Exam 1 Path II Flashcards

1
Q

Which of the following is more likely to develop neoplastic alimentary tract disease?

  • a. dogs and cats
  • b. ruminants and pigs
  • c. horses
A

dogs and cats

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2
Q

Which of the following is more likely to develop infectious alimentary tract disease that are poorly controlled by vaccination?

  • a. dogs and cats
  • b. ruminants and pigs
  • c. horses
A

ruminants and pigs

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3
Q

Which of the following is more likely to develop intestinal displacement?

  • a. dogs and cats
  • b. ruminants and pigs
  • c. horses
A

horses– colic

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4
Q

Portals of pathogen entry into the GI tract?

A
  • (1) Ingestion (*most common*)
  • (2) Coughed up and swallowed
  • (3) Systemic hematogenous route
  • (4) Migration through the body (ie. parasites)
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5
Q

Cleft Palate (Palatoschisis)

A

Common in calves Central defect in the midline fusion of the palatine shelves resulting in communication b/w the oral and nasal cavity.

Tongue may protrude through the abdnormalities

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6
Q

Causes of Palatoschisis and Cheiloschisis?

A
  • often a genetic disorder
  • toxins = ingestion of Veratrum californicum and other teratogenic plants like lupines, poison hemlock in cattle and sheep
  • maternal exposure to drugs during pregnancy
    • griseofulvin in queens and mares
    • steroids in primates
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7
Q

Common sequela of Palatoschisis?

A

(1) aspiration pneumonia due to the communication b/w the cavities (2) starvation (unable to generate suction to suckle)

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8
Q

Malocclusion

A

Congenital abnormalities of the oral cavity. Failure to the upper and lower incisors to interdigitate properly. May result in difficulties in the prehension and mastication of food. Brachygnathia – shorter lower jaw Prognathia – protrusion of the lower jaw

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9
Q

Brachygnathia

A

Brachygnathia – shorter lower jaw

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10
Q

Prognathia

A

Prognathia – protrusion of the lower jaw

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11
Q

Other names for Cleft Lip ?

A

“Harelip” Cheiloschisis

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12
Q

Dental Attrition

A

loss of tooth structure by mastication

The degree of tooth wear depends on the tooth, the animal species and the types of food.

Abnormal wearing is MOST COMMON in herbivores results in “step mouth”

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13
Q

Peridontal disease

A

Resident bacterial films and the acid and enzymes they produce to enamel, gingival and periodontal ligamental damage

See:

–Dental Plaques

–Dental calculus (tartar & mineralized dental plaque)

–Decrease alveolar bone and gingival recession and loss of teeth

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14
Q

Wooden Tongue Etiology?

A

Actinobacillus ligniersesii - gram neg rod primarily in cattle, occasionally in swine and sheep

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15
Q

Thrush (Candidia albicans)

A

Often is observed in young animals (especially if on long-term antibiotic treatment) or in animals with underlying debilitating diseases see yellow/white plaques on mucosal surface that are the hyphae/yeast of the Candidia

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16
Q

What are lingual lesions manifestations of? (ulcerative and necrotizing glossitis)

A

–renal failure –viral disease (BVD, FMD) Other Etiology: Infectious agents, trauma, chemical injury, auto-immune, idiopathic

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17
Q

Lymphoplasmacytic Gingivitis & stomatitis is common in:

A

cats that are FeLV or FIV positive. FCV can also be involved. See Infected gums and mucous membranes

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18
Q

Feline chronic gingivo-stomatitis (FCGS)

A

Feline chronic gingivo-stomatitis (FCGS) Cinical signs: oral pain, dysphagia, ptyalism and weight loss. Etiology: unclear. Dental plaque, FCV, and immune-mediated mechanisms appear to be involved. FCGS is also common in FIV positive cats.

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19
Q

Chronic ulcerative (lympho-plasmacytic) paradental stomatitis

A

Chronic ulcerative (lympho-plasmacytic) paradental stomatitis Most common in older dogs Etiology unclear but associated with chronicperiodontal disease and immunosuppresion. Looks similar to feline lymphoplasmacytic gingivitis

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20
Q

Common cause of vesicular stomatitis in cats?

A

Calciviral infection

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21
Q

Reportable/Foreign Vesicular Stomatis (4 disease) and host?

A

–Foot and Mouth Disease (Picornavirus) – Ruminants, pigs (cloven hoofed animals) NOT HORSES –Vesicular Stomatitis (Rhabdovirus) – Ruminants, pigs and horses (only one in horses) –Vesicular Exanthema of Swine (Calicivirus) – ONLY PIGS –Swine Vesicular Disease (Enterovirus) – ONLY PIGS

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22
Q

Foot and Mouth Disease Pathogenesis

A

Viral ingestion/inhalation–> pharynx –> viremia –>oral mucosa & epidermal sites (oral cavity and coronary bands –> lesions develop in areas subjected to mechanical injury –>vesicle à ulcer/erosion –> sloughing

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23
Q

Clinical Signs of Foot and Mouth Disease

A

Vesicular Stomitits

drooling saliva (ptyalism), lameness due to coronary band lesions, sloughing of the hoof, lesion in areas susceptible to mechanical injury.

Tiger Heart- acute myocardial degeneration and necrosis (pale stripes) that cause high death in young animals

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24
Q

Vesicular Exanthema

A

Vesicular Stomitits only in pigs

caused by calcivirus

Vesicular/Ulcer lesions on nose, face and feet

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25
Q

What is the name of this? What are 3 etiolgy? Pathogenesis?

A

Erosive-Ulcerative Stomatitides

(1) dogs and cats with renal disease
(2) BVD in cattle (subtle lesions)
(3) MCF in cows (more severe)

NO vesicle formation.

Due to presence of vasculitis that leads to damage of the surface epithelium and exposure of the lamina propria.

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26
Q

What is this called? what is the etiology and outcome?

A

Tiger Heart

acute myocardial degeneration and necrosis (pale stripes) that causes high mortality in young animals

Seen in Foot and Mouth Disease

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27
Q

Disease name? Etiology? Description? Histology?

A

Bovine Papular stomatitis

Etiology: Parapoxvirus

Papules on the nares, muzzle, oral cavity.

Usually present in immunosuppressed individuals.

Appear as “Coin-Shaped papules and Ulcers”, the virus is closely related to pseudocowpox virus that causes “milker’s nodule in humans (hands)”.

See proliferation/raised epithelium due to hyperplasia of keratinocytes.

See ballooning degeneration and eosinophilic intracytoplasmic inclusion bodies

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28
Q

Names? Etiology? Complications? Host?

A

Oral Necrobacillosis

Fusobacterium necrophorum (filamentous bacteria part of normal flora)

in calf, sheep and pigs

“Calf Diptera” – ulcerative/necrotizing inflammation in oral cavities, pharynx and laryngitis

Complication- problems eating and aspiration pneumonia due to necrotic exudates

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29
Q

What is the expected etiology of Feline eosinophilic granuloma? Why do they think this?

A

Etiology believed to be immune mediated hypersensitivity due to response to corticosteroid therapy

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30
Q

What breed is gingival hyperplasia most common in?

A

Boxers

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31
Q

What is an Epulis and what is its prognosis?

A

Tumor of the periodontal ligament– type stroma

Fibromatous and ossifying epulis are benign.= GOOD PROGNOSIS

Treat surgically

Histological- proliferation of periodontal epithelium embedded into fibroblast stroma

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32
Q

Acanthomatous ameloblastoma

A

(previously known as acanthomatous epulis)

locally aggressive and often recur after excision – poor prognosis

behaves like squamous cell carcinoma (except this tumor does not metastasize)

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33
Q
A

Canine oral papillomatosis

Papilomavirus-induced papilliform or cauliflower-type lesions (“warts”) in the lips and oral mucosa
It is transmissible and usually affects animals younger than 1 year-old.

Lesions regress spontaneously and immunity is long-lasting.

Verrucous lesion composed of thick keratinized stratified squamous epithelium covering a pedunculate connective tissue core.

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34
Q

Oral Melanomas

Most Common Species? Prognosis? Predisposions?

A

Most common in dogs.

Poor prognosis. Around 90% of oral melanomas in dogs are malignant – see pulmonary metastases

Predisposing factors: Smaller breed and oral pigmentation

May lose pigmentation =amelanotic

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35
Q

Where are Squamous cell carcinomas common in cats and dogs?

A

Tonsils and tongue

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36
Q

Primary congenital megaesophagus

Cause? Location? Complications? Species most common in?

A

Caused by persistant right aortic arch (PRAA) primarily in dogs (German Shepards are predisposed)

Occurs when the right aortic arch develops instead of the left. This leads to the ligamentum arteriosum forming a vascular ring around the esophagus, causing compression.

The dilitation will be located directly cranial to the heart.

Side effects: weight loss, accumulation of feed, regurgitation, aspiration pneumonia

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37
Q

Secondary Acquired Megaesophagus

3 main causes? Location?

A

Causes:

(1) Idiopathic

(2) Maniestation of myasthenia gravis- immune mediated destruction of ACh receptors causes relaxation of the esophagus
(3) Polymiositis

Location: immediatly cranial to the stomach

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38
Q

Choke

Cause? 2 Common locations? Consequence?

A

Cause: Due to obstruction (potatoes, apples, corn cobs)

Location: where impaired dilatation due to hard structures

(1) Dorsal to the larynx
(2) Thoracic Inlet

Consequence:

(1) Impaired eating and drinking
(2) Compression necrosis

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39
Q

Reflux Esophagitis

A

Reflux of gastric acid causes chemical burns on the distal/aboral esophagus.

Most common cause of esophageal erosion and ulcers.

Common in pigs due to the high incidence of gastric ulcers that damges the esophageal portion of the stomachc and leads to an increase in reflux.

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40
Q

What is this? What causes it?

A

Erosive-ulcerative esophagitis due to BVD (pestivirus)

See multiple variable sized and shaped ulcers.

Lesion are also seen in the oral cavity and sometime the intestines.

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41
Q

Spirocerca lupi esophagitis

A

Spirocerca enters the stomach mucosa –> travel through the aorta to the esophagus

Causes caseous granulomatous esophagitis that usually has communication with the lumen so that eggs can be released.

May lead to malignant neoplastic transformation causing the formation of mainly osteosarcomas and fibrosarcomas.

Common in dogs in the caribbean

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42
Q

Ruminal Tympany or Bloat

Primary vs. secondary?

