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Path 2 > Newton Alimentary > Flashcards

Newton Alimentary Flashcards

1
Q

What is a primary facial cleft called?

A

Cheiloschisis

Hair lip → normal in rabbits

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2
Q

What pathological event causes cheiloschisis?

TQ

A
  • Incomplete fusion of nasofrontal and maxillary processes.
  • involves lip (superficial) or lip & nostrils (deep)
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3
Q

What are the two types of primary facial clefts?

A
  • Superficial →cleft lip
  • Deep →cleft lip + nostrils (uni or bilateral)
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4
Q

What is a secondary facial cleft called?

A

Palatoschisis

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5
Q

What pathological event causes palatoschisis?

Sequella?

A
  • Incomplete fusion of the palatine processes

Affected animals:

  • can’t nurse properly
  • aspiration pneumonia
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6
Q

What species have a genetic predisposition to developing a facial cleft?

A
  • Cattle: Charlois, Hereford
  • Dogs: Boxers
  • Cats: Siamese, Abyssinian
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7
Q

What toxins can cause facial clefts and

in what species?

A
  • Cattle: Lupines
  • Sheep: Veratrum Californicum → steroidal alkaloids
  • Swine: Poison Hemlock, Crotalaria
  • Cats: Gruseofulvin
  • Primates: steriods
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8
Q

Ingestion of Steroidal Alkaloids inhibits the Hedgehog Signaling Pathway in lambs. Tell what body part is affected if the ewe ingests this toxin on:

day 14, days 17-19 d & days 28-31?

A
  • day 14 → deformities of the head
  • day 17-19 → deformities of the trachea
  • day 28-31 → shortened metatarsal & metacarpal bones (limbs)
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9
Q

What mandibular malformation results in parrot mouth?

A

Brachygnathia Inferior

(mandible too short)

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10
Q

What maxillary malformation results in “bull dog face”?

A

Brachygnathia Superior

(maxilla too short)

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11
Q

What mandibular malformation results in prolonged mandibles?

A

Prognathia

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12
Q

What mandibular malformation results in a missing lower jaw?

A

Agnathia

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13
Q

How does the dental lamina normally form?

A

Gingival epithelium (ectoderm) invaginates down into jaw (mesenchyme).

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14
Q

What makes enamel?

A

Ameloblasts

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15
Q

What develops the Dental papilla?

A
  • mesenchymal tissue = pulp
  • odontoblasts = dentin
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16
Q

What 3 things develop the dental follicle?

A
  • Cementoblasts → cementum
  • Osteoblasts → boney socket of teeth
  • Fibroblasts → peridontal ligament
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17
Q

Describe brachydont (simple) teeth.

A
  • Crown→above gum
  • Root→ below gum line
  • Pulp→ inner core, nerves & vessles
  • Have demarcation between root & crown
  • Fibrous peridontal ligament holds tooth in socket
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18
Q

Who has brachydont teeth?

A
  • Carnivores
  • Pigs (except tusks)
  • Ruminants (lower incisors)
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19
Q

Describe hypsodont (complex) teeth.

A
  • high crown teeth w/ root
  • crown & pulp grow throughout life
  • no demarcation between root and crown
  • infundibulum: cementum and enamel invaginations
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20
Q

Who has hypsodont teeth?

A
  • Horses
  • Rodents
  • Rabbits
  • Ruminants →cheek teeth
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21
Q

What are the 3 typs of developmental teeth abnormalities?

A

Anadontia = no teeth (rare)

Oligodontia = too few teeth (rare)

  • Pseudo-oligodontia = failed/delayed eruption

Polydontia= too many teeth

  • Psuedo-polyodontia = retained deciduous teeth
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22
Q

What are dentigerous cysts?

A
  • Heterotrophic polydontia AKA ear tooth
  • Epithelial lined cavity + keratin + abnormal tooth
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23
Q

Who gets dentigerous cysts?

A

Horses →under their ears

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24
Q

What is the cause of enamel hypoplasia?

A

damage to ameloblasts → segmental brownish, thin to missing enamel.

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25
Q

Etiology of enamel hypoplasia?

TQ

A
  • K9 Distemper → dogs < 6 mo. old
  • BVD → calves in utero
  • High fever in young animals
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26
Q

Where is chronic fluorisis most common?

A

down stream of aluminum plants

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27
Q

What are 3 types of abnormal pigmentation of teeth?

