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Smith LA Medicine > Ch 32 > Flashcards

Ch 32 Flashcards

1
Q

H: where on rectal palpation would you locate the mesenteric root of the colon, and what would it feel like?

A

Crl to mesenteric artery, mildly taut band of tissue running from dorsal midline, ventrally

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2
Q

What are the 7 locations of focus in an equine abdominal FLASH ultrasound?

A

Ventral, gastric, splenorenal, right middle third abdomen, duodenal, left middle third, thoracic

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3
Q

Roughly where should the stomach be located on AUS?

A

Left, ICS ~9-13. Past ICS 14 is distended

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4
Q

How thick should the stomach, colon, and SI wall be on AUS?

A

7 mm, 4mm, 3mm

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5
Q

Where would you scan to assess for colon volvulus, and what finding would indicate such?

A

Ventral by the xiphoid colon wall 9+mm , nonsacculated colon replacing sacculated ventrally, or distended mesenteric vessels indicates possible volvulus

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6
Q

What ultrasonographic finding would support dx of colon impaction?

A

Flattening of sacculations, hyperechoic border casts strong acoustic shadow at the mucosal surface. Ventrally. Gas may prevent dx

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7
Q

Where would you locate the small colon on US?

A

Left paralumbar fossa, medial or ventral to spleen

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8
Q

What is normal inner diameter of the small intestine?

A

3 mm

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9
Q

What are the main ddx for SI nonstrangulating lesion?

A

Ileal impaction, adhesions, mural hematoma, chronic infiltrative disease

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10
Q

Where would you locate normal liver on AUS?

A

Right, ICS 6-14 between diaphragm and colon

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11
Q

Where can you locate the duodenum on AUS?

A

Right: at the caudal pole of the kidney, and middle abdomen between liver and right dorsal colon

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12
Q

Where would you locate the right dorsal colon on AUS?

A

Right, ICS 10-12, ventral to the liver

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13
Q

How does esophageal rupture appear on radiography?

A

Gas bubbles dorsal to the trachea

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14
Q

What is the most reasonable way to test fecal samples for rotavirus?

A

Screen with agglutination test, repeat test any positives with ELISA or PCR

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15
Q

Sensation to the mouth, cheeks, and lateral tongue is supplied by which nerve and branches?

A

Maxillary and mandibular branches of the trigeminal nerve (CN V)

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16
Q

Motor and sensation innervation are provided to the tongue by which nerves?

A

Motor: Hypoglossal (CN XII)
Sensation: lingual and glossopharyngeal (CN IX)

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17
Q

Which muscles of the jaw contribute to closure?

A

Masseter and temporalis

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18
Q

Which equine teeth have infundibulae?

A

Incisors and UPPER cheek teeth

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19
Q

How much endotoxin is needed to induce endotoxemia in horses?

A

< 1 ug in the blood

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20
Q

Which cytokine is considered the link between innate and acquired immunity?

A

IFN y (gamma)

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21
Q

How do bradykinin and platelet activating factor influence vascular permeability?

A

Increase permeability by promoting active retraction of endothelial cells

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22
Q

What is the predominant cause of death due to severe sepsis and septic shock?

A

Myocardial depression (secondary to effects of inflammatory mediators and apoptosis of cardiomyocytes)

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23
Q

Tell me major points about Polymixin B and its use in a sepsis context

A

-Broad spectrum cyclic peptide antibiotic
-Potentially fatal complications include nephrotoxicity and respiratory paralysis
-Can safely give 2-3 times daily at 6000 U/kg

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24
Q

Which of these is not an NSAID: dipyrone/metamizole, flunixin, aspirin, phenylbutazone, firocoxib?

A

Dipyrone/metamizole

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25
Q

What are ddx for increased peritoneal fluid in ruminants?

A

Late pregnancy, congestive heart failure, caudal vena cava thrombosis, peritonitis, impaired mesenteric blood flow and transudation, ruptured bladder (looks like it)

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26
Q

How do you locate and recognize the reticulum on ultrasound?

A

In L cranioventral abdomen, between xyphoid process and cranial to the let mammary vein, has periodic biphasic movements, and the musculophrenic vein between the diaphragm and abdo wall. Smooth walled

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27
Q

How does hardware disease appear on ultrasound?

A

Heterogenic fluid accumulates between the abdo and reticular walls, and the reticulum has abnormal motility with < 1 contraction/minute. Also increased wall thickness and deformation, and abscessation

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28
Q

Where can you visualize the omasum ?