A

Ruminal Tympany or Bloat= Over distention of the rumena dn reticulum by gases produced during fermentation

  • Primary - associated with new diets of highly fermentable products that cause the formation of stable foam
  • Secondary- due to physical obstruction of the esophagus that prevents eructation of gas
    • Obstruction can be due to vagus indigestion, esophageal papillomas, and lymphosarcomas that cause lymphanditis
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43
Q

Clinical signs of Ruminal Tympany

A
  • Distended left abdomen and paralumbar fossa.
    • (pregnancy causes right side distention)
  • Respiratory signs due to increase pressure on the thoracic cavity
  • Cranial congestion due to pressure on blood vessels
  • Frothy ruminal content (primary bloat)
  • Decreased/Acidic ruminal pH (primary bloar)
  • Bloat Line at the thoracic inlet
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44
Q

Traumatic Reticulitis

A

Traumatic reticulitis/ “hardwear disease”

Caused by ingestion of sharp objects (bovine lips prevent them from being very discriminat when eating) that then enter the reticulum. During rumination, the contractions of the reticulum causes perforation of the object into the reticulum wall.

If severe, the forign object may also puncture the diaphram, pericardium (pericarditis & CHF), heart or lungs (pneumonia).

Animals appear in pain, be reluctant to more or stant on unlevel group to prevent any further pressure on the foreign object.

Magnets are sometimes fed to cattle to prevent reticulitis.

To check for traumatic reticulitits during necropsy you should feel between the diaphram and reticulum for any forign bodies or fibrin adhesions.

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45
Q

Chemical Ruminitis/ Lactic acidosis/ Grain Overload

A

Chemical Ruminitis

Common in feedloack cattle due to high carbohydrate diet that leads to an increase in fermentation in the rumen –> acidic pH–> damage and necrosis of the mucosa

See sloughing of the mucosa that exposes VERY RED, inflammatory submucosa with areas of necrosis, degeneration and pustules (compare to post-mortum ruminal sloughing)

Can treat by surgically removing ruminal contents and replacing them with a healthy ruminal contents from slaughtered animals.

If survive you will have development of Stellate ulcers and/or portal showering of bacteria

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46
Q
A

Stellate ulcers

Ruminal scars of animals that survive grain overload

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47
Q

What are complications of grain overload?

A
  • Sudden death
  • Portal showeing of bacteria - mucosal damage causes ruminal flora to enter the sytemic circulation via the portal vein. See hepatic abcesses and necrosis
  • Fibrinonecrotising ruminitis
  • Secondary mycotic ruminitis (picture)
  • Stellate ulcers
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48
Q

What is this? What species does it commonly occur in?

A

GDV- Gastric Dilatation volvulus

Occurs in dogs and sows after they eat/drink large amounts and then excersise

K9 Clinical signs: progressive abdominal distention, non-productive retching, hypersalivation and restlessness.

Stomach looks dilated, red, swollen and friable.

Spleen may be displace to the right side due to the gastrosplenic ligament.

Surgical emergency! if wait to long you can have venous infarction –> necrosis–> intraluminal hemorrhage.

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49
Q

Abomasal displacement

Species? Right vs. Left? Clinical signs?

A

Occurs most often in post-parturient dairy cows and calves

Left-sided is most common: generally non-fatal due to only partial obstruction of abomasal flow

Right-sided: Represent ~15% of the abomasal displacement. 20% of these result in abomasal volvulus.

Clinical Signs: abdominal pain, elevated heart rate, anorexia, dehydration, depressed peristalsis with lack of feces and abomasal tympany (high-pitch ping elicited by percussion).

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50
Q

What is this? When does it occur? How do you tell it is not post-mortem change? How do you prevent it?

A

Gastric Impaction/Rupture

Occurs in horses due:

(1) intestinal obstruction (ilius) –> adynamic (paralytic) or mechincal ileus that inhibits bowel motility and gastric emptying. ** MOST COMMON**
(2) high grain diet with large amounts of water– due to exspansion
(3) Chronic diaphramatic hernia - may see gastric contents within the thoracic cavity
(4) Persimmon ingestion

Prevention

Horses are unable to vomit, so if a horse is colicing you should pass a nasogastric tube to releive the pressure.

How to tell it is ante-mortem: Hemorrage!

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51
Q

Where do gastric ulcers typically occur in pigs? What are the clinical signs? What is a common cause?

A

Gastric ulcers in pigs typically occur in the esophageal portion of the stomach (was covered by stratified squamous epithelium).

Clinical signs: due to chronic internal bleeding there is melena & anemia (white pigs will look very pale). In severe cases, the ulcer may perferate –> peritonitis –> death

Cause: Finely ground feeds stimulate excessive Cl production in the stomach. High wheat compenents in feed also plays a role.

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52
Q

What is the etiology of gastric ulcers in horses? where do they commonly occur in foals?

A

Etiology: stress, immunosuppression, highly fermentable diets, NSAIDs, ideopathic

In young horses: near margo plicatus & ideopathic

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53
Q

NSAID induced gastric ulcers in horses

Why does it occur?

A

Often occurs after using NSAIDs in colic patients. Colic patients are typically dehydrated, thus even normal doses of NSAIDs can cause issues.

Occurs due to NSAIDs reducing prostoglandins that become PGE2 & PCl1- which have a protective role.

May also see intestinal ulcerations.

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54
Q

Why do dogs with cutaneous mast cell tumors develop gastric ulcers?

A

Mast cell tumors cause the release of histamine into the blood. Histamine binds to receptors on parietal cells and causes them to increase HCl secretion

If severe, dogs may develop perforated gastroduodenal ulcer that can lead to fatal peritonitis.

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55
Q

What is this? Which species does it commonly occur in? Where and Why does it occur?

A

Gastric Inflammation of a Pig in the fundus region of the stomach

Occurs secodnary to endotoxemia or bacterial sepsis (salmonellosis is most common, e.coli, glassers disease) that causes gastric venous infarction.

Gastric mucosa will be dark red and may have fibrin exudate and an increase of mucous production.

This occasionally is seen in ruminants and horses

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56
Q

Gastric Inflammation

Where and why does is most commonly occur in pigs?

A

In the fundus of the stomach

Secondary to bacterial sepsis - ie salmonellosis

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57
Q

What would cause this swollen and red cut section of the stomach mucosa to have a gritty consistency and whitish color?

A

Uremic gastritis in small animal patient with renal failure

Gritty consistancy and whitish color is due to diffuse mineralization.

Diffuse mineralization can be seen as diffuse black dots on histology with a Von-Kossa staining.

Uremia lead to vascular lesions that cause damage to the mucosa of the stomach and intestines.

Clinical signs of uremic gastritis include chronic vomitting and diarrhea.

May also see ulcerative glossitis in renal failure patients

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58
Q

What causes Bacterial gastritis/abomasitis?

AKA Braxy (bradshot)

A

Clostridium septicum causes Bacterial gastritis/abomasitis - Braxy (Bradshot)

Clostridium septicum is a gas producing bacteria, thus it will present as fiable, edematous, hemorragic necrotising and emphysematous gastritis

Occurs after ingestion of frozen food that contain the bacteria and cause mucosal damage.

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59
Q

What is this lesion? What is the pathogenesis?

A

Mycotic gastritis/abomasitis caused by angio-invasive fungi (Aspergillus, Absidia, Rhizopus, Mucor spp. etc.) that have a predilection to blood vessels and cause mycotic vasculitis/perivasculitis and thrombosis that result in round focal areas of ischemia.

Multifocal lesions are necrohemorragic and typically covered with a fribinonecrotic exudate mixed with fungal hyphae

Common sequel of long-term antibiotic therapy, immunosuppresion, debilitating conditions (sepsis) and grain overload.

Can confirm fungal hyphae around blood vessels via GMS stain.

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60
Q

What is going on with this horse? what is the clinical signifigance?

A

Parasitic gastritis due to Gasterophilus nasalis and intestinalis = Bot fly larvae

Gasterophilus nasalis is located close to the intestines

G. intestinalis is close to the esophageal portion of the stomach

NO CLINICAL SIGNIFIGANCE- even in severe infestation

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61
Q

What is this abnormality in the abomasum? Etiology?

A

Proliferative (hyperplastic) abomasitis due to Ostertagia spp.

“Moroccan leather” appearance

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62
Q

What is this large nodule near the margo plicatus of a horse?

A

Draschia megastoma (nematode) brood pouch causing a Granulomatous gastritis.

Will be able to find nematode within…

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63
Q

What parasite will most likely cause bottle jaw and pale mucous membranes in sheep and goats? Why do you see these clinical signs?

A

Trichostongylid nematode Haemonchus contortus“Barber pole worm”

Severe parasitic abomasitis results in chronic blood loss –> anemia & hypoproteinemia & melena

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64
Q

What is the most common gastric tumor in horses? Where is it commonly located?

A

Gastric squamous cell carcinoma

Arises in the esophageal portion of the stomach. It may looked depressed or proliferative, may be surrounded by digested blood.

It is locally aggressive and will penetrate and invade all muscle layers of the stomach wall and then cause peritoneal carcinomatosis via transcoelomic transplantation.

Clinical signs: weight loss and internal bleeding (anemia & melena)

One of the most common tumors in horses in general.

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65
Q

What are the large ulcerative nodules seen in the stomach of this horse?

What species can these occur in?

What do you have to differentiate this from in horses?

A

Gastric Lymphosarcoma

Occurs in ANY species!

Have to differentiate from Drashia.

Lymphosarcomas are located everywhere and will have a solid appearance and no presence of parasites.

Ulcers seen in esophageal portion of the stomach of the picture is probably due to the stress of the animal having a tumor.

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66
Q

What is a common cause of gastric lymphosarcoma in older cows?

A

Bovine Leukemoa virus = Enzootic Leukosis

Enlarged lymph nodes and multicentric lymphosarcoma.

Abomasum folds will be thickened and nodular. On a cut surface there is presence of a solid pale-tan tissue.

Mass in the submucosal causes compression of blood vessels –> ischemia –> necrosis.

May have ulceration and see melena.

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67
Q

What is Atresia coli?

A

Atresia coli is the most common segmental anomaly of the intestines in domestic animals.

Range from stenosis (incomplete occlusion of the intestinal lumen) to atresia (complete occlusion/ obliteration of the intestinal lumen).

Due to ischemia of gut during fetal development.

Autosomal recessive trait in hosteins calves

Will be unable to deficate and have abdominal distension due to megacolon.

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68
Q

What is atresia ani?

A

Atresia ani = imperforate anus

Females may be able to survive this condition longer if they form a concomitant recto-vaginal fistula.

Will have distended megacolon –> abdominal distenstion

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69
Q

What breed is lethal white syndrome most prevelent in?

A

American Paint Horses

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70
Q

What is wrong with this calf?