A
  • Chronic Fluorisis
  • Congenital Erythopoetic Porphyria
  • Tetracycline
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28
Q

Pathogenisis of chronic flurosis?

A
  • Occurs during odontogenesis (6-36 mo. in cattle)
  • Excess flouride disrupts enamal formation
  • teeth are soft, chalky enamel with yellow, brown to blackish spots
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29
Q

What helps prevent chronic fluorisis in cattle?

A

selenium supplementation

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30
Q

What is “pink tooth”?

A

Congenital erythropoetic prophyria

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31
Q

What is the etiology of congenital erythropoetic porphyria?

A
  • 2° to porphyrins in dentin
  • Inherited→defective heme pigment synthesis in erythrocytes
    • uroporphyrinogen 3 cosynthetase defect →type 1 porphyrin deposits
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32
Q

What does tetracycline do to teeth?

A

Deposits Ca2+ in enamel→turning teeth yellow-brown.

(Will fluoresce under UV light/Wood’s Lamp)

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33
Q

What is pulpitis?

A

Inflammation of dental pulp→ 2° to tooth DAMAGE

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34
Q

What is periodontitis?

A
  • Inflammation of soft tissue surrounding tooth (gingivitis)
  • 2° to bacterial plague/dental tartar → toxins & mechanical irritation.
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35
Q

What type of teeth do dental caries occur in?

A

Brachydont Teeth

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36
Q

What causes dental caries?

A
  • Microbial enzymes & Acids→De-Calcification of enamel and Dentin
  • Pulpitis
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37
Q

What type of teeth do Infundibular impaction occur in?

A

Hypsodont Teeth

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38
Q

2 other names for Infundibular Impactions?

A
  • Infundibular necrosis
  • Infundibular caries
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39
Q

What is the etiology of Infundibular impaction?

A
  • Acid from food degradation by bacteria causing demineralization of enamel and cementum
  • leading to pulpitis and periodontitis
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40
Q

What is the etiology of feline external resorptive neck lesions?

A

2° to odontoclastic resorption of cementum in the neck/root of tooth → resorptive cavity that collects food and dental plaque→ inflammation

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41
Q

What is step mouth and what type of teeth does it occur in?

A
  • 2° to lost/broken tooth of opposite jaw leading to molar/premolar elongation
  • Hypsodont teeth
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42
Q

What is wave mouth and what type of teeth does it occur in?

A
  • 2° to multiple lost/broken teeth of the opposite jaw
  • Hypsodont teeth
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43
Q

What is shear mouth & what type of teeth does it happen in?

A
  • Irregular wear of molar/premolars leading to sharp points on medial and lateral aspects
  • Hypsodont
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44
Q

What is the normal slope of horse teeth?

A

15%

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45
Q

Define Cheilitis

A

Inflammation of the lips

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46
Q

Define Stomatitis

A

Inflammation of the oral mucosa

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47
Q

Define Glossitis

A

Inflammation of tongue

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48
Q

Define Gingivitis

A

Inflammation of the gums

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49
Q

Define Pharyngitis

A

Inflammation of the pharynx

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50
Q

Define Tonsilitis

A

Inflammation of the tonsils

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51
Q

What viruses causes Vesicular Diseases of the mouth?

(all are reportable in large animals)

A
  • Foot & Mouth - picorna
    • (cattle, swine sheep/goats)
  • Vesicular Stomatitis - rhabdovirus
    • (all LA, only one in USA)
  • Swine Vesicular Exanthema - Calicivirus
  • Swine Vesicular Dz - Enterovirus
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52
Q

What are the clinical signs of viral stomatitis in LA?

A
  • Vesicles
  • Ulcers
  • Salivation
  • Lameness
  • Fever
  • Anorexia
  • + abortion
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53
Q

What are the zoonotic vesicular dz’s?

A

Parapox stomatitis:

  • Bovine papular stomatitis
    • Milker’s nodules
  • Contageous ecthyma of sheep & goats
    • Orf
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54
Q

Non-viral causes of vesicular stomatitis?

A
  • Pemphigus vulgaris (Autoimmune stomatitis) →acantholysis & ulcers
    • auto-antibodies to desmosomal protiens in epithelium
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55
Q

What are the 5 types of ulcerative stomatitis in SA

A
  • Feline Ulcerative Stomatitis →Glossitis
  • Feline Lymphoplasmacytic Stomatitis-Pharyngitis
  • Oral Eosinophilic Granuloma Complex
  • Chronic Ulcerative Paradental Stomatitis
  • Uremia
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56
Q

What is the etiology of:

  • feline ulcerative stomatitis/glossitis
  • feline lymphoplasmacytic stomatitis-pharyngitis
  • oral eosinophilic granuloma complex?
A
  • Unknown
  • FUSG→ oral tissues
  • FLSP→ glossopalantine arches
  • OEGC:
    • Cats = Upper lip
    • Huskies = tongue
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57
Q

What is the etiology of Chronic Ulcerative Paradental Stomatitis?

