C16 Gastrointestinal Pathology III Flashcards

1
Q

Congenital anomalies;
* Segmental anomalies of the intestine - how common, how severe, how they arise, characteristics, most common

A
  • Segmental anomalies
    o Common and varying severity (stenosis to complete atresia)
    o Usually due to segmental ischemia in utero causing necrosis
    o Distention oral to the atresia, aboral segment will be small and empty
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2
Q

most common segmental anomaly in horse and cow

A
  • Most commonly atresia coli – spiral colon in Holstein calves, anywhere in foals
    o Genetic, possible association with rectal palpation of cows <42 days gestation?
    o Fail to pass meconium, +/- abdominal distention
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3
Q

atresia ani; how it occurs, what species, associations

A
  • Atresia ani
    o Hereditary in calves and pigs, possible in any species
    o Associated with vitamin A deficiency
    o Failure of perforation of the membrane separating the anus
    ectoderm from hindgut, or rectal atresia
    o Can occur alone or with other malformations (not just GI)
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4
Q
  • Congenital colonic aganglionosis; other name, how it arises, what is it, progression
A
  • Congenital colonic aganglionosis
    o AKA lethal white foal syndrome (overo X overo breeding)
    o Defective neural crest migration means no myenteric plexus
    o No GI motility = stenosis of small colon
    o Distention of oral segments, colic and death within 48 hours
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5
Q

acute GI obstructions usually occur where?chronic?

A
  • Acute usually involve the upper SI, chronic involve the ileum and colon
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6
Q

possible causes of GI obstructions

A

o Blockage by a luminal mass
o Stenosis due to a lesion in the wall (intrinsic)
o Extrinsic compression
o Functional (failure of muscle to contract normally), ex
adynamic ileus due to peritonitis or pain, ischemia

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7
Q

what is a strangulation obstruction? common example? often accompanied by what other issue?

A

o Simultaneous obstruction and ischemia
o Ex. pedunculated lipomas in horses

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8
Q

consequences of GI obstruction, despite cause

A

Regardless of cause, consequences are similar
o Fluid and gas distention and ileus oral to obstruction: may cause pressure ischemia
and eventual perforation, severe distention impairs venous outflow (congestion)
o Aboral gut is collapsed and empty

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9
Q

consequences of upper GI obstructions

A

Upper GI obstructions: vomiting, dehydration
o Metabolic alkalosis (lethal if rupture does not happen first)

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10
Q

consequences of lower GI obstructions

A

Lower GI obstructions: less vomiting, milder metabolic disruptions
o Allow more absorption of fluid proximal to obstruction so distention is slower
o Eventually lead to acidosis, dehydration, catabolism (once animal stops eating)
o Cecum/colon impaction in horses often cause ischemia and rupture
o Pigs with rectal stricture can have marked distention of the entire gut and abdomen

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11
Q

reasons for aquired stenosis

A

o Mural abscess/hematoma, neoplasia, post-ulcerative fibrosis

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12
Q

common foreign bodies, esp in cats

A

Foreign bodies
o Literally anything, obstructive by themselves or nidus for enteroliths
o Linear foreign bodies common in cats

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13
Q

typical presentation of linear foreign body

A

-One end becomes fixed (base of tongue, pylorus)
-The free end stretches out and the gut pleats along it due to peristalsis
-This can ‘saw’ through the mucosa

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14
Q

colon impaction - is it common? features? consequences?

A

o Common, features depend on species (but can be fecal impaction in any species)

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15
Q

colon impaction in dogs - common signs and cause

A

o Voluntary suppression of defecation due to pain (inflammation, neoplasia) o Especially common with prostatic neoplasia

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16
Q

colon impaction in cats - common signs and cause

A

o Megacolon in persistent obstipation (but megacolon often idiopathic)
o Manx: spinal cord problems (‘rumpies’ > ‘stumpies’)

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17
Q

colon impaction in horses - common characterstics, causes, consequences

A

o Cecum/colon, mostly at sites of narrowing (pelvic flexure, transverse, small colon)
o Dehydration, coarse hay, dental disease, and sandy soil predisposes
o Can impact with feed, feces, or sand, all predispose to torsion and displacement
o Sand ingestion can cause impaction or chronic colitis

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18
Q

how can extrinsic compression obstruction arise

A

o Neoplasia, abscesses, peritonitis, adipose necrosis (cows)
o Adhesions (develops gradually as the adhesion forms)
o Pedunculated lipomas (horses), incarceration in hernias

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19
Q

how can a functional obstruction arise? characteristics?

