Test 2: 11 upper Flashcards
List the 4 BASIC MECHANISMS of DIARRHEA
1) Hypersecretion of structurally intact mucosa
2) Malabsorption/maldigestion
Mircrovillus Damage
Absorptive enterocyte necrosis/loss
Crypt cell necrosis/loss
Crypt hyperplasia
3) Exudation/effusion
lam propria/vascular necrosis
lam propria infiltration
4) Dysmotility
Suddenly develop diarrhea (yellow, watery to paste-like- no blood or melena) in calf. PE and autopsy findings, what’s the primary mechanism of diarrhea in this case?
Hypersecretion of a structurally intact epithelium
ETEC (enterotoxigenic E coli)
(see the lovely microvilli in the EM photo only “touched” by the insidious fimbriae that stir up so much dysfunction?!).
How quickly would you expect the diarrhea to resolve once ETEC has been eliminated by appropriate antimicrobial therapy?
Because there’s no structural damage- once the ETEC is gone and not inducing secretion- the diarrhea should resolve pretty instantly.
Does withdrawing food have an effect on the recovery time when infected with ETEC?
No- because the diarrhea is purely SECRETORY. All brush border enzymes are working as are the chylomicrons/lacteals to absorb lipids.
Autopsy reveals thin-walled, dilated small intestinal loops filled with yellow watery contents with few flecks of tan debris
histo: -Effacement of microvilli by numerous gram negative bacilli -Mild villus blunting with villus epithelial sloughing
Based on clinical and pathologic findings, what is the most likely pathogen?
Attaching & Effacing E. coli (AEEC)
or crypto
What is the primary mechanism of diarrhea with AEEC?
Microvillus damage/destruction → Malabsorption/Maldigestion
How long would it take these rabbits to recover from their diarrhea if the pathogen was eliminated by appropriate antimicrobial therapy when infected with AEEC?
Fairly quickly. The epithelium can turn over within a few days so as long as the ones with the “squashed” microvilli are replaced by new ones up the pipline…bunnies are good
Provide the name of a ZOONOTIC protozoan pathogen that causes similar microvillus damage to AEEC.
Cryptosporidium- very common in our neonatal dairy calves
10-year-old Welsh pony with acute onset of red-brown pipe-stream diarrhea.
The CBC reveals severe leukopenia. She has an increased PCV and Total solids
Provide a morphologic diagnosis for the gross lesions in the large colon.
SALTD
Severe acute diffuse necroulcerative and hemorrhagic colitis with diphtheritic membranes
Provide the mechanism of diarrhea that takes into account the capillary fibrin thrombi and red brown fluid within the large colon.
Exudative/Effusive from pathogen invasion of lamina propria → capillary fibrin thrombi → vascular necrosis & ischemic mucosal necrosis → intraluminal hemorrhage & protein leakage
Salmonella or clostridium
Based on the clinical and pathologic findings, name the pathogen you most suspect. leads to Exudative/Effusive diarrhea with hemorrhage and protein leakage
Salmonella (remember Salmonella in horses also causes leukopenia).
Name two other common equine pathogens that could produce similar lesions (-hint- they produce exotoxins).
Clostridium perfringens & C. difficile. Typically, C. perf & C. diff produce more hemorrhage- but lesions can look similar to Salmonella (see laboratory specimen)
Speculate on how this pony likely acquired salmonella
Unfortunately, this is a common scenario we see at NBC with farms that rescue animals from auctions. The horse probably acquired the infection from the calf. Salmonella is more common in bovids and can “shed” the organisms when immunosuppressed/stressed. Horses are MUCH more sensitive to Salmonella and acquire serious infections even with relatively small doses of bacteria. The clinical signs of the calf also point to this being the most likely scenario.
red to purple, dilated, thin-walled small intestinal loops that have regularly spaced, well -demarcated, 2-3mm diameter depressed oval foci within the wall (“Punched-out Peyers patches)
Based on clinical and pathologic findings, which pathogen do you most suspect?
Feline Panleukopenia Virus
What is the primary mechanism of diarrhea in feline panleukopenia?
Crypt cell necrosis → malabsorption/maldigestion
is feline panleukopenia contagious to cats and humans
cats- yes
humans- NOT zoonotic
Based on the clinical and autopsy findings, provide the name of the pathogen (genus & species/subspecies) you most likely suspect.
cow
Mycobacterium avium subsp. paratuberculosis (aka M. paratuberculosis)- Johne’s Disease
Why does Johne’s Disease stain positive with acid fast?
Mycolic acid within the cell wall
Mycobacterium avium subsp. paratuberculosis
What is the mechanism of diarrhea that resulted in the hypoproteinemia cause by Johne’s disease
Exudation/Effusion by increasing hydrostatic pressure as well as via epithelial erosions
What is the secondary mechanism of diarrhea for Johne’s disease
Malabsorption/Maldigestion via protein effusion/exudation → osmotic drawl of fluid into the lumen
Exudation/Effusion by increasing hydrostatic pressure as well as via epithelial erosions
Is Johne’s contagious to other members of the herd?