A
  • 2° to dental plague→lymphocytes & plasma cells →gingival ulceration, bone resorption/tooth loss
  • Maltese & CKCS
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58
Q

What is the etiology of Uremia?

A
  • 2° to chronic renal dz→increased urea in blood/saliva→vascular & tissue damage
  • urease producing bacteria in mouth
  • excessive ammonia →ulceration
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59
Q

What are 3 types of bacterial stomatitis?

A
  • Oral Necrobacillosis→fibrinonecrotic
  • Actinobacillosis→chronic granulomatous inflammation w/ fibrosis
  • Actinomycosis →pyogranulomatous
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60
Q

Pathology of oral necrobacillosis?

(calf diptheria)

TQ

A
  • 2° to trauma/damage
  • Fusobacterium necrophorum
    • Gram (-)
    • potent toxins→ulcerative gingivitis (grey-tan)
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61
Q

Pathology of actinobacillosis?

(wooden tongue)

TQ

A
  • 2° to trauma/damage
  • Actinobacillus lignieresii
    • Gram (-)
    • goes to regional lymph nodes
    • chronic granulomatous inflammation w/ fibrosis
    • rigid tongue
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62
Q

Pathology of Actinomycosis?

(lumpy jaw)

A
  • 2°to trauma/damage
  • Actinomyces bovis
    • Gram (-)
    • sulfur granules
    • granulomatous inflammation (mandible) → destruction of bone
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63
Q

What is fungal stomatitis caused by?

A

Thrush = Candida albicans (commensal)

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64
Q

Pathology of thrush?

A
  • 2° to immonocomp/prolonged antibiotics/ hyperglycemia
  • overgrowth→greyish, pseudomembrane on tongue and esophagus
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65
Q

What animals get gingival hyperplasia?

TX?

Ddx?

A
  • Middle-old aged Brachycephalic breeds
  • Surgical removal
  • Must distinguish from Epulis (oral tumor)
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66
Q

What percentage of alimentary tumors are oral neoplasms?

A

75%

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67
Q

What causes papillomas and in what species are they most common?

A
  • Papilloma virus
  • Dogs: < 1 year
  • Young horses (he doesn’t say that but it’s TRUE!)
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68
Q

What is the appearance and pathology of papillomas?

A
  • Cauliflower to papillary shaped warts
  • Small in # most are benign
  • They regress spontaneouly leaving long lasting immunity
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69
Q

What is the pathology of melanoma and

what species is it most common in?

A
  • Common in older dogs
  • Very aggressive–>90% malignant
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70
Q

What is the pathology of SCC?

A
  • Can metastasize
  • ALL are Locally invasive
  • Can involve bone
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71
Q

What species get SCC?

A
  • Felines: 60% of oral tumors
    • Tongue
  • Dogs: Tonsils & metastasis from other sites
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72
Q

Pathology of fibrosarcoma?

Who gets most often?

TQ

A
  • Can involve bone
  • Felines → 20% of oral tumors
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73
Q

Plasmacytoma pathology

(Oral Plasma Cell Tumor)

A
  • Can occur anywhere in the oral cavity
  • Looks aggressive histologically but it’s not
  • Locally invasive
  • NO metastasis
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74
Q

What is Epulis?

A
  • Gingival tumor → Firm, grey/pink
  • Locally invasive
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75
Q

Pathology of Fibromatous epulis?

TQ

A
  • Stromal - arise from periodontal ligament
  • Benign
  • Dosen’t invade bone
  • Clinically indistinguishable from gingival hyperplasia
  • Carnassial & canine teeth of brachycephalic breed
76
Q

Pathology of Acanthomatous Epulis?

A
  • Epithelial
  • Malignant
  • Will invade bone
  • Will reoccur after removal
  • need to differentiate from SCC
77
Q

What are the 2 types of dental oral neoplasms?

A
  • Ameloblastoma
  • Odontoma
78
Q

What is the etiology of Ameloblastomas?