A

Lethal White Syndrome / Congenital Colonic Aganglionosis

Autosomal recessive genetic disorder in which completely/mostly white horses will lack of myenteric and submucosal parasympathetic ganglia in the wall of the ileum, cecum and colon. Leading to intestinal immotility and colic shortly after birth.

Grossly on necropsy the large colon and cecum will be reduced in size and you will not see any parasympatheitc ganglion.

Foal is unable to eliminate the “first feces”/Meconium that contains sloughed cells and other contents –> colic.

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71
Q

What is this? What is is composed of?

A

Entrolith

Composed of concentric lamellae of magnesium, ammonium phosphate (struvite) deposit around a “nucleus” foreign body such as a nail, wire etc.

Vary in size, some may weight up to 10 kg.

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72
Q

What is a Trichobezoar?

A

Trichobezoar= Hair ball!!

Found in cats, dogs and cattle. Can cause obstruction.

Not as heavy as enteroliths.

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73
Q

What is a Phytobezoars?

A

Phytobezoars= plant material impregnated with some phosphate salts

May be found in the colon of horses.

If mixed with hair it is referred to as phytotrichobezoars

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74
Q

In which species are Ascarid impactions most severe in?

A

Pigs and Foals

May cause obstruction

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75
Q

What is this? What is the most common cause?

A

Rectal Stricture in pig due to salmonellosis (S. typhimurium)

Salmonella causes vasculitis of the cranial hemorrhoidal artery –> ischemia –> helaing by fibrosis –> stricture and stenosis.

Pig will also have abdominal pain and distention due to megacolon.

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76
Q

What is a common cause o Rectal stricture in pigs?

A

Salmonella typhimurium

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77
Q

Internal vs. external hernia

A

Internal hernia: Displacement of intestine through a normal or abnormal foramina within the abdominal cavity (rare).

Examples: incarceration (entrapment) of loops of the intestine within the slit-like epiploic foramen, or a rent (tear) in the omentum or mesentery.

External hernia: Displacement of loops of intestine, omentum and occasionally other viscera (hernial contents) outside the abdominal cavity.

Displaced contents are inside of a pouch (hernial sac, formed by the peritoneum and the skin) which protrudes through the hernial ring - an opening in the abdominal wall which could be acquired or natural (e.g.: vaginal ring of the inguinal canal).

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78
Q

What is eventration?

A

Eventration= When displaced abdominal contents are not covered by parietal peritoneum or skin the lesion.

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79
Q

What is happening here? causes?

A

Diaphramatic Hernia

Due to trauma or congenital (loose diaphramatic hiatus)

Will se respiratory sigsn and hear abdominal sounds within the thorax,

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80
Q

What is incarceration of a hernia?

A

Incarceration= fixation of loop of intestine within the hernia.

Can lead to venous infarction, sepsis and death

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81
Q

What is happening to this horses left colon? sequel?

A

Torsion!

Wrapping of the intestines around itself.

Sequel= venous infarction –> congestion –> necrosis –> endotoxemia –> septic shock

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82
Q

What is intestinal volvulus?

A

torsion of a piece of intestines along its mesenteric axis

Segment will be dark red due to congestion, as well as edematous and friable.

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83
Q

What are the arrows pointing to?

A

Pedunculated lipoma

Benign tumor of adipose tissue that arises from the mesentery.

Tumors may have a stalk/peducle attached to them that can twist around section of intestions.

Common in old horses.

If necrosis of the center of a large lipoma there will be dystrophic mineralization and the lipomas will become heavy and more likely to twist around intestines.

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84
Q

Intussescipiens

Vs.

Intussesceptum

A

Intussescipiens- portion “eating” the other section of intestine. Outside

Intussesceptum- smaller portion within another section of the bowel. Inside.

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85
Q

What are some predisposing factors to intussusception?

A

Enteritis –> increased peristaltic activity

Parasite infestation

Ideopathic!

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86
Q

What do you call inflammation of the cecum?

A

typhlitis

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87
Q

What are typical signs of inflammation of the intestines?

A

diarrhoea which leads to dehydration, acidosis,
malabsorption, hypoproteinemia, electrolyte imbalance.

Can have portal showering of bacteria & fatal endotoxic shock

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88
Q

What lesions will you see in animals with BVD (Pestivirus)?

A

Payer patch necrosis & areas of subtle ulceration in the oral cavity, forestomach and intestines.

May be mild or subclinical.

Mucosal disease (most severe form) occurs commonly in persistantly infected (immunotolerant) animals that develop/obtain a cytopathic strain of the virus.

Affected animals are usually 6-12 months of age.

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89
Q

Malignant Catarrhal Fever

A

MCF infects a variety of ruminant (bison, cervids) and sheep in the USA.

Low morbitity, high mortality

Produces fibrino-necrotizing vasculitis with prominant perivascular infiltrates on many organs and tissues (ex. kidney)

Also damages lymph node tissies.

Vasculitis will lead to erosion and ulceration in the oral cavity, Gi tract and on the coronary bands.

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90
Q

Enteric Coronaviral Infection

A

Transmissible gastro-enteritis (TGE) in pigs and common cause of neonatal diarrha in calves (w/ rotovirus and cryptosporidium).

Causes severe villous atrophy/blunting of the tios and sides of the villi

Gross: intestinal wall will be very thin (due to villous atropy) and you will see fluid and gas as the intestinal contents.

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91
Q

Enteric rotoviral infection

A

Causes diarrhea in young animals (all species)

Causes damage to surface/tip enterocyes resulting in variable degreems of strophy

Subclinical infections are common in piglets.

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92
Q

Parvovirus enteritis

A

Caused by CPV-2 and Feline Panleucopenia virus.

Targets fast resplicating cells in the intestinal crypts cells and bone marrow (in Feline form)

Serosal surfaces will look granular and red.

Causes Segmental fibrino-hemorrhagic enteritis, necrosis of peyers patches, and issues associated with bone marrow suppresion (in cats)

May see unique regenerative changes in the remaining crypt cells or intranuclear inclusions.

FeLV in older cats will produce similar enteritis lesions.

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93
Q

What is wrong with this cat?

A

FIP -very important cat disease

Two forms: (can have both)

(1) Wet form: peritoneal and thoracic perfusion due to vasculitis
(2) Dry form- solid puogranulomatous lesion due to vasculutis

Will commonly see gray plaques on the surface of the intestines, liver and spleen. Also in alignment with the blood vessels of the cortex of the kidney

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94
Q

What is wrong with a cat with a kidney that looks like this?

A

FIP

maybe lymphosarcoma

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95
Q

Name me four types of E.coli (from chart in lecture 3A)

A

Enterotoxigenic colibacillosis= Secretory diarrhea (enterotoxininduced) in Neonatal pigs, calves and lambs

Septicemic colibacillosis=Failure of passive transfer of maternal antibodies in Neonatal calves, pigs, foals. Enteritis is not common –sudden death or subacute & chronic disease (meningitis, polyarthritis etc)

Post- weaning colibacillosis= Similar to enterotoxigenic colibacillosis with secretory diarrhea & mild or no lesions

Weaner pigs Attaching & Effacing - attached to surface enterocytes and cause villus atrophy. Some may not produce toxins. In Pigs, dogs –less common in other animals.

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96
Q

What is probably wrong with this pig?

A

Edema disease (enterotoxemic colibacillosis)

Caused by strains of E. coli that produce the edema toxin that cause endothelial cell injury in arterioles resulting
in fluid loss and edema.

It is most common in pigs a few weeks after weaning.

Will see diffuse edema, specifically a swollen face, periorbital edema and edema of the mesentery of the spiral colon.

Affected animals may exhibit focal bilaterally symmetric encephalomalacia (Cerebrospinal angiopathy of swine) after the acute phase due to blood vessel damage that leads to cerebral edema and degenerative changes.

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97
Q

What is the most common cause of clostridial enterotoxemia?

A

Clostridium perfringens Type D

See severe hemorrhagic lesions in the intestines

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98
Q

Which animals are most commonly affected by clostridial enterotoxemia?

A

young, best nourished animals in the group

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99
Q

What toxin of C. perfringes type D causes focal symmetrical encephalomalacia (FSE) in sheep?

A

Angiotoxin/Epsilon toxin

toxin has predilection for blood vessels within the brain

(Will also see severe hemorrhagic enteritis)

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100
Q

What C. perfringens causes clostridial enteritis in chickens?

A

Type A (& C)

Lesion are similar to Type D= necrohemorragic enteritis

Will see layer of gram negative bacilli on surface layer of intestines in histology.

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101
Q

Tyzzer’s Disease

A

Clostridium piliforme

Main target is liver, but lesion also on intestines (port of entry) and heart

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102
Q

Colitis X

A

Clostridium perfringens typa A & Clostridium difficile

Fibrinonecrotizing Typhlocholitis in horses

Result of dysbacteriosis ( associated with antibiotic therapy or dietary change) leadin to proliferation of toxigenic clostridia

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103
Q

Salmonellosis

A

ALL species are pathogenic

Disease range from enterocolitis to septicemis

Causes ulcerative & fibrinonecrotizing enterocolitis

Intestinal contents will be malodorous and contain mucus, fibrin and occasionally blood (feces: “septic tank odor”).

Mucosa will be thickened (edema), friable, with areas of hemorrage and necrosis with fibrin and mucous on surface

Stress factors play a role

Zoonotic and nosocomial (common in horse hospitals)

Complications of disease:

embolic mycotic pneumonia (multifocal necrohemorragic with red margins due to secondary angioinvasive fungi)

Rectal strictures –> megacolon

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104
Q

Horse

A

Fibrino-necrotizing entero-colitis

DDx: Salmonellosis or Colitis X

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105
Q
A

Embolic mycotic pneumonia

Sequel of Salmonellosis

Due to opportunistic angiovasive fungi from intestinal contents

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106
Q

Pig

A

Button Ulcers

DDx: Chronic Salmonellosis -or- Hog Cholera (CSF)

Can lead to rectal stictures –> megacolon

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107
Q

Pig

A

Lawsonia intracellularis

Porcine Proliferative Enteropathy (PPE)

Common in the enterocytes of the ilium** and late jejunum of weaner and young pigs.

Intestines will have “garden hose appearance” due to the mark thickening

May become proliferative hemorrhagic enteropathy in older animals= intestinal contents will be blood. High mortality, low morbidity.

Use silver stain to see bacteria.

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108
Q

Swine dysentery

A

Swine Dysentry (Spirochetal colitis)

Caused by Brachyspira hyodysenteriae

Affect pigs 8-24 wks (low incidence in USA)

Large bowel diarrhea with mucus and blood in feces

Will had edema/thickening of the wall, ulceration, hemorrage, fibrin, mucous (bacteria induces goblet cell hyperplasia) within the large intestines.