A

-At the visceral border of the liver

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29
Q

Which part of the ruminant stomach chambers has a thick, multilayered crescent-shaped wall, just oral to the cranial duodenum?

A

The pylorus!

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30
Q

How would you identify a displaced abomasum on ultrasound? Volvulus?

A

The pylorus is medial to the r mammary vein or close to the ventral midline. The distended abomansum may block the liver too. The pylorus is more cranially displaced in the case of volvulus

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31
Q

Which is the most sensitive way to test for F. hepatica or Dicrocoelia dendriticum infection?

A

Percutaneous puncture of the gallbladder for eggs

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32
Q

How does hepatic lipidosis appear on ultrasound?

A

Decreased image contrast, poor imaging of vascular structures, attenuated liver, increased beam impedance

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33
Q

How is parietal pain communicated (hint, via which nerves)?

A

Pain sensation travels through the peripheral spinal nerves and localizes over the affected area

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34
Q

How is visceral pain transmitted?

A

Via sensory fibers in the autonomic nerves, and is diffuse and difficult to localize

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35
Q

How do ruminants with parietal pain present?

A

-No colic signs
-Splinting abdomen, lack of withers test response or grunting
-Reluctance to move
-Tonic reflex contractions of the abdominal muscles

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36
Q

Which ddx for acute abdomen require emergency surgery?

A

-Abomasal volvulus
-Abomasal bloat in neonates
-Mesentery root torsion
-Intestinal volvulus/strangulation
-Cecal volvulus/torsion

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37
Q

Which DDx for acute abdomen require only medical management?

A

-paralytic ileus
-Enteritis
-enterotoxemia
-acute pyelonephritis
-Urinary tract dz
-Acute liver disease
-Cholelithiasis
-Pleuropneumonia

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38
Q

For which ddx of acute abdomen can you institute medical management before surgery?

A

-Intestinal foreigh body or obstruction
-intussusception
-Intestinal adhesions
-Atresia coli
-hernia
-urolithiasis
-ruptured bladder
-uterine torsion

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39
Q

For which ddx of acute abdomen can medical management be attempted to achieve resolution before considering surgery?

A

Acute traumatic reticulits
-cecal dilation
-abomasal ulcer
-hemorrhagic bowel syndrome
-peritonitis
-fat necrosis
-reticuloperitonitis

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40
Q

Where would you observe distension in the following disorders? SI disorders, cecal and colonic, abomasal, rumen, ?

A

SI: bilateral, ventral
Cecal and colonic: right paralumbar fossa
Abomasal volvulus: caudal to last righ in R paralumbar fossa
Rumen: upper left abdomen, or papple shape if chronic indigestion

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41
Q

describe the R sided ‘pings’ for the following: abomasal volvulus or r displacement, cecal dilation/volvulus, peritonitis, normal, duodenal gas?

A

Abomasum: 13-9th rib, high pitch
Cecal: R paralumbar fossa and caudal quadrant to hip
Peritonitis: bilateral low pitch ping in upper paralumbar fossa
Normal: monotone 15-20 cm under the last rib is normal spiral colon
Duodenum: changing pitch ping

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42
Q

Describe the L sided pings associated with L abomasal displacement, ruminal collapse, and pneumopetioneum

A

L abo displacement: Dorsally, 8-13th rib
Ruminal collapse and penumopertoneum: dorsally, L paralumbar fossa, cranially to 11th rib

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43
Q

Metabolic alkalosis is associated with which abdominal disorders of ruminants?

A

abomasal volvulus, intussusception, cecal disorder, abo ulcers, peritonitis, renal dz, reticuloperitonitis
Bonus: often see hypoK+ and hypoCl-

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44
Q

Metabolic acidosis is associated with which diseases of ruminants?

A

severe D+, enteritis, SI strangulation or obstruction, urinary tract disease

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45
Q

What is the max flow rate of fluids through a 14 g IVC in an adult cow?

A

15-20 ml/kg/h

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46
Q

What fluid rate is advised to resuscitate critically ill neonatal ruminants?

A

80-90 ml/kg bwt/hr

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47
Q

You have a dehydrated but not critically ill ruminant; over what amount of time should you replenish fluids?

A

correct deficits over 2-8 hours

48
Q

What are the max fluid rates for resuscitation in adult ruminants and dehydrated calves?