A

o Adynamic (paralytic) ileus common: surgery, peritonitis, postpartum (horses)
o Segmental to diffuse, flaccid and distended intestines

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20
Q

Torsion vs volvulus?
- what is each
- which is more common?

A

Torsion:
* Around long axis of organ
* Less common

Volvulus:
* Around mesenteric axis of organ
* More common

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21
Q

Mesenteric volvulus
- common cause of sporadic death in what animal?
- which direction
- risk factors?
- what other species / age group, and cause?

A

o Common cause of sporadic deaths in pigs
o Usually counterclockwise, highly fermentable diet
and rock ingestion predisposes
o Also common in suckling ruminants – rapid eating leads to gas production or hypermotility

22
Q

Intussusception
- what is it?
- what orientation, usually?
- naming convention?

A

o Telescoping of one segment (intussusceptum) into another (intussuscipiens)
o Usually an oral segment into an aboral one
o Conventionally the intussusceptum is named before the intussuscipiens

23
Q

Intussusception
- age group, cause?
- associated with what?
- causes what? signs?
- limited by what?
- sequelae?
- problems that affect surgical correction?

A

o Often young animals and idiopathic, can be associated with linear foreign body, parasites, enteritis, previous surgery, mural lesions, or agonal
o Usually cause partial to complete obstruction +/- blood in feces
o 3 layers, length limited by degree of tension on the mesentery
o Tension and compression of mesenteric veins cause infarction of intussusceptum
o Adhesions form and prevent reduction, usually leading to necrosis and gangrene

24
Q

Intussusception
- which part is dilated, vs empty and contracted?
- most common spot in dogs?
- ever in lambs, calves?
- associated with what in horses, and location?

A
  • side of ‘inner’ part may be dilated
  • side of ‘outer’ part may be empty and contracted
    <><>
    dogs
  • Most common
  • Usually ileocolic
    <><>
    occasional in labs, calves
    <><>
    in horses:
  • Cecocolic associated with tapeworms, Salmonella, cyathostomes
25
Q

Eventration
- what is it?
- cause?

A
  • Eventration: displacement outside the abdominal cavity
    o Often congenital, ex. schistosomus reflexus, patent umbilicus, diaphragmatic hernia
    o Acquired often related to trauma, can be external, subcutaneous, intramuscular
26
Q

Cecal and colonic dilation, tympany, and torsion
- common in cows? when?
- cattle risk factors? pathogenesis?
- pathogenesis in horse?
- causes what problems?
- sequelae? survivors may get what?

A

o Uncommon in cows, usually within 2 months postpartum
o High concentrate rations predispose (increased VFAs -> atony -> distention -> rotation)
o Similar pathogenesis in horses
o Compresses abdominal organs, venous return, and diaphragm (dyspnea)
o Painful, may die of hypovolemia or acidosis before rupture occurs
o Acidosis causes mucosal ulceration -> endotoxin absorption -> laminitis in survivors

27
Q

why is the horse colon prone to displacements

A
  • The horse colon is only attached near the cecum (prone to displacements)
28
Q

Right dorsal displacement of the horse colon
- what is this? orientation?
- visible on PM when opened in what position
- how does this progress?
- Tx?

A

o Pelvis flexure ends up pointing cranially, leading to obstruction and colic
o Visible when carcass is opened in left lateral
o Often starts with pelvic flexure impaction and often some degree of torsion is present
o Surgical correction required
<><><><>
- Heavy impacted pelvic flexure moves cranioventrally
- This pulls the right colons ventral to the cecum
- Right colons distend with gas, float up and twist

29
Q

Left dorsal displacement (AKA nephrosplenic entrapment) in the horse?
- how does this occur?
- may cause what?

A

o Left colons move dorsally between the spleen and body wall
o They get stuck between the spleen and kidney, and rotate so the ventral colon is dorsal
o Nephrosplenic ligament laxity predisposes but the cause is usually unknown
o May cause impaction, colonic ischemia, or compress splenic vein (congestion)
o Colic signs are intermittent if not impacted

30
Q

Colonic volvulus in the horse
- common cause of what?
- leads to?
- what happens?
- possible consequences?

A

o Common cause of colic, leads to venous infarction
o Right ventral colon rotates 270-720°
o If >360°, causes obstruction, ischemia, enterotoxemia
o May involve part of the cecum
o Can lead to postmortem diaphragmatic rupture due to pressure from trapped gas
and/or ingesta

31
Q

Internal hernia
- common?
- anatomy?