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109
Q

Rhodococcus equi

A
  • Causes an enterocolitis in young horses
  • Virulent factors allow the bacteria to survive within the cytoplasm of macrophages and cause chronic disease
  • Typically R. Equi is associated with suppurative pyogranulomatous pneumonia in foals.
  • The enteric lesions are ulcerative and pyogranulomatous and are associated with prominent regional lymphadenitis.
  • Also, causes osteomyelitis in horses
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110
Q

Foal

A

Pyogranulomatous lymphadenitis, R. equi

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111
Q

Foal

A

Rhodoccocus equi pyogranulomatous pneumonia

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112
Q

Cow, Older then 19 months

A

Johne’s Disease (Mycobacterium avium paratuberculosis)

Chronic disease of rumunants

Characterized by D, emationation and hypoproteinemia.

Usually occurs in animal older than 19 months

Low morbidity

Lesions are most likely in the ileocecal area= cerebriform appearance due to granulomatous inflammation (M0 are the main component). Also found in the lieum, cecuma and proximal colon.

Acid fast stain will confirm diagnosis

Sheep typcally have subtle lessions but will exhibit prominant/thickened lymphatic vessels due to pyogranulomatous lymphangitis

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113
Q

Sheep/Goat

A

Johnes Diseas

Sheep typcally have subtle intestinal lessions but will exhibit prominant/thickened lymphatic vessels due to pyogranulomatous lymphangitis

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114
Q

Boxer (dog) colon

A

Granulomatous Colitis due to special strain of E. coli

Genetic component

See multifocal ulcerative lesions of the colon that may have raised borders due to the pyogranulomatous reaction.

Will see macrophages containing gram negative bacteria in the lamina propria.

Clinical signs: diarrhea, sometimes bloody –> ematiation

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115
Q

Cryptosporidiosis

A

Causes diarrhea in calve. Usually associated with other etiology (corona, rotovirus)

Will see protozoal organism (basophilic blebs) on the apical surface of the enterocyte

causes a reduced absorptive surface –> diarrhea

ZOONOTIC!!!!!

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116
Q

Goat and sheeps

A

Coccidial enteritis

In sheep and goats, it causes hyperplasia of the mucosa –> grey raised nodules

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117
Q

Coccidial enteritis

A

Coccidia parasitize epithelial cellls of the intestines–> deaht of cells –> necrophemorrhagic enteritis.

Clinical Signs: bloody diarrhea, loss of condition, hypoproteinemia.

Proliferative enteritis in goats and sheep.

Male parasites will be blue, and females will be red on stain.

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118
Q

Ancylostoma caninum & Uncinaria stenocephala

A

Canine Hookworms

Blood sucking parasites that cause significant anemia and hypoproteinemia in puppies

Larvae may be found in colostrum.

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119
Q

Horse

A

ANOPLOCEPHALA PERFOLITIA

Cause issues at the ileocecal valve –> ilial hypertrophy –> colic

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120
Q

Trichuris spp.

A

Whipworm

Parasitize the cecum and colon of domestic animals.
Most infections are subclinical
Severe infections may lead to bloody diarrhea, weight loss, dehydration and anemia.

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121
Q

Pig. DDx? Which is most common?

A

“Milk spot liver”= fibrosis of the conntective tissue capsule and periportal fibrosis.

Etiology: *Ascaris suum & renal worm (Stephanurus dentatus)

Ascaris suum is most common

Stephanurus dentatus is common in free-range pigs in St. Kitts.

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122
Q

Intestinal tumors are most common in which species?

A

Dogs and cats

Most primary tumors are carcinomas

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123
Q

What are most primary tumors in the intestines?

A

Carcinomas

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124
Q

What is the most common form of neoplasm in cats?

A

Lymphosarcoma (LSA)

The alimentary form of LSA has the highest incidence in cats.

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125
Q

Where do most lymphosarcomas of the intestines arise from? what is the exception

A

Lymphosarcomas in the intestines are usual manifestation of multicentric lymphosarcomas.

The exceptions may be in cats, in which the alimentary form of lymphosarcomas are primarily from the intestines.

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126
Q

what is the largest visceral organ?

A

LIVER

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127
Q

How much cardiac output does the liver recieve? how is it divided?

A

25% cardiac output
67% portal vein / 33% hepatic artery

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128
Q

Why woudl you want to know the % body weight the liver is?

A

In necropsy, to determine if the liver size is abnormal.

Carnivores 3-4% body weight
Omnivores 2% body weight
Herbivores 1% body weight

(NO NOT MEMORIZE %)

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129
Q

What is in the portal triad?

A

Bile ductules (3-4)
Branches of portal vein
Hepatic artery
Nerves and lymphatics

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130
Q

How does blood flow travel in the liver?

A

portal triad –> central

toxic injury near portal triad

hypoxic injury near central vein

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131
Q

What direction does the bile flow in the liver?

A

central vein –> portal triad bile ducts

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132
Q

What are the other names of the 3 Liver Zones? Where are they located?

A

Zone 1 or centroacinar (periportal) surrounds the portal triads
Zone 2 or midzone is the intermediate or midlobular area
Zone 3 or periacinar (centrilobular) surrounds the central veins

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133
Q

What cell makes up 80% of the liver mass?

A

Hepatocytes!

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134
Q

Kuffer cells

A

regional macrophages

participate in immune and regenerative response

135
Q

Stellate/ Lipocyte/ Ito cells

A

produce and maintain entracellular matric and store vitamin A

Ito cells play role in fibrosis (drug target)

136
Q

7 functions of the liver?

A
  1. Bilirubin metabolism
  2. Bile acid metabolism
  3. Carbohydrate metabolism
  4. Lipid metabolism
  5. Xenobiotic metabolism
  6. Protein synthesis
  7. Immune function
137
Q

How much injury can a liver have before there are obvious clinical signs? What are ways to catch liver injury early?

A

Clinical signs appear after approximately 75% of the parenchyma is injured

Liver enzymes (AST, ALT, LDH, alkaline phosphatase, gammaglutamyl transpeptidase) can be elevated early; thus they are commonly used as biomarkers of liver injury

138
Q

Portals of entry of injurous agents to the liver?

A
  1. Hematogenous
  2. Retrograde through biliary and pancreatic ducts
  3. Direct extension through the liver capsule (example: trauma through the abdominal wall, rib cage, lumen of the gastrointestinal tract)
139
Q

6 Mechanism of Liver Injury?

A
  1. Metabolic bioactivation of chemicals to reactive species
  2. Stimulation of autoimmunity
  3. Stimulation of apoptosis
  4. Disruption of calcium homeostasis
  5. Canalicular injury
  6. Mitochondrial injury
140
Q

5 different responses to liver injury?

A
  • Atrophy (whole organ, individual cell)
  • Hypertrophy and hyperplasia
  • Regeneration of parenchyma
  • Replacement by fibrosis
  • Biliary hyperplasia
141
Q

What are 4 causes of liver atropy?

A

Increased catabolism /Decrease anabolism (ie portal shunt)
Decreased blood flow
Decreased bile flow
Pressure

142
Q

What % of liver can regenerate within a week!

A

60%

143
Q

What are liver stem cells called? what can they differentiate into?

A

Oval (stem) cells can differentiate into hepatocytes or bile duct epithelium

144
Q

What is required for liver regeneration?

A
  1. Intact framework (reticulum fibers)
  2. Good blood supply
  3. Patent bile ducts
145
Q

What is a regenerative nodule?

A

Hepatocellular regeneration due to sustained or repetitive hepatocellular injury is often nodular.

Histolofically looks like an unorganized cluster of cells, lacks a capsule.

Surrounding area in pucture also has bile duct hyperplasia due to response to injury

146
Q

What happens during liver fibrosis?

A
  • Increased amount of connective tissue within the liver
  • Ito (stellate) cells also proliferate

Significance is dependent upon effects on normal hepatic function and type of collagen (removal and remodelling)

147
Q

dog

A

End stage liver / Liver Cirrhosis

In cases of chronic injury, regeneration can result in hepatocellular nodular proliferation/regeneration with fibrosis (post-necrotic scarring) between nodules and impaired blood and bile flow.

Liver usually reduced in size

148
Q
A

Severe bilary hyperplasia

149
Q

Horse

A

Capsular fibrosis/perihepatitis in horses (incidental lesion)
Due to: Resolution of peritonitis, Parasitic migration, friction

• Also known as “perihepatitis filamentosa”

150
Q

Cattle or horse

A

Focal areas of pale discoloration

Adjacent to mesenteric attachment= incidental
Seen occasionally in cattle and horses

151
Q

What causes liver rupture? What are the common sequelas?

A

Rupture etiology: Trauma or Enarged Liver

Sequela: death due to hemoperitoneum -or- healing by spider web fibrosis (picture)

152
Q

Liver post-mortem changes

A

Occur rapidly- especially if hot environment
Pale, irregular foci
Greenish black discoloration near the intestine
Emphysema

Liver autolysis will make your histology slides crappy

153
Q

What are the three tpes of LIVER DEGENERATION AND
NECROSIS- PATTERNS?

A
  1. Random (Single cell, Multifocal, Piecemeal necrosis)
  2. Zonal
  3. Massive
154
Q

describe the pattern of necrosis/degeneration

A

Random, multifocal liver necrosis

Size: Etiology: Infections= bacterial (pig salmonellosis), viral (equine herpes), parasitic.

155
Q

Describe! What is a Common cause?

A

Centrilobular or Zone 3/ periacinar necrosis

commonly due to hypoxia

156
Q

Decribe the type of liver necrosis? How common is this?

A

Midzonal/Zone 2 necrosis

Very rare. Seen in yellow fever.

157
Q

Describe! What is a common etiology?

A

Periportal necrosis

Common Etiology= toxic

158
Q

Massive hepatic necrosis

A

necrosis that involved entire lobule or contiguous lobules

can be caused by hepatosis dietica in swine (vit E/ selenium deficiency)

159
Q

Hepatosis dietetica

***KNOW THIS****

A

Associated with Vitamine E/Selenium deficency and generation of free radicals.

One of the most common causes of massive hepatic necrosis.

May see jaundice and complete necroisis of nodule (seperated by prominant CT)

160
Q

Calf

A

Congenital cyst

Developmental abnormality

161
Q
A

Congenital bilary cyst

Due to abnormal development of bile ductules - cyst will have a thin wall, lined by a single layer of bilary epithelium

Usually an incidental finding

162
Q
A

CONGENITAL POLYCYSTIC LIVER DISEASE

Multiple cysts are located in the liver and kidney. Can cause pressure necrosis of the surrounding parenchyma.