A

Adult: 40 ml/kg/hour
Calf: 80 ml/kg/hour
*crystalloids

49
Q

Describe briefly how to administer hypertonic crystalloids IV to resuscitate ruminants?

A

give 4-5 ml/kg over 8-10 minutes, then offer fresh water or give isotonic fluids IV. Avoid a rate of hypertonic solution of over 1 ml/kg/min can induce potentially fatal hypotension though

50
Q

What are potentially harmful effects of magnesium hydroxide in ruminants with suspected GI obstruction?

A

decreased potassium absorption, metab alkalosis, sedation, increased ruminal pH, and decreased ruminal microbial activity

51
Q

Which prokinetic is the best choice in goats? Is this the case in cattle too?

A

Goats: use metoclopramide at 0.5 mg/kg IV or IM to increase myoelectric activity of the duodenum. But it’s ineffective alone when used in cattle and sheep. Cattle and sheep respond more to bethanecol or erythromycin

52
Q

What are the ddx of secondary indigestion in ruminants? (2ary to systemic illness)

A

Abomasal reflux
2ary microflora inactivity or motor inactivity

53
Q

What are the ddx of primary indigestion motor disorders in ruminants?

A

Traumatic reticuloperitonitis
Bloat: frothy, free gas
Reticulitis/rumenitis
Ruminal parakeratosis
Vagal indigestion
Cardia obstruction
reticuloomasal orifice obstruction
diaphragmatic hernia

54
Q

What are the ddx of reticuloruminal fermentative disorders?

A

Rumen flora inactivity
Simple indigestion
Acute or subacute ruminal lactic acidosis
Rumen alkalosis
Ingesta putrefaction

55
Q

Briefly, describe the normal number and nature of ruminal contractions

A

3 contractions in 2 minutes, with one associated with gas eructation

56
Q

Where can you auscultate reticuluar contractions?

A

ICS 7, at the level of the CCJ can head tinkling sound

57
Q

How long does it take for ingesta to pass through the adult bovine GI tract?

A

1.5-4 days

58
Q

How long should fibers in cattle manure be, and what does elongated fibers indicate?

A

Should be 0.5 cm. Fibers 1-2 cm indicate TRP, tooth disease, obstructive indigestion, or poor quality roughage

59
Q

How can you differentiate increased vagal nerve tone from primary cardiac conduction disturbance in cattle with bradycardia (40-60 bpm)?

A

Give 30 mg atropine SC. Not super useful though. Also keep in mind that postfasting heart rates may drop below 50 bpm

60
Q

What are your differentials for vomiting in ruminants?

A

diaphragmatic herniation of the reticulum, actinobacillosis inflaming the reticulorumen, obstructive indigestion, reticuloomasal orifice obstruction, azalea or rhododendron or sneezeweed toxicity, or organophosphate toxicity

61
Q

What are the causes of decreased motor discharges in the ruminant GI tract (concerning primary cycle activity)?

A

Decreased excitatory input to gastric centers
Increased inhibitory input to the gastric centers
Depression of the gastric centers
Defective vagal transmission of motor impulses
Other…

62
Q

What are the 3 most important excitatory inputs to the gastric centers?

A
  1. Low threshold tension receptors in the reticulum
  2. Buccal receptors in the reticulum
  3. Acid receptors in the abomasum
63
Q

What are the four most important inhibitory inputs to the gastric center?

A
  1. High threshold tension receptors in the reticulum and cranial dorsal ruminal sac
  2. Tension receptors in the abomasum
  3. Epithelial receptors that detect high [ ] of nondissociated VFAs in the rumen
  4. Pain from any site
64
Q

What is the effect on motility when poorly-digestible roughage accumulates in the forestomach?

A

The musculature is stretched beyond its ability to contract forcefully, so the high-tension receptors adapt and instead of inhibiting motility, weak and ineffective motility is allowed to occur. Then the rumen is weak and unable to adequately release gas

65
Q

What is the shortest period in which ruminal papillae can grow or regress in response to a feeding change?

A

Three weeks

66
Q

How do the proportions of VFAs in the rumen influence the development of ruminal paraeratosis?

A

High energy diets with high proportions of propionate and butyrate, and reduced acetate, lead to parakeratosis and more acidic ruminal fluid pH

67
Q

What are the 4 types of vagal indigestion?

A
  1. failure of eructation
  2. failure of rumen outflow
  3. failure of abomasal motility and outflow
  4. partial pyloric obstruction
68
Q

What are the types of abomasal ulcers?

