing enteropathy, does not usually cause diarrhea, Weight loss, death
difficult to do fecal flotation

246
Q

Is Cryptosporidiosis from C. parvum zoonotic?

A

Yes

247
Q

Cryptosporidiosis

A

Lines the surface of enterocytes
Histolesions: decreased villus height and fusion, hyperemia, increased mononuclear inflammation of the mucosa
Zoonoti

248
Q

Giardiasis

A

Malabsorption due to damage to the microvillous border
Can be subclinical
Zoonotic

249
Q

What kind of diarrhea does Giardia cause

A

Malabsorptive due to damage to the microvillous border

250
Q

Pythium insidiosum

A

fungus like - water mold
usually affects the GI tract of dog but can also occur in skin
Leads to abdominal mass +/- obstruction

251
Q

Oomycetes (Pythiosis)

A

Granulomatous inflammation with non-staining organims
Cause: Pythium insidiosum
Usually affects the GI tract of dogs (can also occut on skin)
Finding: abdominal mass +/- obstruction

252
Q

What about history is important when considering diarrhea?

A

1) Number of animals affected
2) Duration, colic/diarrhea/vomiting, color of it
3) indoor vs outdoor, antibiotics treatment
4) Change in diet, indiscriminate eater
5) Access

253
Q

Pulpy kidney and encephalomalacia in lambs in caused by what C. perfingens

A

Type C (A, e toxins)

254
Q

Inflammatory bowel disease

A

Lymphoplasmacytic enteritis/gastroenteristis leading to malabsorption and protein losing enteropathy
Presence of eosinophils can suggest atopy or food hypersensitivity

255
Q

What can cause Protein Losing Enteropathy

A

1) Physical or functional lymphatic obstruction
2) Cellular mediator release that increases vascular permeability
3) Mucosal inflammation
4) Increased pressure in lymphatics

256
Q

PLE

A

Loss of albumin +/- loss of globulins, antithrombin, magnesium, calcium, cholesterol
can look like shag carpet grossly and will be float in water
caused by lymphatic obstruction, cellular mediator release that increases vascular permeability, mucosal inflammation, or increased pressure in lymphatics
Leading to diarrhea, vomiting, weight loss, edema, effusion, hypercoagulable state

257
Q

What can result in protein losing enteropathy

A

-Diarrhea
-Vomiting
-Weight loss
-Edema
-Effusion
-Hyper coagulable state

258
Q

What dog breeds does histiocytic ulcerative colitis or granulomatous colitis typically occur in?

A

Young boxers and french bulldogs

259
Q

Boxer Colitis

A

Histiocytic ulcerative colitis or granulomatous colitis seen in young Boxers
Leads to blood mucoud diarrhea, anemia, hypoalbuminemia, and weight loss
Caused by infiliration of histiocytes that contain PAS positive material
Caused by invasive E Coli

260
Q

Histiocytic ulcerative colitis /granulomatous colitis

A

seen in young Boxers
Leads to blood mucoud diarrhea, anemia, hypoalbuminemia, and weight loss
Caused by infiltration of histiocytes that contain PAS positive material
Caused by invasive E Coli

261
Q

What is the cause of Histiocytic ulcerative colitis /granulomatous colitis

A

invasive E Coli leading to the infiltration of histiocytes that contain PAS positive material

262
Q

How can you diagnose histiocytic ulcerative colitis

A

With the Periodic Acid Shift stain

263
Q

What can cause right dorsal colitis in horses

A

NSAIDs

264
Q

What might happen if a horse ingests blister beetle with cantharidin

A

necrohemorrhagic enteritis

265
Q

Atresia

A

complete occlusion as seen in with
Atresia ilei
Atresia coli
Atresia ani
Leads to abdominal distension and obstruction

266
Q

Persistent Meckel Diverticulum

A

Derived from the omphalomesenteric duct (stalk of the yolk sac)
Can be confused with the cecum
No importance clinically

267
Q

What is the clinical importance of a Persistent Meckel Diverticulum

A

there is none, other than it gets confused with the cecum

268
Q

White lethal foal syndrome

A

Inherited autosomal recessive disorder seen in paint horses leading to a mutation in the endothelin receptor B gene
Aganglionosis
Absence/Reduction of ganglion cells of the myenteric plexus (hypocellular) causing constipation and stasis and enterocolitis

269
Q

What is another name for Aganglionosis

A

White lethal foal syndrome

270
Q

Obstruction and Function Disorders

A

1) Obturation or occlusion (luminal) - plication
2) Compression (outside)
3) Stenosis (Stricture or scarring
4) Displacements
5) Functional (ileus or absence of peristalsis)

271
Q

Intussusceptum

A

the entrapped segment during intussusception

272
Q

Intussuscipiens

A

the enveloping segment during intussusception

273
Q

Intussusception

A

telescoping to the intestine where the ileium telescopes inside ascending colon obstructing the intestinal contents and can cause blooding

blood vessels become trapped between layers leading to edema, strnagulation of bowel, gangrene, sepsis, shock, and death

causes: irritability, hypermotility

274
Q

Causes of intussusception

A

irritability and hypermotility

275
Q

Intestinal Torsion

A

Rotation along the long axis
can cause luminal and vascular compromise - infarction
results in a sharp line of demarcation due to obstruction of venous blood flow

276
Q

Volvulus

A

twisting on the mesenteric axis
can cause luminal and vascular compromise - infarction

277
Q

What is the sequela to vascular compromise to the intestine?