A
  • Adult Dogs
  • Epithelial ameloblasts from enamel organ
  • Locally invasive with bone destruction
79
Q

What is the occurence & pathology of odontoma?

A
  • Rare - occurs in immature animals
  • originates in enamel organ and contains dentin and enamel
80
Q

Pathology of tonsilitis?

A

Inflammation of tonsils via oropharynx or blood stream

(NOT via lymphatics)

81
Q

What are the neoplasms of tonsils?

A
  • Lymphoma
  • SCC (Dogs)
82
Q

Define Ptylism

A

excessive salivation

83
Q

Define Aptylism

A

reduced or no salivation

84
Q

What are sialoliths (salivary caculi)?

RARE

A
  • 2° inflammation of salivary gland
    • Sloughed cells & inflammatory cells form a NIDUS → can block the salivary gland
    • Hard, chalky & white to yellow concretions of Ca2+ phosphate
    • Painful
85
Q

What are sialoadentitis and what is the etiology?

A
  • Inflammation of the salivary glands
  • Caused by:
    • Rabies
    • Strangles (strep equi)
    • Canine distemper
    • hypovitaminosis A
86
Q

Pathophysiology of dilation of slivary ducts?

2 Results?

TQ

A
  • 2° to obstruction
    • Ranula = dilation of sublingual salivary duct
    • Salivary mucocele = ruptured or torn salivary duct
      • 2° to trauma w/ bloody salivary secretions
87
Q

What is the etiology/pathology of salivary duct infarction?

A
  • Unknown etiology
  • Usually unilateral
    • Grossly firm & swollen glands
      • can be confused with neoplasms
88
Q

What are the neoplasms of the salivary glands?

A
  • Adenoma & Adenocarcinomas (rare)
  • Metastasis to regional LN & lungs
89
Q

What are the functional disorders of the esophagus?

A
  • Esophageal Achalsia
  • Cricopharyngeal Achalasia
  • Megaesophagus
90
Q

What is the pathophysiology of esophageal achalasia?

A
  • Lower Sphincter dysfunction
  • Defective esophageal muscle contractility
91
Q

What is the pathophysiology of cricopharyngeal achalasia?

A
  • Upper Sphincter dysfunction
  • dysfunction of Inhibitory neurons (doesnt relax)
    • Difficulty swallowing
    • regurgitation
    • Aspiration pneumonia
92
Q

What is the pathophysiology of Megaesophagus?

(esophageal ectasia)

A

Problem with peristalsis in the the cervical-mid esophagus leading to dilation.

93
Q

What are the two types of megaesophagus?

TQ

A

Congenital

  • Idiopathic : neruromuscular disorders
  • PRAA: vascular ring anomaly (Aorta, PA, Ductus Arteriosis) TQ!!!

Aquired

  • 2° to damage/inflammation
94
Q

Types of Acquired Megaesophagus?

A
  • Myasthenia gravis→ auto-antibodies
  • Hypothyroidism → muscular atrophy
  • Toxins → nerve damage
95
Q

Lesions of Acquired Megaesophagus?

A
  • Flaccid→ up to 3x enlargedment
  • Regurgitation
  • Aspiration pneumonia
  • Ulceration
96
Q

What are the 4 types of choke & their pathology?

A
  • Intraluminal → 2° to foreign bodies →pressure necrosis
  • Periesophageal- 2° to:
    • vascular ring anomalies →PRRA (most common)
    • inflammtion
    • muscular hypertrophy (terminal esophagus)→ horse
  • Stenosis→2° to esophageal damage→fibrosis
  • Perforation
    • Cellulitis
    • Eso-respitatory fistulae
    • Esophageal diverticulum
97
Q

What 4 things cause inflammation of the esopagus (esophagitis)?

A
  • Gastric Reflux
  • Viral- erosions & ulcers
  • Fungus (myotic)
  • Parasitic
98
Q

What Viruses cause esophagitis?

A
  • BVD
  • Malignant Catarrhal Fever
  • IBR
  • Feline Calici Virus
99
Q

What fugus causes myotic esophagitis?

A
  • Candida albicans→ 2° to immunosuppresison/prolonged antibiotic use
  • Phythium insidiosum →chronic pyogranulomatous esophatis (dogs) →2° fibrosis
100
Q

What are the 4 types of esophagial neoplasms?