A
  1. Nonperforating
  2. Nonperforating with severe bleeding
  3. Perforating with local peritonitis
  4. Perforating with diffuse peritonitis
69
Q

How are nonperforating abomasal ulcers subtyped?

A

1a Erosion with minimal defects
1b Deeper erosions with focal mucosal hemorrhage
1c Craters coated in fibrin, center depression
1d Radial wrinkles with central point

70
Q

How would you expect the PCV to differ between cattle with abomasal ulcers vs intussusception vs hemorrhagic bowel syndrome?

A

Ulcers: decreased
HBS: normal or increased
Intussusception: increased

71
Q

For which disease should cattle over 5 years old with bleeding abomasal ulcers be tested?

A

Bovine leukosis virus

72
Q

When is blood transfusion recommended for cattle with abomasal bleeding ulcers? Briefly, what is important to remember when transfusing cattle?

A

-If PCV is 14% or below, transfuse
-Usually 4-6L is enough
-No crossmatching needed unless repeated over more than 3 days

73
Q

Which medications can assist closing the esophageal groove (to deposit medications into the abomasum)?

A

-Vasopressin
-Copper sulfate
-10% sodium bicarb

74
Q

Which H2 antagonist is most effective in sheep to increase abomasal pH?

A

IV ranitidine

75
Q

At what point in the production cycle do abomasal ulcers most commonly occur in cattle?

A

Within the first month after calving

76
Q

Which forestomach disease is associated with suffolk sheep?

A

Abomasal dilation and emptying defect

77
Q

What dietary factor may cause secondary abomasal impactions?

A

poorly-digestible roughage

78
Q

What clinical and diagnostic signs usually accompany abomasal impaction?

A

-Fluidy rumen, abomasum is a firm mass palpable behind the right costal arch, may or may not have hypoCl- metabolic alkalosis

79
Q

Which prokinetic is most effective to increase abomasal emptying rate?

A

Erythromycin IM

80
Q

Which type of abomasal impaction has the best prognosis?

A

when only the pyloric antrum is affected

81
Q

Jejunal atresia is heritable in which breed of cattle?

A

Jerseys

82
Q

How is intestinal tract atresia/stenosis graded?

A
  1. membranous diaphragm with perforation
  2. cordlike intestinal remnant
  3. Blind ended with complete intestinal separation (MOST FREQUENT)
  4. Multiple sites of atresia
83
Q

Briefly, how does an intussusception develop? Which ages and breeds are predisposed?

A

The oral portion of the gut is usually engulfed and propelled distally by peristalsis of the enveloping portion. Calves < 2 months , and Brown Swiss

84
Q

How are the three classifications of cecal distension described?

A
  1. Dilation: gas distension, apex displaced toward rectum, rectally palpable
  2. Retroflexion: folded dorsally or ventrally, volvulus, with apex pointed cranially
  3. Torsion: distended and rotated on its long axis , apex toward rectum and transrectally palpable
85
Q

What are the most important clinical findings for diagnosing cecal dilation?

A

-ping from tuber coxae to cranially
- transrectal palpation of gassy cecum
*bonus: hypocalcemia

86
Q

Which animals are predisposed towards developing fat necrosis?

A

Abdereen Angus, Jersey, adult animals, possibly endophyte infested fescue

87
Q

Which agent causes jejunal hemorrhage syndrome?

A

Clostridium perfringens toxins

88
Q

What is pseudoobstruction, and how is it treated?

A

A functional ileus commonly seen in adult lactating dairy cattle mimicig complete obstruction but may respond to manipulation during celiotomy, or medical management

89
Q

What kind of organism is C. perfringens, and which strain is commonly found in the GI tract of healthy animals?

A

Gram-positive, toxin-producing, anaerobic spore-forming rod. Type A

90
Q

What causes Yellow Lamb Disease, and which species cannot be affected?

A

Caused by C perf type A, which causes RBC, platelet, and leukocyte lysis. Goats and horses are resistant. At necropsy, see icterus

91
Q

What is Lamb Dysentery?

A

caused by C perf type B. Lambs < 1 week have yellow-brown diarrhea, die rapidly. Necrotising enteritis and ulcers in the SI. Also neuro signs . Vaccine exists. Not in Americas

92
Q

What disease is caused by C perfringens type C? How?