A

-Increased intestinal permeability
-Endotoxemia
-Sepsis
-Rupture
-Peritonitis

278
Q

Different kinda of intestinal displacements

A

1) Equine colonic displacement
2) Displacement and entrapment (Equine epiploic foramen entrapment and hernias- umbilical, diaphragmatic, inguinal, scrotal)
3) rectal prolapse

279
Q

Common intestinal neoplasms

A

-Lymphoma
-Adenoma/Adenocarcinoma
-Sarcomas
-Carcinoids
-Polyps

280
Q

Intestinal/Alimentary lymphoma

A

Soft, white to tan, homogenous, soft mass or diffuse thickening of the GI wall leading to stenosis and ulceration

281
Q

What is the most common GI neoplasm of cats and ruminants leading to stenosis and ulceration

A

Intestinal/alimentary lymphoma

282
Q

What is the most common GI neoplasm in dogs and sheeps?

A

Intestinal adenocarcinoma
often have metastasized by diagnosis

283
Q

Mesenchymal neoplasms of the GI tract

A

leiomyoma, leiomyosarcoma, gastrointestinal stromal tumors, hemangioma/hemangiosarcoma

284
Q

What effect can mast cell tumors have on stomach and GI tract

A

predispose to gastric and GI ulceration and perforation

285
Q

What do beavers have near their esophagus

A

cardiogastric gland, normal stricture, near the oesophagus entrance

286
Q

Hepatic stricture

A

epithelium cells from the hepatic diverticulum and mesenchymal stroma surrounds vessels of the vitelline venous plexus
Caudal hepatic diverticulum develops into the gallbladder

287
Q

Hepatocytes and biliary epithelial cells share_____

A

a common embryonic origin

288
Q

Hepatic artery

A

supplies oxygen rich blood to the liver. approx 20% of blood to the liver

289
Q

Blood leaves the liver through the hepatic vein which quickly enters the ________

A

caudal vena cava

290
Q

Stellate (Ito) cells

A

Cells in the liver that store vitamin A and play a role in hepatic fibrosis

291
Q

What do the stellate (ito) cells store

A

Vitamin A, play a role in hepatic fibrosis

292
Q

Oval cell

A

Cells of the liver, of bone marrow origin, function in liver regeneration
differentiate into hepatocytes and biliary cells

293
Q

Space of Disse

A

gap between endothelial cells and hepatocytes

294
Q

What separates hepatic plates?

A

vascular sinusoids

295
Q

Why are there microvilli of hepatocytes

A

take in, produce, and move products out

296
Q

Kupffer cells

A

resident histiocytes
clear infectious agents and senescent cells
involved in cytokine driven interactions with hepatocytes, endothelial cells, lymphocytes and stellate cells
can function as antigen presenting cells

297
Q

What are the resident histiocytes of the liver

A

Kupffer cells

298
Q

What way does bile move in the liver

A

opposite of the flow of blood

from the centrilobular area through midzonal to the periportal area (inner to outer)

299
Q

Zonal necrosis of the liver

A

pattern of hepatocellular degeneration and necrosis where it is pale, enlarged, friable, and enhanced lobular patter
1) Centrilobular (periacinar, zone 3) is the least oxygen in region and susceptible to hypoxia, seen with severe anemia or right sided heart failure. Also has the greatest enzymatic activity where activated compounds are turned into toxic forms
2) Midozonal necrosis: seen in pigs and horses with aflatoxicosis
3) Toxin exposure lacking requirement of metabolism by oxidases

300
Q

What portion of the liver is most susceptible to hypoxia

A

Centrilobular, receives the least amount of oxygen

301
Q

What portion of the liver is damaged in pigs and horses with aflatoxicosis

A

Midzonal

302
Q

What portion of the liver has the greatest enzymatic activity and therefore targeted when metabolism is needed for activation of toxic metabolite

A

Centrilobular

303
Q

What portion of the liver is most susceptible to immediate toxins that do not need to metabolized to be toxic?

A

Periportal because these cells lack oxidases and therefore are not readily broken down here

304
Q

Bridging necrosis (Liver)

A

can link centrilobular areas or centrilobular to periportal areas
confluent areas of liver necrosis

305
Q

Massive necrosis (liver)

A

Necrosis of the entire hepatic lobule
Regeneration does not occur because all hepatocytes in the lobule are affected

306
Q

Can regeneration occur when all hepatocutes in a lobule are affected?

A

NO

307
Q

What is a common cause of random necrosis?

A

infectious agents

308
Q

Individual cell necrosis results in ______

A

proliferation and regeneration of hepatocytes

308
Q

What area of pattern of necrosis is it if necrosis is occuring around the portal vein?

A

Zonal, periportal necrosis

309
Q

Massive necrosis inhibits_______

A

hepatic replication. replacement occurs through the ductular reaction

310
Q

What does prolonged liver regenerative effort with damaged reticulin result in?

A

nodular proliferation which distorts the architecture

311
Q

Parenchymal regeneration of the liver can occur if_____

A

normal reticulin scaffolding remains intact without collapse

312
Q

Hepatic fibrosis

A

occurs in hepatic injury
collagen scaffolding can extend into parenchyma
Stellate cells change towards a myofibroblastic function producing collagen synthesis
Perisinusoidal fibrosis affects hepatic function with capillarization of the sinusoids

313
Q

What stains can be used for hepatic injury evaluation?

A

Trichrome (Blue stains collagen) and Reticulin (Tells if you have collapse of lobule)

314
Q

Periacinal hepatic fibrosis can occur with _____

A

toxic injury and chronic passive congestion

315
Q

Periportal fibrosis can result from______

A

chronic inflammation and some toxins

316
Q

What can result in multifocal hepatic fibrosis

A

migrating nematodes

317
Q

Hepatic cirrhosis

A

a diffuse process characterized by fibrosis and conversion of normal liver architecture into structurally abnormal lobes
-Parenchymal loss with increased reticulin network
-Fibrous tracts
-Hepatic regeneration between fibrous bands
-Vascular alterations such as acquired portosystemic shunts

318
Q

What can 5 things can cause hepatic cirrhosis

A

1) Chronic toxic insult
2) Chronic hepatitis or cholangitis
3) Chronic biliary obstruction (typically portal)
4) Chronic passive congestion (central vein fibrosis)
5) Inherited disorders (copper, iron, dissecting hepatic fibrosis)

319
Q

At end stage liver cirrhosis can you determine the inciting causes?