Cair terriers, West Highland white terries, and Persian cats are predisposed.
May result in mortality due to liver or renal failure. NOT incidental (compared to incidental bilary cysts)

163
Q

What breed are predisposed to develop congenital polycystic liver disease?

A

Cair terriers

West Highland white terries

Persian cats

164
Q
A

Diaphramatic hernia of the liver

Congenital abnormality due to missing part of the diaphram or a very thin wall of the diaphram.

(could also be traumatic)

165
Q

In the liver, which circulatory disturbance is most likely to occur?

a. congestion
b. infarction
c. ischemia

A

CONGESTION

Infarction/ischemia are rare due to high collateral circulation and double circulation (arterial and portal vein)

166
Q

What gross characteristics would you see in ACUTE liver congestion?

A

Slight enlargement of the liver

Prominant reticular pattern- due to congestion of centrilobular areas

167
Q

What would you grossly see in CHRONIC passive congestion?

A

“nutmeg liver” - due to right sided heart failure (picture)

Reticular pattern due to zonal congestion

168
Q

Histological appearance of chronic passive congestion of the liver?

A

Congestion around central veins
Hepatocytes around portal areas are often unremarkable
Midzonal fatty change is occasionally seen

169
Q

What is the Budd-Chiaria syndrome?

**NEED TO KNOW THIS**

A

Budd-Chiaria syndrome= hepatomegaly, ascites, and abdominal pain.

It is caused by thrombosis of the hepatic vein and the adjacent inferior vena cava.

Probable causes of thrombosis include conditions producing thrombotic tendencies or sluggish flow such as myeloproliferative disorders, infections, trauma and
neoplasia.

170
Q

Gross appearance of congenital portosystemic shunts?

A

Blood within the portal venous system bypass the liver and drain into the posterior vena cava, or the azygous vein.

Gross:

  • Hepatic encephalopathy and ascites are seen in congenital cases in dogs and cats.
  • Decrease size fo the liver because it has been deprived of primary perfusion by portal hepatotrophic factors such as insulin, glucagon and amino acids.
171
Q

Histological appearance of congenital portosystemic shunts?

A

Small hepatocytes

Portal veins are small/abscent in small portal triads

Multiple, more prominant, hepatic arterioles

172
Q

Acquired shunts in liver

A

Acquired shunts have multiple, thin walled and tortuous blood vessels and evidence of liver disease

Due to chronic portal hypertension..

173
Q

Telangiectasis

A

Telangiectasis

Definition: presence of focal areas in which sinusoids are dilated and filled with blood.
Gross appearance: irregular, circumscribed, dark-red foci of cavernous ectasia of sinusoids.

Common in: cattle and old cats

Clinical Signifigance: NONE!

Histologically: Dilation of sinusoids

174
Q

Bovine

A

Telangiectasis= focal areas of silated sinusoids within the liver

NO clinical significance

Also commonly seen in older cats (picture)

175
Q

Which species commonly get Telangiectasis?

A

Cattle and older cats

No clinical signifigance. Focal dilitation of the sinusoids of the liver. Grossly appear as irregular dark red foci.

176
Q

5 Mechanism of Hepatic Lipidosis?

A
  1. Excessive entry of fatty acids into the liver
    • ​consequence of (1) excessive dietary intake of fat or (2) increased mobilization of fat from adipose tissue due to increased demand (lactation, starvation, and endocrine abnormalities).
  2. Decreased oxidation of fatty acids within hepatocytes.
  3. Increased esterification of fatty acids to triglycerides.
  4. Decreased apoprotein synthesis
    • ​​subsequent decreased production and export of lipoprotein from hepatocytes.
  5. Impaired secretion of lipoprotein from the liver
177
Q

Gross appearance of hepatic lipidosis?

A

Enlarged

heavy

uniform light yellow or orange

cuts with ease

greasy

rounded edges

smooth surface

tissue will float in water or fixative

178
Q

Mdx & Disease name of the liver on the right

A

Mdx: Diffuse hepatic lipidosis

Condition: Hepatic lipidosis

179
Q

What stains can you use to confrim hepatic lipidosis?

*** NEED TO KNOW***

A

(1) Oil red O - have to do a frozen stain, normal processing will wash fat out of cells.
(2) Osmium tetroxide- binds to lipids and keeps them within cells. Prevents washing out during normal processing. Lipids will appear black. VERY BAD FOR THE ENVIRONMENT

180
Q

What is the significance of hepatic lipidosis?

A

Depends on the cause, severity and duration.

  • Lesion is reversible in mild cases
  • could lead to hepatic necrosis, fatty cysts, fat embolism and liver rupture with internal hemorrhage.
  • Fatty livers are also more susceptible to toxic damage and traumatic injury.
181
Q

What conditions are characterized by fatty liver?

A
  • Physiological Fatty Liver ( late pregnancy, peak lactation, dietary excess, TWINE PREGNANCY IN EWES)
  • Fasting in obese animals

  • Bovine fatty liver syndrome- occurs in obese dairy cattle a few days after parturition when another event causes them to go off feed.
  • Feline fatty liver syndrome- poorly defined/ideopathic. In either obese or anorexic cats. Causes icterus, hepatic failure and hepatic encephalopathy (picture)
  • Equine hyperlipemia - occurs in obese ponies od shetland breed. Pathogenesis unknown. See pale discoleration and rounded edges of liver
  • Endocrine disorders
  • Toxic and anoxic injury
182
Q
A

Equine hyperlipemia

Common in obese Shetland breed ponies

Unknown pathogenesis

**Pale discoloration and rounded edges**

183
Q

What are two common endocrine disorders that cause hepatic lipidosis?

A

diabetes mellitus and hypothyroidism.

The increased lipolysis results in increased access of fatty acids, coinciding with shortage of ATP (due to reduced glucose availability), concluding with reduction in lipoprotein synthesis.

184
Q

Fatty degeneration

A

Accumulation of fat within cells arising as a consequence of cellular injury is called fatty degeneration.

Injury to hepatocytes can lead to accumulation of fat because of decreased formation and/or export of lipoproteins by hepatocytes and decreased oxidation of fatty acids within hepatocytes

185
Q

What 3 conditions lead to an excess storage of glycogen in hepatocytes?

A

Diabetes mellitus
Hyperadrenocorticism (steroid induced hepatopathy)
Glycogen storage diseases

186
Q

Why does Excessive levels of endogenous or exogenous glucocorticoids cause extensive swelling of hepatocytes?

A

Glucocorticoids induce glycogen synthetase and enhance hepatic storage of glycogen –> excess accumulation –> swelling

187
Q

What will you see grossly and histologically with steroid induced hepatopathy?

A

Gross: Enlarged, pale liver due to swollen hepatocytes (particularly in the midzonal areas)

  • Differential diagnosis is hepatic lipidosis/ fatty change; thus a special stain (PAS stain) should be used to distinguish these two conditions.

Histologically: “feathery” cytoplasm. Glycogen accumulation around a centrally located nucleus. Enlarged cells. Confirm with PAS stain

188
Q

Which breeds are predisposed to hepatic amyloidosis?

A

Abyssinian cats

Siamese cats

Chinese Shar-Pei dogs

189
Q

Where does amyloid accumulate in the liver?

A

Space of Disse

190
Q

When/Why does hepatic amyloid occur in animals?

A

Hepatic amyloidosis usually occurs as a consequence of prolonged antigenic stimulation such as chronic infection or repeated inoculations of an antigen.

191
Q

Special stains for: Amyloid, Glycogen, Lipids & Copper

A

Amyloid: Congo Red

Glycogen: PAS
Lipid: Oil Red O

Copper: Rhodanine or Rubeanic acid

192
Q

What liver condition commonly occurs when an ewe has a twin pregnancy?

** KNOW THIS***

A

Ketosis

193
Q

5 causes of Cu toxicosis/Cu accumulation in the liver?

A
  • Dietary excess in ruminants
  • Grazing on pasture low in molybdenum (common in ovine)
  • Hepatic (cholestatic) disease (accumulates in bile –> injury)
  • Chronic liver disease
  • Hereditary disorders (Bedlington and West Highland terriers, Dalmatians , cats, LEC rats)
194
Q

What breeds are predisposed to copper toxicosis?

A

Bedlington and West Highland terriers

Dalmatians.

Also reported in cats
Long Evans Cinnamon (LEC) rats are human model for Wilson’s disease

195
Q

What is the Rhodaine stain used for?

A

Copper

196
Q

How do agents that cause hepatitis reach the liver?

A

Hematogenous/ blood-borne route (most common)
Ascending route: reaching the liver by ascending the biliary system
Direct extension from the peritoneum

197
Q

Cholangiohepatitis

A

inflammation of bile ductules and liver parenchyma

198
Q

Etiology? Edx?

A

Etiologic diagnosis: Parasitic hepatitis.
Etiologic agent: Fascioloides magna

199
Q

What is a likely cause of this in a young animal/fetus? What will you see on histology?

A

HERPES VIRUS

Discrete off-white foci are seen in young animals and fetuses with Herpes viruses.

Necrotic hepatocytes often contain intranuclear inclusion bodies (INIB) and are surrounded by inflammatory cells.

Agents include:

  • Bovine Herpes virus 1: Infectious Bovine Rhinotracheitis (IBR)
  • Equine Herpes virus 1: Equine Viral Rhinopneumonitis (EVR)
  • Canine herpes virus 1
  • Pseudorabies in pigs.
200
Q

What disease will cause:

gall bladder edema

corneal edema “blue eye” in survivors

enlarge, congested and friable liver

serosal petechia, ecchymosis and paint-brush hemorrhages

A

Canine adenovirus 1= Infectious canine hepatitis (ICH)

AKA Rubarth’s disease, Fox encephalitis, Hepatitis contagiosa canis

Highly contagious peracute disease

See intranuclear inclusion bodies

Pathogenesis: Oral exposure to urine → tonsilitis → viremia → virus has tropism for hepatocytes, vascular endothelium, renal epithelium, and mesothelium

Clinical signs: peracute onset, with vomiting, diarrhea, petechia in mucosal surfaces, hemorrhagic diathesis (=excessive bleeding)

201
Q

What are the histological features of ICH?

A
  • *Periacinar individual cell necrosis** of hepatocytes
  • *Intranuclear basophilic inclusion bodie**s in hepatocytes, endothelial cells, biliary epithelium and Kupfer cells
  • *Endothelial damage** in various organs
  • *Minimal inflammation** (peracute)
202
Q

Which disease will cause dish rag liver in horses?