A
  • Papilloma - “wart”
    • Cattle
  • SCC
    • Cattle & Cats
  • Fibroma/Fibrosarcoma/Osteosarcoma
    • 2° to Spirocerca lupis→dogs
  • Leiomyoma/Leiomysarcoma →RARE in all species
101
Q

What are the protective mechanisms of the monogastric stomach?

TQ

A
  • Intact layer of epithelial & mucus cells
  • Gastric mucus
  • Bicarb
  • Microcirculation/bloodflow
  • Prostaglandins
    • inhibits HCl secretion
    • stimulates bicard & mucus secretion
    • vasoDILATION
  • Mucosal immune system
102
Q

What are the two tumors that can cause gastric ulcers?

A
  • Gastrinoma (parietal cell)→ HYPERsecretion of HCl
  • Mast Cell Tumor →histamine released-→increased HCl

(Both injure epithelium)

103
Q

3 ways the stomach can dilate and rupture?

A
  • Dogs
    • Acute K9 Gastric Dilation & Volvulus (GDV)
  • Equine
    • Acute Equine Gastric Dilation
  • Gastric Rupture
104
Q

What is the pathophysiology of acute cainine gastric dilation and volvulus (GDV)?

A
  • Deep chested dog→ 2° to large meal/excessive H2O intake→ food swells
  • Clockwise rotation of stomach (from ventral veiw) causes:
    • congestion
    • infarction
    • splenic enlargement
    • ishemia/hypoxia
    • acid-base imbalances
  • Will result in cardiac arrhythmia, shock, failure if don’t TX
105
Q

What is the pathophysiology of Acute Equine Gastric Dilation?

A

2° to overeating or excessive water intake→ grain swells

106
Q

What is the pathophysiology of gastric rupture?

A
  • 2° to severe dilation
  • Usually greater curvature, parallel to omental attachment
    • accompanied by muscle tearing, hemorrhage, shock, peritonitis
107
Q

What can cause gastritis?

(7)

A
  1. Acute hemorrhagic, gastritis (garbage gut)
  2. Trauma (FB)
  3. Parasitic
  4. Bacterial
  5. Fugal
  6. Neoplasia
  7. Uremia
108
Q

What parasites can cause gastritis?

A
  • Equine:
    • Bots
    • Drachia megastoma →margoplicata region
    • Tricostrongylus →Morroco leather appearance
  • Cats/Dogs:
    • Ollulanus tricuspic
    • Gnathostoma spp.
    • Physaloptera spp.
109
Q

What fungus can cause gastritis?

A

Pythium insidiosum

110
Q

Match the animals with their gastric neoplasia.

  • Dog, Cat, Horse, Llama
    • Adenocarcinoma
    • Gastric Mast Cell Tumor
    • Lymphoma
    • SCC
    • Leimyoma/Leiomyosarcoma
A
  • Dogs
    • Adenocarcoma
    • Gastric MCT
  • Cats
    • Lymphoma
  • Horse/Llama
    • SCC
  • Rare in any species
    • Leimyoma/Leiomyosarcoma
111
Q

What are the 2 types of bloat?

A
  • 1° bloat → Frothy
    • Legume bloat
    • Feedlot bloat
  • 2° bloat → Obstructive
112
Q

Pathology of Legume Bloat (1°)?

A

Lush pastures →

cholorplast proteins stabilize gas bubbles & they don’t burst →

gas accumulates in rumen

113
Q

Pathology of Feedlot Bloat (1°)?

A

feed high carbs →get an increase in encapsulated bacT →

their thick capsules increase the vicosity of the rumen fluid→

gas is entraped & builds up

(Increased carbs, decreased roughage = increased gas producing bacT)

114
Q

Pathology of Obstructive Bloat?

A

2° to the inability to eructate:

  • Choke
  • Vagal nerve damage
  • Recumbency → cardia of esophagus becomes occluded
115
Q

Lesions of Bloat on Necropsy

TQ

A
  • distended rumen
  • sawhorse appearance
  • marked edema of head & neck
  • Bloat line
    • Cervical esophagus→ congested
    • Thoracic esophagus → pale
    • increased thoracic pressure 2° to increased abdominal pressure
  • Compressed lungs
  • Bulging diaphragm
116
Q

When can you DX Frothy Bloat on Necropsy?

A
  • Best is 1-2 hrs post-mortem
  • foam is completely gone 8-10 hours post mortem
117
Q

Pathology & Lesions of Postmortem Tympany?

A
  • No bloat line
  • postmortem degeneration of all the tissues in carcass
118
Q

Pathology of Grain Overload (Engorgement Toxemia)?