A

NO

320
Q

Portal hypertension induced hepatic injury

A

diffuse liver fibrosis with chronic injury due to increased portal blood flow resistance and pressure elevation
collateral vascular channels open, shunting of portal vein into the central vein
Can lead to ascites. enhanced by hypoalbuminemia as (enhanced loss into intestinal lumen and reduced albumin synthesis)

321
Q

If a patient presents with ascites, what likely happened

A

portal hypertension, shunting of blood from portal vein into the central vein through collateral vasculars
enhanced by hypoalbuminemia

322
Q

Canaliculi

A

within the centrilobular (periacinar areas)
drain to canals of Herring lined by hepatocytes and biliary epithelium
then to cholangioles which drain to intralobular bile ducts

323
Q

Flow of Bile

A

Canaliculi > Canals of Herring > intralobular bile ducts > gallbladder via common hepatic ducts

324
Q

3 functions of Bile

A

1) Excretory- waste products eliminated in the bile
2) Digestion- intestinal secretions aid in the digestion of lipids within the intestine
3) Buffers- neutralizes the pH of ingesta released from stomach

325
Q

What is the difference between cholestasis and hyperbilirubinemai

A

Cholestasis: blockage of bilirubin flow

Hyperbilirubinemia: increased bilirubin (conjugated or inconjugated) in blood

326
Q

Where does bilirubin conjugation occur?

A

in the liver

327
Q

Causes of prehepatic hyperbilirubinemia

A

Hemolysis- too much bilirubin for excretion

328
Q

Causes of intrahepatic hyperbilirubinemia

A

1) liver injury affection the ability of hepatocytes to metabolize and excrete bile
2) Inherited abnormalities of bile synthesis inhibiting excretion

329
Q

Causes of extrahepatic hyperbilirubinemia

A

-Obstruction of extrahepatic bile ducts
Intraluminal-calculi, parasites or
Extraluminal- neoplasia, adjacent inflammation (pancreatitis)

330
Q

Icterus/jaundice

A

yellow discoloration of the tissues when bilrubin concentration must reach 2mg/dL
Maximus accumulation takes 2 days

331
Q

What might you see if a horse has been deprived of feed for multiple days

A

icterus as hepatic bilirubin uptake is decreased

332
Q

You are performing a necropsy on an animal with icterus. What systems will you check for the cause of icterus

A

Prehepatic: Spleen, blood, urinary tract
Hepatic: Liver
Post-Hepatic: Gallbladder, cystic duct, Duodenal papilla

333
Q

Liver zone 1

A

Periportal area, low enzymatic activity

334
Q

Liver zone 2

A

Midzonal area between the centrilolobular and portal areas

335
Q

Liver zone 3

A

Centrilobular areas, least amount of oxygen, greatest enzymatic activity

336
Q

Circulatory disorders of the liver

A

1) Disturbances of outflow (passive or venous congestion
2) Disturbances of inflow (Anemia, congenital porto-systemic shunts, portal hyper tension
3) Incidental (Telangiectasia)
4) Infarction- liver lobe torsion

337
Q

How might acute passive liver congestion occur

A

acute right sided failure, can result in nutmeg liver

338
Q

How might chronic passive liver congestion occur

A

valvular endocardiosis in dogs

339
Q

What can chronic passive liver congestion lead to

A

Centrilobular hypoxia leading to atrophy (Degeneration, necrosis), sinusoidal ocngestion, periportal hepatocellular steatosis, and bridging hepatic fibrosis

340
Q

Hepatic Steatosis

A

buildup of fat in the liver, can be from chronic passive congestion or other reasons tba

341
Q

Would you expect passive congestion to cause icterus?

A

No, its an issue of blood flowing out of the liver

342
Q

What clotting factors are made in the liver

A

5, 7, 9, 10

343
Q

Bleeding tendencies with liver disease

A

-Impaired synthesis of clotting factors
-Reduced clotting products (fibrin degradation products, activated coagulation factors, plasminogen factors)
-Metabolic abnormalities affecting platelet function

*Clotting factors made in liver
Chronic disease factor II also deficient (Biliary obstruction, impaired fat absorption limiting vitamin K uptake from the intestine > inactivity of factor 2, 7, 9, 10

344
Q

What clotting factors are impacted with biliary obstruction

A

impaired fat absorption (affects 2, 7, 9, 10)

345
Q

Liver failure has reduced production of factors 5, 7, 9, 10. What other factor do you also see affected in biliary obstruction due to limited vitamin K uptake from the intestine

A

Factor II

346
Q

What region of the hepatic lobule is most severely affected by anemia?

A

Centrilobular region

347
Q

Congenital portosystemic shunts

A

Blood is shunted from the abdominal organs to the systemic circulation, bypassing the liver
Liver is unable to metabolize and detoxify the blood. Deprived of factors to enhance development (hepatic atrophy and insufficiency)
Can lead to stunted, hepatic-encephalopathy (ammonia) and ammonia biurate crystals

348
Q

What dogs do you typically see single extrahepatic shunts in

A

Small and toy breeds
Portal vein to caudal vena cava, portal vein to azygous vein

349
Q

What dogs do you typically see single intrahepatic shunts in?

A

Large breeds
Failure of ductus venosus to close at birth (often left side of liver)

350
Q

What do you typically see with congenital portosystemic shunts in cats?

A

almost always extrahepatic and left gastric is the most common

351
Q

What can lead to an acquired portosystemic shunt?