A

Equine serum hepatitis aka Theiler’s disease

Caused by Pegivirus (used to be ideopathic)

Disease usually occurs 1-2 months after injection with a biological products of equine serum origin e.g. pregnant mare serum or tetanus antitoxin, but can occur without any such inoculation.

Clinical signs are acute even though liver lesions may appear older.
Characterized by icterus, ascites, petechiae, and hepatic encephalopathy due to severe hepatic fatty degeneration and some necrosis, cholestasis, mononuclear infiltration and slight fibrosis and regeneration.

203
Q

What disease will result in a single large area of necrosis seen in a liver (picture) as well as intravascular anemia and hemoglobinuria in cattle and sheep?

A

Bacillary hemoglobinuris

Caused by Clostridium haemolyticum which produces a B toxin.

Occurs in cattle and sheep when the liver is injured.

(ie. Migrating liver flukes create an anaerobic environment for latent spores of the organism to germinate and elaborate the toxins.)

204
Q

Which disease will causes small and numerous areas of liver necrosis and dark coloration of skin?

A

Black disease/ Infectious necrotic hepatitis

caused by Clostridium novyi type B

Dark discoloration of skin is due to severe sub-q venous congestion

lesions of fluke infestions or migration through the liver are also associated with it

205
Q

Tyzzer’s Disease

A

Caused by Clostridium piliforme (previously known as Bacillus piliformis)

.It causes multifocal necrotic hepatitis and colitis.

Diagnosis is done by demonstrating bundles of large, long bacilli in hepatocytes stained with silver (Warthin-Starry) stain.

Seen especially in rodents and immunocompromised or very young animals (foals, calves, kittens, puppies)

206
Q

Liver of young animal

A

Tyzzers disease- Clostridium piliforme

Diagnosis is done by demonstrating bundles of large,
long bacilli in hepatocytes stained with silver (Warthin-Starry) stain.

207
Q

Leptospirosis

A

Disease characterized by jaundice
Pathogenesis varies according to serotype of Leptospira sp..
Lesions are often due to ischemic injury following hemolytic anemia.
Cholestasis has also been implicated as a cause of icterus
Leptospira grippotyphosa has also been associated with chronic active hepatitis in dogs.

Demonstrate lepto via silver stain (warthin starry)

208
Q

Liver abcesses are due to….

A

hematogenous infection or secondary to omphalophlebitis

seen in cattle as a complication of chemical rumenitis or traumatic reticulitis.

Abscesses may be few or many and are usually caused by mixed bacterial flora including Fusobacterium necrophorus, Trueperella pyogenes (formerly known as Arcanobacter pyogenes), Streptococci and Staphylococci.

The left lobe is more frequently affected.

Use NAG- neoplasia, abcess or granuloma

209
Q

What is the significance of liver abcesses?

A

Could be incidental finding at abattoir or necropsy

May heal, become encapsulated and sterile

May cause focal adhesive peritonitis, or diaphragmatic adhesions (photo)

May break into hepatic vein or vena cava and cause thrombophlebitis, endocarditis, pulmonary abscesses or massive endotoxic shock

Generalized infection in young animals

Toxemia if numerous.

210
Q

Causes o granulomatous hepatitis?

A

Occurs secondary to fungal infections (Blastomycosis, Histoplasmosis),
bacterial diseases such as tuberculosis (confirm via acid fast stain)

211
Q
A

Mycotic infection of the liver

Usually seconday to mycotic ruminitis in cattle or part of a systemic mycosis

Have red rim, but no campule

Etiology:

Aspergillus fumigatus and other Zygomycetes in ruminants
Histoplasma capsulatum
Cryptococcus neoformans

Coccidioides immitis
Sporothrix schenckii

212
Q
A

Fasciola hepatica

Larvae migrate through the liver and matureflukes reside within the bile ducts

Prominennt areas of bile duct, due to inflammation and fibrosis, may look like cords.

Causes chronic fibrosing cholangitis

213
Q

Pipe stem liver

A

Fasciola hepatic

causing chronic fibrosing cholangitis that looks like cords

214
Q

Etiology?

A

Hydatid cysts/ intermediate stage of Ecchinococcus granulosus

Dog is the definitive host.

215
Q

Rabbit. What is wrong with the right liver?

** IMPORTANT***

A

Proliferative cholangitis

Etiology: Eimeria stiedae
Gross appearance: multiple, raised, off-white nodules scattered throughout the liver

216
Q

Etiology? Mdx? Disease name?

A

Etiology: Histomonas meleagridis

Disease name: Black head
Pathogenesis associated to Heterakis gallinarum
MDX: Multifocal granulomatous hepatitis (“target lesion”) and Diffuse granulomatous typhilits

217
Q

What will ingestion of Blue-green algae cause?

A

It is a hepatotoxic plant. Microcystin is the main preformed toxin.

It blooms in late summer or early fall

Lesion include:

  • *Acute hemorrhagic gastro-enteritis**
  • *Acute centrilobular to massive hepatic necrosis**
  • *Chronic liver disease** in survivors
218
Q

What are the main lesions you will see in Pyrrolizidine alkaloid toxicity on gross and histology?

A

Pyrrolizidine alkaloid toxicity- due to alkaloids being convered to toxic pyrrolic esters by the liver p450 system,

Common in cattle, horses, pigs, goats, sheep

Gross: Hepatopathy

  • Acute: periacinar necrosis
  • Hepatic veno-occlusive disease
  • Chronic with fibrosis (most common form)

****Histology******

  • Portal fibrosis*
  • Biliary hyperplasia*
  • Megalocytosis** (toxin is antimitotic)
  • Absent parenchymal regeneration
219
Q

Alsike Clover

A

Toxin plant in north america

Causes Chronic liver disease and photodynamic dermatitis

Histology: Fibrosis, bile duct hyperplasia, & portal hepatitis
NO megalocytosis

220
Q

4 Common Mycotoxins

A

A. Aflatoxins- B1 is most common and potent (carcinogen). Chronic > Acute

B. Sporidesmin- toxic to bile duct epithelium –> cholangiohepatits. Photosensitization & facial edema in sheep

C. Phomopsin- grows on lupins, chronic liver damage in herbivores

D. Poisonous mushrooms- dogs, fatal acute periacinar to massive hepatocellular necrosis

221
Q

copper toxicosis is common in _______\_

A

Sheep

Cu accumulates in liver lysosomes and is release as a consequence of stress–> lipid peroxidation and massive hepatic necrosis

222
Q

4 Hepatotoxic therapeutic drugs

A

• Trimethoprim-sulfonamide - Doberman pinschers
Carprofen - especially Labrador retrievers
• Ivermectin - collies and shelties NO
• Anticonvulsants: primidone, phenytoin and phenobarbital

223
Q

Hepatic Encephalopathy

A

Manifestation of liver dysfunction and failure –> depression, behavior changes, mania, convulsions, head pressing

Causes:

Acute liver disease- horse and ruminants

Portosystemic shunts - dogs and cats

Chronic liver disease - any animals

Pathogenesis:

Blood accumulation of neurotoxic substances bypassing the liver
Requires shunting of >10-15% of portal blood
Main toxic substance is ammonia
Ammonia bypasses the liver**→ increased levels reach the general circulation → go through the blood-brain barrier causing encephalopathy.

224
Q

What causes elevations in bilirubin?

**KNOW THIS***

A
    1. Overproduction of bilirubin (prehepatic jaundice)
      * Hemolysis - intra- or extra-vascular
  1. Decreased uptake, conjugation or secretion of bilirubin (hepatic jaundice)
    • Severe hepatocellular injury
    • Impairment of flow within canaliculi (intrahepatic cholestasis)
  2. Reduced outflow of bile in extrahepatic bile ducts and gallbladder (post hepatic jaundice)
    • Mechanical obstruction of bile ducts (extrahepatic cholestasis) or gallbladder (cholelithiasis)
225
Q

What are Metabolis Disturbances of Hepatic Failure?

A
  • Hemorrhagic diathesis or bleeding tendencies
    • Impaired synthesis of clotting factors
    • Reduced clearance of products of clotting cascade
    • Impaired platelet function
    • Impaired absorption of vitamin K
    • Disseminated intravascular coagulation (DIC)
  • Hypoalbuminemia
    • Decreased synthesis in chronic liver disease
    • Loss in ascites or via the gastrointestinal tract
226
Q

What does this indicate?

A

Acquired portosystemic shunts

227
Q

What should you suspect if a dogs paw ahs crusting erosions and scaling at the mucocutaneous junctions and footpads?

A

Hepatocutaneous syndrome (Superficial necrolytic dermatitis)

A rare cutaneous problem in liver disease in dogs

228
Q

What are the 3 main causes of Photosensitization?

A

Photosensitization is due to activation of photodynamic pigments by UV light

  1. Primary
     St John’s wort (Hypericum perforatum)
     Chlorpromazine
     Phenothiazine
  2. Secondary (hepatogenous)
    • Occurs in herbivores with impaired excretion of phylloerythrin
    • Is the most common form
  3. Congenital
    • Abnormal metabolism of heme –> Retention of porphyrins
229
Q

What are non-neoplastic gorwth disturbances of the liver?

A

Hepatocellular nodular hyperplasia - age related change only in dogs
Regenerative nodules
Bile duct hyperplasia

230
Q

Cholangioma

A

benign hepatic tumor of bile epithelium

common in cats

231
Q

Most malignant tumors in the liver are ________

a. primary (from hepatocytes, bile duct or mesenchymal tissue)
b. seconday (other organs)

A

Secondary

232
Q

Ruminant Liver. Benign or malignant?

A

Hepatocellular Adenoma= beinign neoplasm of hepatocytes

Seen in young ruminants s a single, non-encapsulates, red-brown nodule. It is composed of well differntiated hepatocytes and the portal arease are NOT seen in the neoplastic ares

233
Q

Feline Liver.

Beinign or Malignany? What is is most common in? Gross? Histology?

A

Hepatocellular Carcinoma = Malignant
• Most often seen in dogs

Gross: solitary and involes entire lobe. Cut surface is multilobulated and grey-white to yellow brown

Histology: cells are arranfes in a trabecular pattern (3 or mor cells thick). Hepatocytes exhibit atypical and bizarre forms

234
Q

Cholangiocellular adenoma vs. carcinoma

A

Cholangiocellular adenoma- Benign tumour arising from the bile ducts. Often cystic

Cholangiocellular carcinoma- Relatively common (described in all species)
• Multilobulated, firm, raised, with central areas of depression (umbilicated).