A

High carb intake → Incr. microbe activity & increased VFA production →

rapid drop in pH → change in microbe population →

Strep. bovis makes lactic acid →Acidosis & dehydration →

circulatory collaspe & SHOCK

119
Q

Which ruminants are more prone to grain overload than the other species?

A

New world camelids

(llamas & alpacas)

120
Q

Lesions of Grain Overload?

A
  • large amt of grain in rumen
  • dehydration
  • low rumen pH
    • only if done immediately postmortem
  • rumenitis
121
Q

Sequela to Grain Overload?

A
  • Rumen ulcers
  • Fusobacterium necrophorum (2° invader) → sawdust liver
  • Rumen scars
  • Occasionally see Mycotic Rumenitis due to:
    • Absidia spp.
    • Mucor spp.
    • Rhizopus spp.
122
Q

What parasitic larvae burrow into the rumen causing:

HYPOproteinemia

Anemia

?

A

Paraphistomum spp.

“Rumen Flukes”

123
Q

List types of Rumen FBs.

A
  • Trichobezoars → hairballs (from licking other cattle)
  • Phytobezoars → plant fiber balls
  • Rocks
  • Sand
  • Metal
124
Q

What can be done to help protect the Rumen from damage by Metal FBs?

A

Use a rumen magnet

125
Q

Pathogensis of Traumatic Reticuloperitonitis/Pericarditis?

A

2° to ingest metal objects ( > 4cm) →

FB penetrates the reticulum →

reticuloperitonitis, pericarditis, pleuritis/pneumonia →

FIBROSIS → Congested HF

126
Q

2 BacT associated with Traumatic Reticuloperitonitis/Pericarditis?

A
  • Trueperella pyogenes*
  • Fusobacterium necrophorum*
127
Q

Etiology of Abomasal Ulcers?

(many)

A
  • BVD or Bluetongue (viral)
  • Trauma
  • Lymphoma
  • Displacement/torsion
  • Heavy grain feeding @ paturition→ lactic acidosis
  • Impaction
    • dehydration
  • Arsenic poisoning
  • Dietary change & stress → calves
128
Q

Pathology of Abomasal Dilation & Tympany?

A
  • Young dairy cattle
  • 2° to fermentation of high energy products by gas-producing bacteria in the abomasum
129
Q

Etiology of Abomasal Dilation & Tympany?

A
  • Calves improperly fed milk or milk replacer
  • Inconsistent feeding (once a day only)
  • Inadequate water intake
  • High energy oral electrolytes
130
Q

Lesions of Abomasal Dilation & Tympany?

A
  • Hemorrhage
  • Edema
  • Necrosis
131
Q

Pathology of Displaced Abomasum?

A

2° to Atony (lack of tone) due to high Grain &/o HYPOcalcemia →

gas buildup → displacement

132
Q

Most common form of Displaced Abomasum?

(75% of cases)

A

Left Displaced Abomasusm (LDA)

ventral to the left

133
Q

Which form of Displaced Abomasum can result in rupture?

A

Right Displaced Abomasum (RDA)

dorsally displaced

134
Q

What is the Abomasal Parasite Mnemonic?

What are the parasites?

TQ

A

HOT-C

  • Haemonchus contortus
  • Ostertagia ostertagi
  • Trichistrongylus spp.
  • Coopera spp.
135
Q

List the 2 parasites that damage the Parietal cells of the Abomasum.

A
  • O. ostertagi
  • Trichistrongylus
136
Q

Lesions of Ostertagia ostertagi?

A
  • Maldigestion
  • HYPOproteinemia
  • Nodules →“Morocco leather”
  • Ostertagoisis → mucosal permeability
    • albumin leaks out & pepsinogen leaks in
137
Q

Pathology of Type I Ostertagiasis

A

larvae enter abomasum → two molts in 2½- 3 wks →

early 5th stage larvae mature on abomasal surface

138
Q

Pathology of Type II Ostertagiasis?

A
  • Type I larvae enter abomasum → environmental conditions suck →

enter hypobiotic state (early 4th stage larvae) → can persists for months

  • Hot climates → emerge in Fall
  • Cold climates → emerge in Spring
139
Q

What 4 agents cause Mycotic Abomasitis,

invading vessels & forming “bull’s eye” lesions ?

(often 2° to damage)

A
  • Absidia
  • Aspergillus
  • Mucor
  • Rhizopus
140
Q

Common cause of Abomasal 2° neoplasia?