A

hepatic hypertension leading to multiple vessels being impacted

352
Q

Intrahepatic shunts

A

failure of ductus venosus to close at birth
most commonly large breed dogs
left side of liver

353
Q

Extrahepatic shunts

A

portal vein to the caudal vena cava
portal vein to azygous vein
small breeds of dogs and cats

354
Q

What is a result of congenital portosystemic shunts

A

-Stunted
-Hepatic encephalopathy
-Hepatic atrophy and insufficiency
-Abnormal plasma ammonia leading to ammonia biurate crystals in the urine

355
Q

What has the same histological lesions as a portosystemic shunt

A

Portal vein hypoplasia (microvascular dysplasia) leading to diminished hepatic perfusion leading to portal hypertension
Use clinical data, antemortem imaging, and portal vein pressure for dx.

356
Q

Hepatic microvascular dysplasia (HMD)

A

histological diagnosis when ruled out portosystemic shunt
dogs are often 3-4 years of age
bloodwork less severe
Yorkshire and Cairn terrier most commonly affected but other small breeds are
Definitive diagnosis: proving dogs do not have any shunts but do have abnormal vessels on hepatic biopsy
some dogs can have both

357
Q

Hepatic encephalopathy

A

Neurologic disease (depression, behavioral changes, convulsion) associated with hepatic failure
Unknown metabolites and increased plasma ammonia
Amines are absorbed from the intestine into the portal blood and not appropriately metabolized by the diseased liver
Toxic effects on the brain, seen in congenital or acquired shunts

358
Q

Portal vein thrombosis

A

thrombosis of the extrahepatic portal system
seen in hyper coagulability or inflammatory disorders such as pancreatitis

359
Q

What are some causes of hypercoagulability in the dog

A

*Liver disease
*Cushings
*Protein losing disease
*Neoplasia
*Immune mediated disease
*Infectious disease
* Pancreatitis

360
Q

Causes of prehepatic portal hypertension

A

portal vein thrombosis

361
Q

Causes of intrahepatic portal hypertension

A

chronic liver disease bridging disease
lobular abnormalities
regenerative nodules
lobular dissecting hepatitis
Veno-occlusive disease
amyloidosis
Schistomiasis
Granulomatous disease

362
Q

Causes of post-hepatic portal hypertension

A

thrombosis of hepatic vein or caudal vena cava
congestive heart failure

363
Q

Telangiectasis

A

dilation of sinusoids with hepatocellular loss
variable size dark, red to blue foci
common in cattle and older cats
can be incidental

364
Q

Hepatic lipidosis or steatosis

A

occurs when the rate of triglyceride accumulation within the hepatocytes exceeds metabolic degradation or release of lipoproteins
causes: diet, toxins, hypoxia, ketosis, species syndromes, endocrine diseases

365
Q

What could happen with sheep/goats on a high fat or deitary deficiencies of cobalt and vitamin B12

A

Liver steatosis

366
Q

COMMD1 mutation

A

an autosomal recessive inherited mutation in dogs leading to impaired biliary excretion of copper

367
Q

What does molybdenum do to copper

A

it antagonizes its uptake

368
Q

What animals are most frequently affected by copper toxicity

A

Sheep (but also cattle, goats, and pugs)

369
Q

How might copper toxicity occur

A

1) Excessive intake
2) Low molybdenum
3) Plants w hepatotoxic phytotoxins, pyrrolizidine alkoloids
4) COMMD1 mutation dogs (Dobermans, Labs, Skye and West Highland, Dalmations)

370
Q

How does copper impact the liver

A

Hepatocellular necrosis from reactive oxygen species leading to hepatocellular apoptosis

Hemolysis and hemoglobinuria because decreased hepatic ability to deal with copper leading to elevated plasma copper leading to intravascular hemolysis

Acute: anorexia, abdominal pain, diarrhea, dehydration, and shock

Histologically: centrilobular hepatic necrosis and renal tubular necrosis

371
Q

What is the most common recognizable size of canine chronic hepatitis

A

copper toxicity

372
Q

Where does copper accumulate in the liver

A

centrilobular regions

373
Q

What is the Rhodamine Stain used for

A

copper detection within the hepatocytes

374
Q

What stains copper in the hepatocytes

A

Rhodamine

375
Q

Lobular dissecting hepatitis

A

disease of young dogs, cirrhosis of the liver
similar to chronic active hepatitis but you see mild inflammation and increased fibrosis dissecting hepatic parenchyma isolating hepatocytes

376
Q

Hepatosis dietetic

A

Acute hepatic necrosis in young, rapidly growing pigs
poorly understood but Vitamin E and/or selenium deficiency is like contributing to it because they are antioxidants and prevent oxidative injury leading to hemorrhagic centrilobular to massive hepatic necrosis

377
Q

What might cause hepatosis dietetic in young rapidly growing pigs

A

vitamin e/selenium deficiency

378
Q

Lipofuscin

A

pigment accumulation that increases with age due to incomplete oxidation of lipids

379
Q

Ceroid

A

pigment accumulation due to peroxidation of fat deposits

380
Q

Parasite hematin

A

pigment accumulation due to iron and porphyrin, fascioliasis

381
Q

Hemosiderin

A

pigment accumulation due to the breakdown of erythrocytes

382
Q

What is a consequence of portosystemic shunt
A) Chronic passive congestion
B) Massive hepatic necrosis
C) Nodular regeneration
D) Hepatic encephalopathy

A

D) Hepatic encephalopathy

383
Q

What effect can steroids have on the liver

A

Hepatopathy, steatosis

384
Q

What allows for cobalamin absorption

A

intrinsic factor

385
Q

What secretes glucagon

A

alpha cells

386
Q

What secretes insulin

A

beta cells

387
Q

What secretes somatostatin

A

delta cells

388
Q

Pacinian corpuscles

A

present on the pancreas of cats, mechanoreceptors for pressure and vibration
more suceptible for pain in abdomen
also in humans and primates

389
Q

What is special about the cat pancreatic and common bile duct

A

they merge prior to going through the duodenal papilla while in dogs they enter separately