Yes- via fecal-oral route. Not every cow in the herd develops clinical disease and oftentimes there are “subclinical” shedders of bacteria. The inflammation takes a while to “build up” within intestines and so clinical disease (often beginning with emaciation well before diarrhea develops) is not seen until animals are >2 years-old.
What is the name of these pathogens (provide likely genus & species)?
Toxocara canis
What is the primary mechanism of diarrhea in this case
Dysmotility
Is Toxocara canis zoonotic? If so, how is it spread and what disease(s) is/are seen in humans?
Yes! Fecal-oral route of food/environment/paratenic hosts contaminated with embryonated ova larvae penetrate intestinal wall disseminated to organs associated inflammation Visceral or ocular larval migrans.
Abdominal ultrasound reveals a target-like (“bullseye”) structure surrounded by hypomotile intestines
based on clinical findings and the gross lesion, what is your diagnosis
INTUSSUSCEPTION
Briefly list the steps in the pathogenesis of developing the septic effusion after an intussusception
Intestinal dysmotility → telescoping of proximal segment of intestine into distal segment → compression of collapsible veins/lymphatics in proximal segment → passive congestion with edema → ischemic necrosis → bacterial translocation through devitalized bowel → septic peritonitis with effusion
What evidence to you have that the intestinal hypomotility seen on US represents functional ileus?
Septic peritonitis is one cause of functional ileus (ie HYPOmotile intestines in other segments than the one with the intussusception).
What are the TOP 3 differential diagnoses for these lesions?
- Fibrogingival Hyperplasia- benign “reactive” proliferation; Boxer breed predilection
- Peripheral Odontogenic Fibroma (POF)- benign neoplastic proliferation of odontogenic mesenchyme (including fibrous stroma resembling periodontal ligament as well as mineralized matrix, ie- bone/cementum/dentin) with scattered ameloblastic epithelial “rests”; de novo lesions can arise post-operatively
- Acanthomatous Ameloblastoma (AA)- locally invasive/aggressive neoplastic proliferation of ameloblastic epithelium that is difficult to surgically excise post-operative recurrence and progression is common but does not metastasize
Scattered about the periphery are small island-like aggregates of ameloblastic epithelium (cell rests of Malassez).
Based on the histologic findings, what is your diagnosis?
Peripheral Odontogenic Fibroma (POF)
What is its biologic behavior of POF
benign, non-invasive (although can displace adjacent teeth)
benign neoplastic proliferation of odontogenic mesenchyme (including fibrous stroma resembling periodontal ligament as well as mineralized matrix, ie- bone/cementum/dentin) with scattered ameloblastic epithelial “rests”; de novo lesions can arise post-operatively
If a biopsy report of a mass in the K9 oral cavity describes a population of pleomorphic round to spindle cells containing brown-black pigment granules, what would be your top Ddx and associated prognosis?
In the K9 oral cavity, this is compatible with malignant melanoma, which is a highly aggressive, invasive neoplasm with poor prognosis due to rapid widespread metastasis (lungs, liver, oth viscera).
At 6-months of age, this Great Dane puppy has multifocal pink-tan, soft-to-firm verrucous masses arising within the mouth and on the lips. By 1-year of age, these lesions have disappeared without any treatment.
Q9a: Based on the clinical information and gross features, what’s your diagnosis.
viral papilloma
What is the general mechanism by which papilloma lesions disappear?
Papilloma viral infection → benign neoplastic proliferation of squamous epithelium→ T cell-mediated immune response→ spontaneous regression
You identify this sublingual exophytic lesion in a 15-year-old cat with a history or ptyalism, halitosis and recent anorexia. Histology reveals cords & nests of epithelium with varying keratinization, intercellular desmosomes and a high mitotic index. Some islands of neoplastic cells have central “keratin pearls.”
what is your diagnosis?
Sublingual Squamous Cell Carcinoma
what is the biological behavior of Sublingual Squamous Cell Carcinoma
Malignant- locally aggressive an invasive neoplasm with metastasis to regional lymph nodes & other organs (eg lung, carcinomatosis, etc).
old cat with diffuse expansion and partial effacement of mucosal glands by a population of atypical round cells with large round nuclei, scant basophilic cytoplasm and frequent atypical mitoses.
Based on the clinical and autopsy findings, what is your diagnosis?
Diffuse alimentary lymphoma
Diffuse alimentary lymphoma in a cat is similar to — in cows
Effusion/exudation (similar to Johne’s- but intestinal infiltrates are neoplastic lymphocytes not epithelioid macs/multinucleated giant cells)
what is the primary mechanism of diarrhea of diffuse alimentary lymphoma
Effusion/exudation (similar to Johne’s- but intestinal infiltrates are neoplastic lymphocytes not epithelioid macs/multinucleated giant cells)
What is the secondary mechanism of diarrhea in diffuse alimentary lymphoma
Malabsorption/Maldigestion (similar to Johne’s again!)
In addition to the diffuse form, how else can alimentary lymphoma present in the intestinal tract?