A

o Uncommon, can be through normal or pathological foramina, no hernial sac
o Natural foramen: mostly epiploic foramen SI entrapment in horses
o Omental/mesenteric hernia: entrapment in a tear, usually traumatic and involve SI

32
Q

External hernia
- what is it? anatomy?
- contents?
- sequelae?
- what is incarceration and what may it lead to?

A

o Natural or acquired hernial sac of peritoneum covered by skin and soft tissue
o Hernial ring at the base connects to the abdomen
o Usually contain omentum, intestine, +/- other organs
o Sequelae depend on location and contents, if freely mobile usually no sequelae
o Fixation (incarceration) due to stenosis, adhesions, or distention is serious, may lead
to necrosis, obstruction, perforation, and peritonitis

33
Q

Ventral abdominal wall hernia
- uncommon in what species?
- anatomy?
- spontaeous when?

A

o Uncommon in horses and cattle
o Herniation into subcutis
o Spontaneous in late pregnancy (rule out ruptured prepubic tendon) or traumatic

34
Q

Umbilical hernia
- common?
- cause?
- risk factors?
- species?

A

o Common, congenital, sometimes heritable (Holsteins)
o Patency of the umbilical ring, omphalitis predisposes
o The most common congenital defect in calves but occurs in all species

35
Q

Perineal hernia
- moslty what species, signalment? concurrent dz?
- cause?
- anatomy? possible issue?

A

o Mostly old male dogs with prostatic enlargement and obstipation
o Weakening of perineal muscles combined with pressure from straining
o Mostly unilateral but can be bilateral
o Usually only contain fat but sometimes bladder is involved and may obstruct

36
Q

Diaphragmatic hernia
- common? cause?
- anatomy? rare issue?

A

o Common, usually acquired but sometimes congenital
o Liver and SI most likely to herniate, strangulation is rare

37
Q

Inguinal hernia
- inguinal ring anatomy?
- can progress to what in males?
- possibility in bitches?
- 2 main types?
> how they arise
> how common
> how serious, sequelae
> signalment

A

o Inguinal ring is patent in intact males of all species and in the bitch
o In males, herniation can progress to scrotal hernia (leading to testicular degeneration,
castration complications…)
o In bitches, uterine herniation and strangulation is possible
o Two main types…
<><><><>
* Direct inguinal hernia
o Herniation through a tear in the peritoneum
o Less common and life-threatening (often cause skin necrosis, become fixed by adhesions and strangulate)
o Most frequent in foals (due to pressure of parturition)
<><>
* Indirect inguinal hernia
o More common, contents are contained in the tunica vaginalis
o Congenital in young animals (more common in male dogs)
o Acquired in adults but often idiopathic (more common in bitches)

38
Q

inchemia and infarction of the GI tract are especially common in what species?

A

horses

39
Q

if we have intestinal ischemia and infarction, what is the progression of damage?

A

tips of villi:
- ischemic lesions in 5-10 minutes
<><>
villi:
- Complete epithelial loss and hemorrhage in 1-3 hours
<><>
- Colon less sensitive
> Mild damage 1 hour
> Necrosis 3-4 hours
> Can cause chronic diarrhea and cachexia
<><>
crypts:
- Begin disintegrating in 2-4 hours
- Completely gone in 4-5 hours
<><>
- Tunica muscularis survives for 6-7 hours, contractility permanently lost if ischemic >4-6 hours

40
Q

Ischemia and infarction
- intestinal sample consideration for diagnostics
> timing

A

MUST FIX QUICKLY FOR DIAGNOSTICS!

41
Q

Ischemia and infarction
- when is reperfusion injury possible?
> resembles what?
> less likely in what species?

A
  • Reperfusion injury is possible if necrosis is not complete and ischemia is transient
    o Resembles hypoxic injury, less likely in pigs and horses
42
Q

Ischemia and infarction
* Sequelae depend on?
- preservation vs loss of crypts?
- complete ischemia?

A
  • Sequelae depend on duration and severity of ischemia
    o Preservation of crypts: regenerates in 1-2 weeks (except necrotic muscularis mucosa),
    inflammation persists until the epithelium is restored
    o Loss of crypts: ulceration and surrounding inflammation, healing by granulation followed by re-epithelialization from adjacent surviving mucosa
    > Extensive ischemic ulcers covering large areas don’t heal (often have a fibrinonecrotic
    covering, act as portals for bacteria)
    > In survivors, chronic ulcers may lead to stricture
    o Complete ischemia: full-thickness necrosis (green-black and friable), proliferation of
    anaerobes (produce toxins and gas), gangrene, endotoxemia
43
Q

The most common cause of GI ischemia?
- why?
- causes?
- appearance?
- sequelae?