390
Q

Canine juvenile pancreatic atrophy

A

cause of EPI in young dogs (loss of exocrine pancreas)
Primarily german shepherd, rough coated collies, chows, and english setters
Complex genetic disorders
Infiltration by small lymphocutes leading to atrophy and replacement fibrosis
autoimmune cell mediated process against acinar cells

391
Q

What is a common cause of EPI in young german shephards

A

Canine juvenile pancreatic atrophy

392
Q

EPI is a disease of

A

maldigestion and malabsorption

393
Q

Clinical signs of EPI

A

Weight loss depsite normal to voracious appetite
Poor quality hair coat
muscle atrophy
Pale, soft, voluminous and malodourous feces “cow patty”

Mesenteric torsion, intussusception
Small intestinal bacterial overgrowth from increased volume of undigested nutrients

394
Q

How do you diagnose EPI

A

Signalment and clinical signs
Serum trypsin-like immunoreactivity
<2.5 mcg/L dogs <8 mcg/L in cats
Cobalamin deficiency present

395
Q

Agonal and postmortem finding of the pancreas

A

1) Interstitial hemorrhage from increased central blood pressure preceding the death
2) Autolysis- pancreas autodigests very rapidly- can look like pancreatitis/fat necrosis

396
Q

Acute Pancreatitis

A

necrosis (primary lesion) and acute inflammation
Dogs>Cats
Cause: Not clear but
-High lipid/fat diet
-Abdominal trauma
-Hypotension and re-perfusion
-Hyperlipidemia: Cushings and hypothyroidism

397
Q

Is acute pancreatitis more common in dogs or cats

A

Dogs

398
Q

is chronic pancreatitis more common in dogs or cats

A

Cats

399
Q

Gross findings of acute pancreatitis/ pancreatic necrosis

A

Red swollen parenchyma
Indistinct margins
hemorrhage
edema
fat necrosis / saponification

400
Q

Fat necrosis/saponification

A

Release of pancreatic enzymes (lipase and amylase) leading to the breakdown of adipose into fatty acids and salts leading to necrosis and saponification
chalky, white to yellow deposits over the peri-pancreatic fat
histopath: purple to pink material, fibrin, mineral replacing adipose
surrounded by sheets of neutrophils and hemorrhage

401
Q

How does fat necrosis/saponification occur

A

when pancreatic enzymes such as lipase and amylase are released to breakdown adipose into fatty acids and salts

402
Q

What can zinc toxicity lead to

A

Pancreatic necrosis

403
Q

Zinc toxicity

A

pancreas is a major route of zinc excretion
narrow margin between safe and unsafe exposure
exocrine acini are affected first
ingestion of pennies
Can also lead to heinz body hemolytic anemia

404
Q

Sequelae of pancreatic necrosis

A

can lead to EPI

acutely- cytokine storms leading to SIRS (systemic inflammatory response syndrome) leading to acute respiratory distress syndrome and DIC

Necrotizing panniculitis- inflammation of subcutis due to circulating pancreatic enzymes: phospholipase A, lipase, amylase, and trypsin

405
Q

Findings of Chronic Pancreatitis

A

Pancreas is firm, small, and nodular

Histopath: atrophy, fibrosis (pink bands of tissue) and lymphocytic or lymphoplasmacytic inflammation (blue aggregates)

406
Q

What can cause chronic pancreatitis

A

1) Hepatic lipidosis due to inappetance
2) Repeated episodes of acute inflammation
3) Unresolved/ongoing necrosis or inflammation
4) Atrophy and fibrosis leading to loss of exocrine and/endocrine pancreas such as EPI or Diabetes mellitus

407
Q

Feline Triaditis

A

due to the common bile duct and pancreatic duct merging together at the duodenal papilla
inflammation here can manifest 3
1) enteritis
2) pancreatitis
3) cholangitis or cholangiohepatitis

408
Q

Pancreatic duct flukes

A

-Eurytrema procyonis (carnivores)
-Eurytrema pancreticum (ruminants)
Block the pancreatic duct, cause inflammation, atrophy and fibrosis

409
Q

Pancreatolithiasis

A

Stones in the pancreatic duct
most commonly in cattle (incidental at slaughter)
mineralization following inflammation or necrosis
Rarely cause complete obstruction

410
Q

Exocrine nodular hyperplasia

A

incidental finding that is constant adaptation to nutritional influences
seen in older dogs, cats, and cattle
nodules are pale due to less zymogen granules
can be confused with neoplasia but paler than surrounding pancreas

411
Q

Adenocarcinoma of pancreas

A

tan to white
firm
multinodular
very infiltrative
Histo: acini, islands, cords
can have zymogen granules
can surround by dense stroma=desmoplasia/scirrhous response
carcinomatosis along serosal surface

412
Q

Desmoplasia/Scirrhous response

A

the body response to wall off neoplasms with scar tissue to prevent spread. seem in pancreatic adenocarcinomas

413
Q

Insulinoma

A

most common islet cell tumor
beta cells
secrete insulin and result in hypoglycemia
variable discrete, tan to red masses
common in ferrets (not malignant)
metastasis to liver and lymph nodes
histopath: lobules and packets of polygonal cells separated by fine connective tissue septa

414
Q

Are insulimonas malignant

A

most are, except in ferrets

415
Q

Where do insulinomas typically metastasize to in the dog?