Nodular form- single or multiple masses that expand the wall +/- compress the intestinal lumen diameter → intestinal obstruction
What is the neoplasm you most suspect based on autopsy findings.
Adenocarcinoma with carcinomastosis
Why did the dog have tenesmus?
Adenocarcioma with mural invasion → desmoplasia → stricture & partial intraluminal obstruction
the feeling that you need to pass stools, even though your bowels are already empty
A common vesicular disease in cats is
feline calicivirus
Vesicular diseases in large animals are reportable to investigate potential Foot and Mouth Disease Virus, a disease that has — morbidity and — mortality with severe economic impacts on agriculture.
high
low
If you identify vesicular lesions in the oral cavity of a horse, Foot and Mouth Disease —- be considered as a differential diagnosis. Mechanical disruption of vesicles — result in painful erosions and ulcers.
should not
often
A benign neoplasm that often forms multiple exophytic, verrucous nodules comprising squamous epithelium arising within the mouth or lips of young dogs that often undergoes spontaneous regression is:
Viral Papillomas
A non-neoplastic “reactive” proliferation associated with periodontitis that forms single to multiple firm raised nodules arising from the gingiva that histologically comprising hyperplastic squamous epithelium and edematous proliferative fibrovascular tissue within the submucosa is:
Fibrogingival Hyperplasia
A benign odontogenic neoplasm (periodontal ligament origin) forming single to multiple raised nodules that histologically comprise spindle shaped mesenchyme with dentinous/osseous/cementum islands and scattered islands of bland odontogenic epithelium (ie, rests of Malassez):
Peripheral Odontogenic Fibroma (POF)
A raised, firm-to-hard, locally invasive and aggressive mass comprised of ameloblasts (primitive enamel epithelium) that invades bone, can recur post-operatively, but does not metastasize is:
Acantomatous Ameloblastoma (AA)
A brown-black pigmented firm raised mass arising within the oral cavity that is locally invasive and aggressive with frequent, rapid, widespread metastasis is
Malignant Melanom
One important differential diagnosis for a horse with a malodorous unilateral mucopurulent nasal discharge is — arising from —
Sinusitis
Tooth Root Abscess
in a neonate with dyspnea and/or signs of pneumonia, you should examine the oral cavity for potential
Palatoschisis
In dogs with aspiration pneumonia and history of chronic regurgitation, you should rule out an acquired stricture caused by all EXCEPT
Cardiac ventricular septal defect
In cows and other ruminants, Rumen Acidosis Syndrome is caused by — diets that result in rumen dysbiosis through a fermentation process that creates — volatile fatty acids.
Carbohydrate-rich
excessive
excessive volatile fatty acids cause a — in rumen pH and —protozoa/gram negative bacteria with — acid-producing gram positive bacteria.
drop
decrease
increased
Rumen acidosis often produces secondary bloat (ie, rumen tympany) from ‘stasis’ as well as through an osmotic drawl of fluid into the lumen. Rumen acidosis can lead to rumen ulcers as well as lameness due to —
laminitis
Bacterial emboli arising from rumen ulcers can cause — abscesses, pulmonary — and tricuspid valve —
liver
thromboemboli
vegetative endocarditis
Entire intestine inflammation
Enterocolitis
Cecum inflammation
Typhlitis
mouth inflammation
Stomatitis
Lips inflammation
Cheilitis
tongue inflammation
Glossitis
COX enzyme inhibition–> DECREASED prostaglandin
NSAIDS
Epi-/Norepinephrine mediated VASOCONSTRICTION
stress
Local invasion of neoplastic cells with desmoplasia–> disruption of glands and microvasculature
Adenocarcinoma
Secretion of excess circulating histamine–> increased Parietal Cell secretion
Mast Cell Tumor
Lamina propria invasion–> Capillary fibrin thrombi–> Mucosal necrosis–> Effusion/Exudation
Salmonella
Hypersecretion from a structurally intact epithelium
Enterotoxigenic E. coli (ETEC
Dysmotility from intraluminal impaction
Ascarids
Microvillus damage from zoonotic protozoa–> Malabsorption/Maldigestion
Cryptosporidium
Diffuse granulomatous enteritis–> Effusion/Exudation
Johne’s (Mycobacterium avium paratuberculosis)
Crypt Cell Necrosis–> Delayed repopulation of villus enterocytes–> Malabsorption/Maldigestion
Canine/Feline Parvovirus
Villus enterocyte necrosis–> Replacement by immature enterocytes–> malabsorption maldigestion
Coronaviruses
Microvillus damage from bacteria–> Malabsorption/Maldigestion
Attaching & Effacing E. coli (AEEC)
The most common neoplasm that causes segmental to multisegmental diffuse round cell infiltrates within the gastrointestinal tract of cats, horses, cows, pigs and dogs is:
Lymphoma
All are considered PHYSICAL OBSTRUCTIONS of the gastrointestinal tract except [1] which is considered a FUNCTIONAL OBSTRUCTION.
Linear Foreign Body
Gastric Dilation & Volvulus (GDV)
Ileus
Large Colon Volvulus
Intussusception
Ileus