235
Q

Hemangiosarcoma are ________________\_ origin tumors that arise from the ______ _______

A

Hemangiosarcomas are mesenchymal origin tumors that arise from the right atrium

Animals die when the tumor ruptures

236
Q

What are the steps required for a histology specimen

A
  1. Tissue Collection
  2. Fixation- 10% NBF at 10:1 NBF:tissue. Fixes at ~1 mm/hour for 24 hours
  3. Trimming- lesion & normal. All layers. ~3mm thickness
  4. Processing- replace water with wax. Alcohol –> xylene –> paraffin. 15 hours
  5. Embedding- create mold by putting in paraffin filled block then place on ice.
  6. Microtomy- rough trim before then cut into 2-10 um (4um)
  7. Staining- deparaffinize via xylene, alcohols and water befor staining
  8. Coverslipping
237
Q

When using a microtomy, what thickness should you cut?

A

4um

238
Q

Before processing, what thickness should you trim your tissue ?

A

~3mm thick

ensure it fits in the cassette without smushing it

239
Q

What ate the 3 magic numbers for fixatives/fixing?

A

Use 10 % NBF

at 10:1 ratio of NBF:tissue

It fixes at a rate of ~1mm/hour, so ensure pieces are small

Have tissue in fixative for 24 hours. You may need to change out fixative if feces or blood within

240
Q

Where do hematopoeitic cells originate in the embyro? during gestation?

A

embryo= yolk sac

gestation= liver, spleen –> bone marrow

241
Q

How quickly are neutrophils produced in the bone marrow? platelets? RBC?

A

Neutrophils= hours

Platelets= days

RBC= months

242
Q

Release of immature cells indicates bone marrow
________ or _________

A

Release of immature cells indicates bone marrow
stress or disease

Under normal circumstances only mature cells are
released into the systemic circulation

Hematopoiesis is controlled by soluble stimulatory
factors that include cytokines, hormones and growth
factors

243
Q

What are 4 indications to examine the bone marrow?

A
  1. Unexplained cytopenias (any non‐regenerative anemia)
  2. Maturation defects or morphologic abnormalities in cells
  3. Potential myeloproliferative/lymphoproliferative disease
  4. Potential malignancies metastatic to marrow
244
Q

True or False

Even though bone marrow is present in multiple sites it
responds as a single tissue unit.

a sample taken anywhere
is thought to be representative of the marrow as a whole.

A

True!!!

245
Q

What are two types of evaluationd of bone marrow

A

aspirates (cytology)

Core biopsies (histology)- more invasive but you can see cell organization

246
Q

What is wrong with this neonatal calf?

A

Nothing! The bone marrow is normally this color in neonates due to the bone marrow being active

Ex. normal 13 day old foal (picture below)

247
Q

What is wrong with this goat/sheep? What is the cause? Where else will you see clinical signs?

A

Serous atropy of Fat

Due to starvation of cachexia (caused by disease, inflammation, diet, neoplasia, etc)

Also will see serous atropy of fat at the base of heart and around the kidney.

Common in sheeps and goats

May aslo see osteopenia (picture)

248
Q

What are 3 common causes of bone marrow degeneration/necrpsos?

A
  1. Radiation
  2. Chemical, antineoplastic drugs
  3. Viral infections (parvovirus of feline panleukopenia, canine parvovirus, EIA virus etc.)

Since bone marrow cells are very active metabolically, a variety of insults can interfere with hematopoiesis. Bone marrow necrosis may result in pancytopenia.

[Parvoviruses- infect rapidly dividing cells. In-utero infection in cats causes cerebellar atrophy. Infects cardiomyocytes of puppies.]

249
Q

What is the usual cause of this lesion?

A

Suppurative osteomyelitis is usually the result of bacterial infections.

Tissue will be rich in neutrophils and macrophages.

Septic osteomyelitis= comes from the blood (maybe originating from the umbilical cord/omphalitis)

250
Q

What are common causes of diffuse granulomatous osteomyelitis? what may it result in?

A

Diffuse granulomatous osteomyelitis is usually the result of fungal infections, e.g.: histoplasmosis and coccidiodomycosis.

Osteomyelitis may result in Pancytopenia

Lesion will be rich in macrophages that may contain the causative agent .

Multifocal granulomatous osteomyelitis is seen in tuberculosis of birds(?)

Histoplasmosis can also manifest in other organs as a diffuse granulomatous uveitis, hepatitis and splenitis.

251
Q

Cytauxzoonosis

A

Cytauxozoon felisprotozoa
Often fatal
Bobcats (Lynx rufus) are the reservoir

Two forms

  1. Schizogenous phase –> macrophages (enlarged and filled with parasite) –> systemic illness
  2. Erythrocytic phase –>anemia
252
Q

What will you see in bone marrow hypoplasia/atropy?

A
  • Decreased proliferative activity
  • Usually characterized by increase in yellow marrow
  • Often accompanies marrow degeneration.
  • Sequel will depend on cell line(s) affected

Example: marrow damage secondary to feline panleukopenia virus infection.

Example: myelofibrosis (CT replaces precursors) in scirvey/Vitamin C deficiency

253
Q

Pancytopenia may be the result of …

A
  • myelophthisis, the replacement of myeloid tissue by abnormal tissue:
    • collagen‐rich fibrous connective tissue(myelofibrosis)
    • malignant neoplasia
  • abnormality of hematopoietic cells – aplastic anemia/pancytopenia (destruction of hematopoietic stem cells)
254
Q

What will you see in bone marrow hyperplasia? pathogenesis?

A

One or multiple cell lines may be hyperplastic depending on the stimulus

Gross finding: Red marrow replacing yellow marrow (fat) at metaphysis and endosteal surface of diaphysis.

Pathogenesis: ↓cell numbers in blood caused by increased peripheral demand; or adequate numbers of hypofunctional cells in peripheral blood –> lead to ↑cell production in the marrow in response to poietns and
interleukins.

Example: Bovine Leukocyte Adhesion Deficiency (BLAD) syndrome - in people and dogs (Irish setters). Defect in migration of leukocytes.

horse w/ hyperplasia due to IHA (picture below)

255
Q

What is wrong with this adult horse? common cause?

** NEED TO KNOW***

A

Bone marrow hyperplasia secondary to EIA

Causes of anemia in EIA (1) extravascular immune mediated hemolysis (2) decrease production (3) Inflammation

May see acute thrombocytopenia (due to immune mediated mechanism, they are innocent bystanders)

Horses are infected for life with EIA. They act as reservoirs. the disease can be transmitted by flies and mosquitoes.

256
Q

Which primary neoplasia are most common in the bone marrow?

A

Lymphoproliferative (LYMPHOID) Disease

Marrow and/or extramedullary neoplastic transformation of a lymphoid cell line

  • lymphoma (lymphosarcoma)
  • lymphoid (lymphocytic) leukemia
  • plasma cell tumors

Myeloproliferative (MYELOID) Disease are rarer.

257
Q

What are the three types of Lymphoproliferative (LYMPHOID) Diseases?

A
  1. Lymphoid leukemia
  2. Lymphoma (Leukemic phase)
  3. Plasma cell neoplasia ( multiple myeloma & plasmacytoma)
258
Q

What are the two types of myeloproliferative disease of the bone marrow?

A

Acute forms: rapidly fatal and tend to occur in younger animals, poorly differentiated cells, decrease number of circulating cells

Chronic forms: longer clinical course (indolent), neoplastic cells are relatively well‐differentiated, increase number of circulating cells

259
Q

What are common features of both Myelo/Lymphoproliferative disease of the bone marrow?

A
  • Anemia
  • Hypercellular marrow
  • Leukemic cells in peripheral circulation (especially if chronic)
  • Megaloblastic alterations in erythroid cells
  • Thrombocytopenia (not always present)
  • Hepato/splenomegaly – Myelo/lymphoproliferative disease spreads early to involve the spleen and liver. Animals may present with splenomegaly and/or hepatomegaly
260
Q

What would you call this abnormality? What is possible cause?

A

Hepatosplenomegaly

Due to myelo/lymphoproliferative disease (LSA) due to the early spread of these diseases to the spleen and liver

Also may see anemia, hypercellular bone marrow, leukemic cells in peripheral circulation, megaloblastic alterations in RBC etc.

261
Q

What may be wrong with this cow?

A

Lymphoid leukemia or leukemic lymphoma

May see focal to multifocal whitish masses, that may be hard (picture below)

262
Q

What are three types of plasma cell neoplasias?

A
  1. Multiple myeloma- malignant, from bone barrow, M protein, increase Ig secretion, punched out appearance, monoclonal gammopathy, hypercalcemia
  2. Cutaneous Plasmacytomas- benign
  3. Extramedullary Plasmacytoma - malignant, dogs, cats, horses, + amyloidosis
263
Q

Multiple Myeloma

A

rare, malignant tumor of plasma cells that arise from the bone marrow

have increase secretion of Ig/Ig subunits ( M protein) - monoclonal gammopathy

“punched out” appearance of osteolytic lesions in 25-66% of cases. Starts in active marrow (vertebral bodies, flat bones, pelvis)

hypercalcemia due to osteolysis

Plasma cells will be enlarged, have perinuclear clearing, with nucleas pushed to the side due to increased cytoplasm.

264
Q

Cutaneous vs. Extramedullary Plasmacytomas?

A

Cutaneous Plasmacytomas- Rare ‐ usually benign – skin or mucous membranes
Extramedullary Plasmacytoma- Rare – malignant – dogs, horses, cats; Amyloidosis is a feature

Both are types of plasma cell neoplasias

265
Q

ddx?

A

Multiple Myeloma

“punched out” osteolytic lesions

266
Q

What are 4 types of Histocytic neoplasias?

A
  1. Histiocytic sarcoma - uncommon – malignant tumor of histiocytic (macrophage or dendritic cell) origin
    • frequently in the dog (Rottweiler, Bernese mountain dog); rarely in cat
    • disseminated form= “malignant histiocytosis”
  2. Cutaneous histiocytosis and systemic histiocytosis
    • ​​nonneoplastic canine immunoregulatory disorders
  3. Canine cutaneous histiocytoma- benign – epidermal Langerhans cell origin. “top heavy” nodular lesions.
  4. Feline progressive histiocytosis
    • Initially indolent cutaneous neoplasm; probably of dendritic cell origin
267
Q

________ syndrome= not clearly neoplastic maturation abnormalities of bone marrow cells characterized by ineffective and dysplastic hematopoises –> peripheral cytopenia of one or more cell lines

A

Myelodysplastic (MDS)

It is seen in cats infected with FeLV

268
Q

Which animals normally have hemal nodes (prominent, small, dark red) in their lymph nodes?