A

lymph nodes and liver
mean survival time ranges between 12 to 18 months

416
Q

T/F Herpes virus can cause hepatitis

A

T

417
Q

Why is the first 2 weeks of life the most susceptible to herpesviral hepatitis

A

because of the lack of competent thermoregulation

418
Q

Herpesviral hepatitis typically affects

A

the fetus or neonates
transplacental exposure, birth canal, infected littermates, oronasal secretion from dam

419
Q

Herpesviral hepatitis leads to

A

multifocal, random hepatic necrosis with intranuclear inclusion bodies

420
Q

What are your differentials for centrilobular necrosis of the liver

A

-Toxins (xylitol, aflatoxicosis, acetaminophen, carprogen
-Chronic passive congestion
-Canine Adenovirus 1

421
Q

Canine adenovirus 1 and canine herpesvirus 1 both cause intranuclear inclusions but how do they differ in there hepatic necrosis

A

Canine Adenovirus 1 causes centrilobular necrosis while canine herpesvirus 1 causes random hepatic necrosis

422
Q

T/F Canine Adenovirus causes random hepatic necrosis

A

F: it causes centrilobular necrosis

423
Q

What is the causative agent of canine hepatitis

A

canine adenovirus 1

424
Q

Infectious canine hepatitis

A

Caused by canine adenovirus 1
slight fever to severe depression, marked leukopenia and coagulation abnormalities
Hepatocullar necrosis and endothelial cell damage
immune complex deposition leading to uveitis, corneal clouding and glomerulonephritis
Intranuclear inclusions in liver, dx w PCR and FISH
also reported in wildlife
uncommon with routine vaccination

425
Q

Clinical signs of Infectious canine hepatitis (ICH)

A

-Hepatocellular necrosis and endothelial cell damage ( centrilobular)
-Blue eye/corneal edema
-Glomerulonephritis
-Intranuclear inclusion boddies in the liver

426
Q

Rabbit hemorrhagic disease causative agent

A

Calicivirus

427
Q

Rabbit hemorrhagic disease

A

Calicivirus
Highly contagious, temperature resistance, direct contact, infected rabbit blood
Massive hepatocellular necrosis
NM, CA, CO, NV, TX
Pale enhanced lobular pattern, limp, friable texture
Necrosis is acute
Periportal to midzonal
Reportable to state veterinarian

428
Q

Where does hepatic necrosis from rabbit hemorrhagic disease occur

A

Periportal to midzonal

429
Q

Lymphocyctic cholangitis in cats

A

slowly progressive and chronic
usually >4 years of age
icterus (intrahepatic cholestasis)
Lymphocytes and plasma cells in the portal tracts and surrounding bile ducts
unknown cause
immune mediated?
must be differentiated from chronic suppurative cholangitis which is usually by ascending bacterial infections (cats > 11yo)
can occur with pancreatitis and IBD “Triaditis”

430
Q

Why is the liver a common place for bacteria to manifest

A

bacteria can reach the liver through the portal vein, umbilican veins, hepatic artery, ascending from biliary, parasitic migration, direct extension from tissue adjacent to the liver
Ex: Fusobacterium in toxic ruminits, phlebitis, thrombosis, portal hypertension, septic thromboemoboli into lungs, sidden death, fungal disease with ruminal ulceration
enteric species of bacteria (Francisella, Nocardia, actinomyces)

431
Q

Common bacterial causes of hepatitis

A

-Mycobacterim, tuberculosis
-Rhodococcus equi
-Corynbacterium pseudotuberculosis
-Francisella tularensis
-Salmonellosis: foci of necrosis with macrophages surround paratyphoid nodules

432
Q

Paratyphoid nodules

A

aggregates of macrophages in the liver in response to salmonellosis

433
Q

Clostridium piliforme hepatitis

A

young/immunocompromised animals
well recognized in lab animal
lead to pale foci of hepatocellular necrosis with surrounding neutrophilic and mononuclear infilitrate
Intracellular

434
Q

What stain should you use for Clostridium piliforme (Tyzzer’s)

A

Warthin-Starry or Gomori’s silver stain

435
Q

T/F Clostridium piliform is intracellular

A

T

436
Q

Leptospirosis

A

gram -, thin spiral bacterial
enter body through mucous membranes or skin via contaminated water, bedding and soil, shed in urine, transplacental infection
intravascular hemolysis causing ischemic injury to centrilobular regions
icterus
can cause hepatic dissociation, bile casts, hemosiderin Kupffer cells, chronic active hepatitis

437
Q

What disease causes hepatic dissociation and chronic active hepatitis

A

Leptospirosis

438
Q

What disease causes intravascular hemolysis and ischemic injury to centrilobular regions

A

Leptospirosis

439
Q

What bacteria can cause hepatic infarction

A

Clostridium Haemolyticum (novi type D)

440
Q

What can cause bacillary hemoglobinuria

A

Clostridium Haemolyticum (novi type D)

441
Q

Bacillary hemoglobinuria

A

Caused by Clostridium Haemolyticum (novi type D), found in poorly drained pastures with alkaline pH
After ingestion latent spores become embedded in liver
disease requires anerobic conditions (Fasciola hepatica)
High nitrate diet, liver puncture or biopsy, or other cause of localized hepatic necrosis
Produce beta toxin causing intravascular hemolysis and hemolytic anemia/hemoglobinuria and infarction
Signs: dehydration, anemia, bloody abdominal fluid, liver infarction, kidney petechiations, red to purple urine
dx: PCR, IFAT, IHC on liver
Prevent with vaccinations and control of liver flukes

442
Q

What parasite is associated with clostridium haemolyticum

A

Fasciola hepatica, allows for anaerobic conditions

443
Q

What bacteria is associated with Fasciola hepatica infection

A

Clostridium haemolyticum

444
Q

How does Clostridium cause hemoglobinuria

A

It produces beta toxin that causes intravascular hemolysis and hemolytic anemia

445
Q

How can you prevent bacillary hemoglobinuria

A

-Clostridium vaccination or fluke control

446
Q

Black Disease causative agent

A

Clostridium novyi (type B)

447
Q

Black’s Disease

A

Caused by Clostridium novyi (Type B)
most common in sheep and cattle but can occur in pigs and horses
germinate in regions of lowered oxygen tension and release exotoxin
Hepatic necrosis with migration of liver flukes
exotoxin causes discrete foci of coagulation necrosis and hemorrhage in the liver
Histo: necrosis surrounded by neutrophils and abundant gram + rods