A
  • Venous infarction
    o The most common cause of GI ischemia (thin-walled veins compress more easily)
    o Incarcerated hernias, pedunculated masses, torsion, volvulus, intussusception
    o Displacements can progress to infarction (common cause of colic in horses)
    <><><><>
  • Edema, congestion, hemorrhage (red-black)
  • Sharp demarcation
  • Bloody, gaseous contents
  • Progressive gangrene turns green-black
  • Leads to septic peritonitis regardless of whether it ruptures
44
Q

Arterial thromboembolism in hose
- any other species?
- associated with?
- anatomical location
- appearance?

A

o Rare other than horses, mostly associated with emboli from secondarily infected thrombi (ex. S. vulgaris)
o Most common at watershed regions with limited collateral circulation
> rectum, pelvic flexure, tip of cecum
o Necrotic areas are grey-brown if there is no reperfusion but resemble venous infarction if reperfused (distribution will be different)

45
Q

Shock gut
- mostly what species?
- pathogenesis?
- leads to?
- appearance?

A

o Mostly in dogs, hypoxia due to reflex vasoconstriction and capillary dilation
o Leads to pooling of blood, hypotension, and microthrombi
o Congested SI mucosa and hemorrhagic contents

46
Q

Reduced perfusion – NSAIDs
- species?
- how do we get mucosal ischemia?
- range of possible problems?
- in horses, anatomic location
<><><>
- what if dehydrated?

A

o Causes GI ulceration in horses (even at therapeutic levels) and dogs
o Microvascular damage and/or vasoconstriction -> mucosal ischemia
o Ranges from congestion and edema to erosion and ulceration
o In horses, mostly right dorsal colon
<><><>
Renal papillary necrosis – common if dehydrated

47
Q

Malassimilation and protein loss
- species?
- causes?
- lead to?
- requirement for diagnosis and prognosis?

A
  • Mostly seen in dogs but also diagnosed in horses and cats
    o Usually idiopathic but many possible causes (neoplasia, amyloid, lymphangiectasia,
    some infectious agents)
    o All lead to chronic diarrhea, weight loss, and hypoproteinemia
    o Biopsy required to diagnose and give a prognosis
48
Q

Amyloidosis
- where is it deposited? visible grossly?
- problems caused?

A

o Deposited in GI tract in systemic amyloidosis, usually not visible grossly
o Impairs fluid uptake and/or increases
capillary permeability, leading to protein loss

49
Q

Lymphangiectasia in dogs
- usual cause?
- clinical signs due to?
- appearance?
- sequelae?
<><>
- appearance, gross and histo

A

o Usually due to acquired lymphatic obstruction (inflammation, neoplasia)
o Often no cause can be identified, clinical signs due to malabsorption
o Transmural lymphatic and lacteal dilation +/- lipid laden macrophages
o Hypoalbuminemia leads to ascites and peripheral edema
<><><><>
- Thickened, edematous mucosa with white spots
- Prominent serosal lymphatics
- Dilated crypts with inflammatory cells (‘crypt abscess’)

50
Q

Idiopathic inflammatory bowel disease (IBD)
- species?
- is it a specific disease?
- why can it be hard to confirm?
- hard to differentiate from what other dz?

A

o Mostly dogs and cats, sometimes horses and cows
o Clinical syndrome rather than a specific disease, likely multifactorial
o Diagnosis of exclusion but hard to confirm due to overlap between pathology and
normal variation, lesions often mild compared to clinical signs
o Inflammation can be hard to differentiate from early lymphoma

51
Q

Eosinophilic enteritis in cats
- common? may be part of what syndrome? age?
- what happens?
- signs?

A

o Rare, may be part of systemic hypereosinophilic syndrome (middle aged-old)
o Differentiated eosinophils infiltrate many tissues (SI, liver, spleen, LNs - enlarge)
o Severe diarrhea +/- blood, vomiting, weight loss, peripheral eosinophilia

52
Q

Eosinophilic enteritis in horses
- may be part of what disease?
- signs?
- lesions
- cause?

A

o May be part of multisystemic epitheliotropic syndrome, chronic disease
o Weight loss and diarrhea +/- pancreatitis, dermatitis, no peripheral eosinophilia
o Thickening of GI mucosa anywhere in the tract
o Cause unknown, sometimes GI lesions occur alone