Lesions?

A
  • BLV → Bovine lymphoma
  • Whitish-pale,tan cellular infiltrate
141
Q

Where are the Intenstinal Epithelial Cells

responsible for absorption of nutrients located?

A

Villi

142
Q

Where are the Intestinal Epithelial Cells that proliferate located?

A

Crypts

143
Q

What do Goblet cells do?
Where are they located?

A
  • secrete mucus
  • crypts & villi
144
Q

What are M Cells responsible for?

A

uptake of Ags from the intestinal lumen

145
Q

List the 4 cells types found in the Lamina Propria of the Intestines.

A
  • Lymphocytes
  • Plasma cells
  • MØs
  • Eosinophils
146
Q

What are the natural defense mechanisms of the Intestines?

A
  • Microflora
  • Motility
  • Rapid epithelial turnover
  • Bile salts
  • IgA
  • IgM
147
Q

List the 3 Developmental Dz’s of the Intestines.

A
  • Atresia → failure to develop
  • Persistent Merkel’s Diverticulum
  • Megacolon
    • Congenital
    • Acquired
148
Q

What is the term for failure of the anus to develop?

A

Atresia ani

149
Q

Term for failure of a segment of the colon to develop?

A

Atresia coli

150
Q

Pathogenesis of Persistent Merkel’s Diverticulum?

TQ

A

remnant of Omphalomesenteic Duct→ blind pouch → impactions/inflammation

151
Q

Pathogenesis of Megacolon?

(Congenital/Acquired)

A
  • Congenital
    • failure of neuroblast migration → myenteric plexus doesn’t develop
      • Overo Lethal White (get when breed Overos to each other)
  • Acquired
    • 2° to Colonic n. damage (trauma)
152
Q

List the 6 types of Intestinal Obstructions.

A
  • Intraluminal
  • Intramural
  • Extramural
  • Intussusception
  • Postmortem Intussusception
  • Adynamic ileus
153
Q

Etiology & Pathogenesis of Intraluminal Intestinal Obstructions

(6)

A

w/in the lumen

  • FB → pressure necrosis
  • Enterolith (fecolith) → struvite & nidus (horses)
  • Trichobezoars
  • Phytobezoars
  • Parasites → roundworms, tapeworms in young, dewormed animals
  • Impaction → usually LI of horses
154
Q

Etiology & pathogenesis of

Intramural Intestinal Obstructions.

TQ

A

w/in intestinal wall

  • Strictures → 2° to intestinal injury
    • ex. S. typhimurium in pigs
  • 1° neoplasms → dogs/cats
  • Inflammation → swelling & fibrosis
  • Ileum muscular HYPERtrophy → incidental finding
155
Q

Etiology of Extramural Intestinal Obstructions.

A
  • Adhesions
  • Lipoma
  • Neoplasia
  • Mesenteric fat necrosis → cattle → “We don’t know why it happens. It just does!”
156
Q

Etiology & Pathogenesis of Intussusception.

A
  • when one intestinal segment invaginates into an adjacent segment
  • 2° to intestinal HYPERmotility or irritation
  • Red-black appearance
157
Q

What does intussusceptum refer to?

A

the trapped segment

158
Q

What does Intussuscipiens refer to?

A

the enveloping portion

159
Q

Lesions of Postmortem Intussusception?

A
  • No swelling
  • No color change
  • Invagination is easily pulled out
160
Q

Etiology & Pathogenesis of Adynamic Ileus (Paralytic Ileus)?

A
  • 2° to intestinal HYPOmotility → creates a fxnal pseudo-obstruction
  • Dilation due to
    • Gas
    • Intestinal content
161
Q

Discuss the differences btwn Internal & External Intestinal Displacement,

which leads to herniation, incarceration & strangulation?

A
  • Internal → through a normal opening into the peritoneal cavity
  • External → through the abdominal wall
162
Q

What cases Postmortem Intestinal Displacement?

Lesions?

A
  • Bacteria → make GAS → distention → displacement
  • Rectal prolaspe
  • Intestinal rupture
163
Q

Etiology of Vascular Dzs of the Intestines

A
  • Verminis arteritis, thrombosis, aneurisms
  • Volvulus & torsion
  • > 6 hrs of Ischemia
  • Reperfusion injury (> 3 hours of ischemia)
164
Q

Which parastite likes to get stuck in the CRANIAL mesenteric arteries & cause verminis arteritis, thrombosis & aneurisms.