448
Q

What bacteria causes multifocla hepatic necrosis with black pigment with migration tracts of fluke pigment

A

Clostridium novyi (Type B)

449
Q

Compare and contrast C. hemolyticum and C. novyi

A

spores are spread through fluke larval migration (areas of low oxygen) leading to bacterial proliferation. Both lead to death but hemolyticum toxins lead to intravascular hemolysis while novyi leads to infectious necrotic hepatitis

450
Q

Name some causes of intravascular hemolysis

A

-Leptospirosis
-Bacillary hemoglobinuria
-Copper toxicity

451
Q

What causes milk spotted liver in pigs

A

Ascaris suum migration

452
Q

How might heartworm cause DIC and acute hepatic failure

A

it causes vena caval syndrome

453
Q

Echinococcus

A

caused by ingested hydatid cysts
central necrosis

454
Q

How does Fasciola hepatica differ from Fascioloides magna

A

-Fasciola hepatica inhabits the biliary system while Fascioloides magna inhabits the hepatic parenchyma

455
Q

Where does Fasciola hepatica inhabit

A

the biliary system

456
Q

Where does Fascioloides magna inhabit

A

the hepatic parenchyma

457
Q

Trematode Hepatitis

A

Caused by F. hepatica or magna migration through the liver creates hemorrhagic tracts with fibrotic repair
leads to peritonitis, abscessation, widespread hepatic necrosis infiltration and Clostridium haemolyticum or novyi infection leading to bacillary hemoglobinuria or infectious necrotic hepatitis

458
Q

Heterobilharzia americana

A

trematode of raccoons. ova shed in water from feces by infected racoons, release miracidia penetrate the host snails
Dogs infected wen skin is penetrated by cercariae released by snails
granulomatous diseasee in liver, pancreas, intestine, and mesentery in reaction to adult schistosomes

459
Q

Theiler’s Disease

A

Equine Serum Hepatitis
Received inection of equine serum (such as tetanus antitoxin)
Late summer or early
Increasing evidence for a viral cause
Incubation period is prolonged
Rapid to often fatal
Hepatic failure with hepatic encephalopathy and icterus
intravascular hemolysis in terminal stages

460
Q

What might occur with a horse receiving an injection of tetanus antitoxin

A

Theiler’s Disease (Equine Serum Hepatitis)
Hepatic failure with hepatic encephalopathy and icterus
Intravascular hemolysis with late stages

461
Q

What hepatocytrs have the highest concentration of P450 enzymes

A

Centrilobular hepatocytes

462
Q

Phases of liver metabolism

A

Phase I: chemicals bioactivated to high-energy reactive intermediate molecule (Bioactivation)
Phase II: formation of covalent bonds with polar molecules such as glucuronic acid (Conjugation)
Phase IIIL transport of molecules across the cell membranes into canaliculus

463
Q

Old or young cats: Suppurative cholangitis/cholangiohepatitis

A

Young

464
Q

Old or young cats: lymphocytic cholangitis

A

Old

465
Q

What phase does conjugation happen

A

Phase II

466
Q

What phase does bioactivation happen

A

Phase I

467
Q

What phase does excretion happen

A

Phase III

468
Q

Where does direct toxicity to hepatocytes occur

A

zone 1: periportal (no need to metabolism)

469
Q

Where does indirect toxicity to hepatocytes occur

A

zone 3: Centrilolobular- injury occurs where there is most concentration of enzymes, toxic after metabolism by gi microbes

470
Q

Acute toxic injury to liver

A

regeneration possible if submassive
Massive necrosis causes destruction of reticulin framework/limiting plate resulting in fibrosis

471
Q

Chronic or recurrent toxic injury to liver

A

Necrosis and fibrosis and hepatocellular nodular regeneration- hepatic insufficiency

472
Q

Name toxins of acute hepatic injury

A

1) Acetaminophen (cats)
2) Carprofen (dogs)
3) Microcystin LR (blue-green algae)
4) alpha-amanitin (Amanita mushrooms)
5) Acute aflatoxicosis
6) Xylitol (dogs)

473
Q

What has red/white/blue lesions on histostaining

A

Hepatocutaneous syndrome

474
Q

Acetaminophen toxicity

A

drug is metabolized by glucouronidation and sulfation
cats are deficient inpathways, dogs can still be affected
Causes methemoglobinemia and hepatotoxicity (Renal injury also possible)
liver damage more common in dogs
Centrilobular necrosis

475
Q

Microcystin LR

A

Occur in cyanobacteria algal blooms in late summer/early fall
released by dying bacteria that accumulates on the water
ingested by livestoack
cause hemorrhagic gastroenteritis and hemorrhagic liver
Have centrilobular or massive hepatic necrosis and hemorrhage

476
Q

Amanita mushrooms

A

high mortality rate lead to vomiting, bloody diarrhea to multiorgan failure
Massive hepatocellular necrosis, ductular reaction, hydropic degeneration

477
Q

Xylitol

A

acutely toxic to dogs leads to hyperinsulinemia, hypoglycemia, icterus, and liver failure
vomitting, lethargy, weakness, seizures
found in sunscreens, medications, toothpastes, chewable vitamins, cosmetics, deodorants, and hair care
centrilobular to midzonal or massive necrosis and vacuolar degeneration

478
Q

Aflatoxicosis

A

mycotoxin produced by fungus on feed in hot temperatures
Produced by Aspergillus flavus and parasiticus
metabolized in liver and can lead to carcinogenesis, teratogenesis, immunosuppression, and liver damage with reduced protein synthesis
inappetance, poor growth, hemorrhage, icterus, and death