A

Ruminants

269
Q

______ lymph nodes have a inverted cortex and medulla

A

Porcine

270
Q

What should you suspect if your lymph node had a red color? black? brown? green? orange?

A

Red= blood

Black = anthracosis/carbon, tatoo ink

Brown= melanin, parasite hematin, hemosiderin

Green= eosinophils, blue-green algae

Orange= paratuberculosis in sheep

271
Q

Hemosiderosis: Brownish discoloration observed in lymph nodes draining areas of ________

A

hemorrhage

272
Q

lymphoid tissue proliferation of the outer cortex = _____ hyperplasia

lymphoid proliferation of the inner cortex = _____/_____ hyperplasia

A

outer cortex=follicular hyperplasia

inner cortex= lymphocyte/diffuse hyperplasia

273
Q

______ is a common term for a painful swollen lymph node

A

buboes (bubos)

274
Q

What are DDx for focal areas of necrosis in lymph nodes of CATS

A

toxoplasmosis, salmonellosis, tularemia, yersiniosis,
Tyzzer’s disease, FIP

275
Q

Diagnosis?

Foal has enlarged swollen lymph nodes ( only mandibular, pharyngeal, parotid) with some abscessation and fistulation

A

Strangles- Streptococcus equi ssp equi

276
Q

________ __________ = Streptococcus equi ssp equi abscesses anywhere in the body other than the pharyngeal area

A

Bastard strangles

277
Q

Sheep lymph node.

Top Disease? Etiology?

A

Caseous lymphadenitis

Corynebacterium pseudotuberculosis

See concentric “onion ring” lymph node & eosinophilic (green) pus becomes caseous with age

278
Q

Top DDx for a cow with granulomatous lymphadenitis?

A

Mycobacterium bovis

279
Q

Top DDx for pig with diffuse granulomatous (histocytic) lymphadenitis?

A

PMWS- Porcine Multisystemic Wasting Disease

Porcine Circovirus 2

Lymph node will be increased in size and have uneven color.

Will have B & T Cell depletion –> immunosuppresion

Botryoid intracytoplasmic inclusion in macrophages

280
Q

______ are usually ill when lymphoma is diagnoses

A

Cats

(dogs are usually healthy)

281
Q

Lymphosarcoma can be induced by _____ in cats and _______ in cattle

A

FeLV , BLV

282
Q

Which anatomical classification of lymphomas is most common?

A

Multicentric

283
Q

Alimentary lymphomas are common in _____

A

CATS

284
Q

in animals, which has a better survival profile and response to treatment;

B-cell lymphomas –or–T-cell lymphomas?

A

B-cell lymphomas

285
Q

True or False

Large cell lymphomas with high mitotic rates are slower to progress but response poorly to chemotherapy

A

FALSE

Small cell lymphomas with low mitotic rates are slower to progress but response poorly to chemotherapy

L_arge cell lymphomas_ with high mitotic rates rapidly progress but response well to chemotherapy

286
Q

Malignant lymphomas (most common canine treated neoplasm) affects dog of what ages and breeds?

A

ALL ages and ALL breeds

287
Q

Bovine lymph node.

Etiology/Disease?

A

BLV- bovine enzootic leukosis

The hemorrage and necrosis is characteristic of rapid growing tumors

288
Q

Abomasum of young cow. Etiology/Disease?

A

enzootic leukosis (BLV) with abomasal involvement

289
Q

__________ is the MOST COMMON reported malignency in pigs

*** KNOW THIS*****

A

Lymphoma

290
Q

What would be my best diagnosis for the type of malignancy in this pig?

A

Lymphoma

It is the most common reported malignancy in pigs

291
Q

Which species has the highest incidence of lymphoma?

A

CATS

Lymphoma is the most common hemopoietic neoplasm in cats

FUN FACT: Although it can be caused by FeLV, as FeLV infection rates has gone down the incidence of lymphoma has actually increased (mainly gastrointerstinal lymphomas)

292
Q

Why are endoscopic biopsie for GI lymphomas not always diagnostic?

A

Different types of tumors are located in different areas of the GI tract. A single biopsy of one area will commonly miss the tumor.

Ex. B cell lymphomas are “further down” than T-cells, or are in the stomach.

293
Q

Marek disease is most often in chickens _____ month of age

A

2-5

294
Q

Leukemia virus of birds usually infects birds after the age of ____ months

A

6

295
Q

True or False

Birds have lymph nodes

A

False- they dont have lymph nodes

296
Q

_________ disease causes cutaneous (nodules at base of feathers), ocular (“grey eye”) and diffuse (liver, spleen, etc) lymphocytic infiltrates/lymphoma. As well as peripheral neuritis (sciatic n.)

A

Marek’s (herpesvirus)

297
Q

What disease in chickens will cause these clinical signs?

A

Marek’s disease (Herpesvirus)

298
Q

lack of Ag stimulation, toxins, chemotherapy, infectious agents, ionizing radiation, malnutrition, cachexia, & aging cause what response in the spleen?

A

lymphoid atropy

299
Q

storage of blood and contraction to expel reserve blood are important functions of what organ?

A

Spleen

300
Q

Congestion, acute hyperemia, and acute hemolytic anemia are causes of a __________ spleen

A

bloody

301
Q

Phagocytosis, proliferation of cells, and storage of material (ex. amyloid) are causes of a _________ spleen

A

meaty

302
Q

Hematomas, incompletely contracted areas of spleen, acute splenic infarcts and vascular neoplasma (hemangiosarcoma) are causes of splenic ________ with a________ consistency

A

nodule , bloody

303
Q

What are 6 causes of splenic nodules with a firm consistency?

A
  1. Splenic nodular hyperplasia
  2. Fibrohistiocytic nodules
  3. Primary neoplasms
  4. Secondary (metastatic) neoplasms
  5. Granulomas
  6. Abscesses
304
Q

SCID (splenic hypoplasia), congenital accessory spleens and splenic fissures (horses) are all developmental anomalies that result in a ______ spleen

A

small

305
Q

true or false

accessory spleens are functional

A

false

they lack the proper blood suppy

306
Q

_________ ____________ are gray-white to yellow, hard dry encrustation on the capsule (usually on the margins) of the spleen that are most common in old dogs.

A

Siderotic plaques

307
Q

What is present on this old dogs spleen?

A

Siderofibrosis of the splenic capsule (siderotic plaques/nodules, Gamma‐Gandy bodies).

308
Q

Siderotic plaques are a _______ change, but may be a sequel of ________

A

aging/degenerative , hemorrhage

309
Q

What is wrong with this old dogs spleen?

A

Hemosiderosis (degenerative lesion)

pigment make it look brown

310
Q

Barbiturate-insuced splenomegaly is due to ________ ___________ _________

A

Acute passive congestion

311
Q

Barbituates, gastrosplenic torsion/volvulus and right CHF cause ______ _______ _____ of the spleen

A

acute-passive congestion

312
Q

Acute splenic infarction in pigs should alert you about the possibility of ____ _____ ______

A

Classical Swine Fever (hog Cholera)

313
Q

____ _____ leads to seeding of the omentum and formation of numerous “accessory spleens” –> splenosis

A

Splenic rupture

314
Q
A

Splenic hematoma

315
Q

________ & _________ result in hyperplasic spenitis

A

Aleutian disease of mink and ferrets

Equine infectious anemia

Due to Chronic antigenic stimulation results in hyperplasia of the monocyte‐macrophage or lymphoid/ plasma cell population

316
Q

Acute splenic hyperemia/spenitis with splenomegaly can be seen in a bovine with ______

A

Bacillus anthracis

large bacillus, forms short chains and is characterized by square ends and a distinct capsule.

317
Q

What is going on with this spleen?

A

lymphoid hyperplasia

318
Q

What is the etilogy of White‐grey miliary foci scattered throughout the splenic parenchyma. Causing a Necrotizing (or necrosuppurative) splenitis.

A

Francisella tularensis (Tularemia) - “rabbit fever”

319
Q

Acute multifocal (milary) necrotizing hepatis and splenitis is characterisitc of ______ virus in raptors

A

Herpes

“herpes inclusion body disease (hepatosplenitits) of raptors”

Raptors get infected by consuming pigeons infected (often subclinically) with columbid herpesvirus (CoHV),

320
Q

Multifocal granulomatous spenitis is characteristic of systemic ________ _______ in birds

A

Mycobacterium avium

321
Q

What is wrong with this spleen? what is the clinical signifigance?

A

Nodular hyperplasia

Incidental - slow growing

likely an aging change, formed by a mixture of hyperplastic extramedullary hemopoietic cells, and are prone to rupture from trauma, resulting in hemoabdomen and exsanguination

322
Q

Splenic _________ are benign, but are prone to rupture

A

hemangiona

323
Q

Splenic ____________ are the most common neoplasm of the spleen

A

Hemangiosarcoma

(they are also commonly found on the skin)

Highlt metastaitc, invade the abdominal cavity.

324
Q

White, multi-nodular, firm mass of the spleen is most likely a …

A

Lymphosarcoma

325
Q

Cat

A

Histocytic sarcoma

326
Q

Which 4 viruses cause thymic atophy

A

EHV-1

FeLV

BVD

Canine Distemper

327
Q

SCID in arabian foals and Basset hounds causes thymic _________

A

hypoplasia

328
Q

Thymus inflammation is very rare, but can occur in pigs with ______

A

PCV-2

329
Q

What kind of neoplasm is this? what is the prognosis?

A

Thymic Lymphoma

Results in lung collaps, breathing difficulties and compression of vessels feeding the brain. Poor prognosis, hard to remove.

330
Q

Myasthenia gravis (–>megaesophagus) in dogs and Generalized exfoliative dermatitis (head and pinna) of cat are paraneiplastic syndroms of ______

A

thymoma

331
Q

What are 3 infections of the Bursa of Fabricius?

A
  1. Infectious bursal disease (birnavirus)- lymphoid depletion (3-6 weeks)
  2. Lymphoid leukosis (avian leukosis virus) - neoplastic proliferation of B-lymphocytes
  3. New castle disease (paramyxovirus)
332
Q

Infectious birdal disease occurs in chickens________ weeks of age.

A

3-6 weeks

IBV is the most important disease of concentrated broiler producing areas of the US

Causes lymphoid depletion –> immunodeficiency due to the virus targeting pre-B lymphoctes.

Birds usually die of secondary infections.

333
Q

This is caused by which disease?

A

Infectious bursal disease (IBD)

Other names of this condition: Gumboro disease, Avian infectious bursitis
Etiology: Avian bursal disease virus (Birnavirus)