TQ

A

Strongylus vulgaris in horses

(4th stage larvae)

165
Q

Pathogenesis of Volvulus & Torsion?

A

obstruction → ischemia → infarction

  • Volvulus → twisting on MESENTERIC AXIS
  • Torsion → rotation of Tubular organ along is LONG AXIS
  • Renosplenic Entrapement of LEFT dorsal/ventral COLON
166
Q

What happens to the gut if 6 hrs of ischemia occurs?

A

complete infarction → necrosis of gut wall

167
Q

What happens to the gut if 3+ hrs. of ischemia occurs?

A

Ischemia → reperfusion → free radical damage to tissues

168
Q

Pathogenesis of Lymphangiectasis?

A
  • Dilation of lacteals → increased lymphocytes & plasma cells
  • Congenital
    • lymphatic malformation
  • Acquired
    • 2° to neoplasms, granulomatous dz, or mesenteric dz
169
Q

Clinical Signs of Lymphangiectasis

A
  • Diarrhea
  • Steattorhea
  • HYPOproteinemia
  • Ascites
170
Q

4 basics mechanisms of Diarrhea?

A
  • Hypersecretion
  • Hypermotility
  • Increased Mucosal Permeability
  • Malabsorption
171
Q

How does E. coli cause Hypersecretion → diarrhea?

A

secretes an ENTEROtoxin → increases Cl- secretion

172
Q

Etiology of Increased Mucosal Permeability → diarrhea?

A
  • increased pore size
  • decreased pore integrity
  • disruption of the osmotic gradient
  • imparied lymphatic drainage
173
Q

Etiology of 2° Malabsorption → diarrhea?

A
  • Maldigestion → pancreas
  • Stasis (Ileus)
  • Mucosal transport abnormailities
  • Necrosis of epithelium→ bacT or virus
174
Q

Which 2 viruses effect the intestinal villi?

A
  • Rotavirus
  • Coronavirus
175
Q

Pathogenesis of Rotavirus Enteritis

A

affects proximal 2/3 of SI

  • enterocyte death→ shortened villi → malabsorption/maldigestion
  • products produced → Incr. Cl- secretion to lumen → H2O follows
  • activation of Enteric NS → Increased peristalsis
  • Blocks Na+/Gluc transport
176
Q

What distinguishes Coronavirus diarrhea from Rotavirus?

A
  • WORSE
  • Affects younger animals
  • More virulent
  • Longer duration of dz.
177
Q

Agent of Calfhood Enteritis?

A

Coronavirus

178
Q

Pathogenesis of Transmissible Gastroenteritis of Swine?

A
  • Coronavirus
  • < 10 d piglets → HIGH morbidity & mortality
  • Older piglets → + fever & survive
  • Affects distal 3/4 of villi → severe loss → permanent loss of surface area
179
Q

Paravovirus affects what?

TQ

A
  • CRYPTS!!!
  • lymphocytes
  • BM
180
Q

Pathogenesis of Enterotoxogenic E. coli

(ETEC)

A
  • EXOtoxin
  • Increased Cl- secretion
  • Secretory diarrhea
  • NO morphological changes
181
Q

Pathogenesis of Enterotoxemic/Verotoxogenic E. coli?

(VTEC)

A
  • ENTEROtoxin
  • hematogenous spread
  • Endothelial damage → fluid loss
  • Edema
182
Q

Pathogenesis of Attaching, Effacing E. coli/ Enteropathogenic E. coli?

(AEEC/EPEC)

A
  • Attached to the brush border
  • Decreased enzyme secretion
  • Altered tight jxn proteins
  • malabsorption, maldigestion & diarrhea
183
Q

Pathogenesis of Salmonellosis

A
  • S. typhimurium
  • Acute
    • ulcers
    • fibro-necrotic lesions
  • Chronic
    • button ulcers
    • thrombosis
184
Q

Pathogenesis of C. perfringens infections?

A
  • commensal
  • 4 Toxins → enterocyte degeneration & necrosis → hemorrhage
  • High mortality
185
Q

How do drugs cause gastric ulcers?

TQ

A

Corticosteroids

  • decrease production of epithelial cells & PGF’s

NSAIDS

  • direct damage to mucosa
  • inhibit PGF
186
Q

Patholgoy of Gastric Ulcers in Swine?

TQ

A

hyperkeratosis & parakeratosis in squamous epithelium surrounding cardia of stomach → ulcers bleed into stomach

Path 2 (6 decks)

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