479
Q

What can be seen in subacute aflatoxicosis

A

Steatosis and Cholestasis

480
Q
A
481
Q

What can be seen with chronic aflatoxicosis

A

Bridging fibrosis (chronic) and biliary hyperplasia

482
Q

Pyrrolizidine Alkaloid containing plants

A

Ragwort, Crotolaria, Senecio, Cynoglossum
Convered to pyrrolic esters by hepatic P450
Pigs most susceptible, chronic, lead to hepatic fibrosis
Megalocytosis, hepatic fibrosis, biliary proliferation +/- nodular regeneration

483
Q

A horse present with icterus. Liver biopsy reveals hepatic dissociation, bile casts, and hemosiderin-laden macrophages. What would be a strong differential
A) Leptospirosis
B) Clostridium piliforme
C) Rhodococcus Equi
D) Salmonellosis

A

A) Leptospirosis

484
Q

Hepatocellular nodular hyperplasia

A

common in dogs >6years
Not a result of hepatic dysfunction
multiple are present
Well demarcated and can compress adjacent parenchyma
Contain all elements of normal liver
Cytoplasmic lipid or glycogen common within hepatocytes

485
Q

What should you not do when submitting liver biopsy

A

Say why you need to take the biopsy
Give as much information as you can
Provide what part of the liver

486
Q

What are features of regenerative nodules (e.g hepatic cirrhosis) in contrast to nodular hyperplasia

A

They are not smooth or pale
Disease process (nodular hyperplasia is not)

487
Q

Hepatocellular adenoma

A

single, compress adjacent tissue, variable size, unencapsulate. looks very similar to nodular hyperplasia

488
Q

Is Hepatocellular carcinoma differentiated

A

well differentiated to atypical. but look for invasion at margin mitotic figures, and cellular atypia and help

489
Q

Hepatocellular carcinoma

A

well differential to atypical
Common in ruminants (sheep) and dogs
solitary, involve entire lobe, well demarcated
Friable, more pale, divided into lobules
irregular trabeculae, three or more cells thick
multiple patterns can be found
distant metastasis uncommon

490
Q

3 syndromes of hepatocellular carcinoma in dogs

A

1) Solitary or massive: low mitotic rate, low metastatic rate, usually amenable to surgery

2) Multifocal (nodular)-several masses

3) Diffuse- throughout the entire liver: nodular or diffuse can have metastasis, intrahepatic extension is most common, extraheptatic metastasis can occur to the local lymphnodes and lunges

491
Q

What is the easiest hepatocellular carcinoma to treat in dogs

A

Solitary, can be surgically removed

492
Q

Carcinoid

A

hepatic tumor of the neuroendocrine cells within the biliary epithelium
single or multiple nodules
use IHC to distinguish

493
Q

What is the next common site for hemangiosarcoma after skin, spleen, and heart

A

Liver

494
Q

What animal does not have a gallbladder

A

Rat

495
Q

What is special about hepatosplic and hepatocytotropic T cell lymphoma

A

there is hepatic involvement with the absence of peripheral lymphadenopathy

496
Q

Cholecystokinin

A

released in response of fatty food in intestine tract to stimulate bile emulsification of fats for better absorption

497
Q

What is a result of biliary atresia

A

hyperbilirubinemia

498
Q

Result of choleliths

A

can obstruct the gallbladder or bile ducts. bile cannot be released upon stimulation leading to hyperbilirubinemia and maldigestion of fats
pressure necrosis can rupture and cause acute peritonitis

499
Q

What two viruses can cause cholecystitis

A

1) Rift valley fever
2) Infectious canine hepatitis

500
Q

Gallbladder Edema causes

A

1) Non-sepecific inflammatory diseases
2) Anphylaxis-generalized venous congestion
3) Cardiac disease

501
Q

T/F Biliary hamartoma is congential

A

T - biliary tree developmental abnormality

502
Q

T/F Cholangiocellular carcinoma is benign

A

F- commonly to LN, lungs, or abdominal seeding

503
Q

Cholangiocellular carcinoma

A

neoplasm of biliary epithelium from intrahepatic ducts
single or multiple masses
firm, raised, central depression, pale, unencapsulated
can have scirrhous response (firmness)
Metastasis is common to LN, lungs, or abdominal seeding

504
Q

Cystic mucinous hyperplasia

A

benign
dogs and sheep
cystic spaces that thicken the gallbladder mucosa
asymptomatic but can become issue (gallbladder mucocele)
cause unknown

505
Q

Gallbladder mucocele

A

progressive accumulation of mucin-laden bile
Can result in bile duct obstruction
Can lead to gall bladder ischemia and necrosis, bile peritonitis, and opportunistic infection
tx: with cholecystectomy
predisposing factors: endocrinopathies, hyperlipidemia, gallbladder dysmotilility, cystic hyperplasia

506
Q

What could result from a gallbladder mucocele

A

1) Bile Duct obstruction
2) Gall bladder ischemia and necrosis
3) Bile Periotonitis
4) Opportunistic infection

507
Q

What is the best treatment for gallbladder mucocele

A

Cholecystectomy

508
Q

What can predispose animal to gallbladder mucocele

A

endocrinopathies, hyperlipidemia, gallbladder dysmotility, cystic hyperplasia

509
Q

Are you more supspicious of steroid hepatotopy or hepatic lipidosis in a dog

A

steroid hepatotopy

510
Q

What is your primary differential for multifocal hepatic abscesses in a horse

A

Rhodococcus equi

511
Q

What is your top differential for disseminated foci of necrosis in the liver and spleen of a cat

A

Tularemia or Herpes

512
Q

What is your differential for diarrhea, vomiting, coma, death. Liver with centrilobular to massive hepatocellular necrosis

A

Acute toxicity (Xylitol, Acetaminophen, Aflatoxin, Cyanobacteria, Amanita Mushroom)

513
Q
A

BOD 2 (5 decks)

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