A

-Caused by beta toxin from C perf TypeC (diagnosis by clinical signs + toxin isolation)
-disease = necrotic enteritis or hemorrhagic enterotoxemia
-calves, lambs, foals, piglets
-See yellow/brown diarrhea preceded by colic signs.
-Epsilon toxin can cause neuro signs

93
Q

Briefly, describe the pathophysiology of necrotic enteritis

A

Beta toxin takes effect when the recipient is deficient in trypsin. Neonates lack this because colostrum inhibits trypsin, and adults on diets high in trypsin-inhibitors (legumes, soy, sweet potato) are predisposed

94
Q

Which factors are associated with necrotic enteritis incidence in foals?

A

housing in stalls or dry lots during first few days, previous livestock on farm, low amounts of grass hay fed postpartum, born on dirt, stock horse parentage

95
Q

How is C perf C prevented and treated?

A

-Can vaccinate dams, final dose 2 wks before parturition
-Vaccinate neonates at 8 and 12 weeks
-Tx with support and broad spec abx, and antitoxin

96
Q

What disease process results from C perf type D? What are the signs pre and post mortem?

A

-Animals > 2 weeks old can develop acute or chronic disease from proliferation of C perf D and subsequent epsilon toxin production
-Acute: see ataxia, trembling, respiratory difficulty, coma. Not D+
-Chronic: focal symmetric encephalomalacia , looks like polio
-Subacute: diarrhea

97
Q

Briefly, what is the pathophysiology of C perf D?

A

-Overconsumption of starch leads to C perf D proliferation, and then epsilon prototoxin production which is cleaved to active form in the SI. Epsilon tox increases intestinal permeability, enters the bloodstream and crosses bloodbrain barrier, causes widespread vascular permeability

98
Q

How can C perf type D be treated and prevented?

A

-Treatable only if caught early: antitoxin and sulfa antibiotics
-Prevent: vaccinate during outbreaks and before arrival to feedlots, vax lambs and kids at 2-3 months. Booster sheep annually and goats every 3-4 months
-reduce dietary starch

99
Q

What criteria are used to diagnose C perf type D?

A
  1. Perivascular or mural vascular edema in the brain
  2. Focal symmetrical encephalomalacia
  3. Epsilon toxin in GI contents
100
Q

What causes acorn toxicity?

A

The metabolites of oak tannins and volatile phenols. Gallic acid and phenols are extremely toxic to renal tubules and intestinal epithelium

101
Q

What is acorn calf syndrome?

A

Congenital malformation of calves caused by maternal acorn ingestion during the second trimester pregnant (short legs, wonky hooves)

102
Q

How does acorn toxicosis present?

A
  1. Peracute: recumbency, weakness, perineal/vulvar edema. Low or normal temp. Death. Firm, dark feces
  2. 2 d later: reduced GI motility, listless, hemorrhagic diarrhea , ammonia breath, engorged scleral vessels, alimentary ulceration or perforations may follow
    **Horses: colic, tenesmus, hemorrhagic diarrhea. Possible serum levels of phenols?
103
Q

Which clinpath parameters are altered in acorn toxicosis?

A

Cattle: elevated BUN/CREA, acidosis and very high anion gap, hypoNaCl, hyper K, hyper phos, hypo calcemia.
Protracted cases get high BUN and Crea, and elevated anion gap
Horses: see cattle, and markedly high PCV

104
Q

What is Winter Dysentery, and how does the causative agent result in the clinical signs?

A

Bovine Coronavirus. Most animals recover spontaneously in a few days. The virus destroys epithelial crypts , leading to necrosis and hemorrhage. Incubation period is 2-8 days

105
Q

Which serotypes of Salmonella are specific to cattle, sheep, and horses, respectively?

A

Cattle: S dublin
Horses: S abortus equi
Sheep: S abortus ovis AND S arizonae

106
Q

What is the incubation period of salmonella? What cattle demographics are most commonly affected?

A

1-4 days. Calves 1d-6 months, usually < 2 months, and parturient adults

107
Q

Which is the most sensitive and specific method of diagnosing salmonella?

A

Culture of feces, blood, or tissues. PCR and ELISA are less sensitive and specific

108
Q

Which salmonella serovar is an endemic herd issue vs epidemic?

A

S Dublin tends to be endemic in a herd and shed in low numbers. S Typhimurium is epidemic and shed in higher numbers

109
Q

Which cattle are at greatest risk of becoming S Dublin carriers?

A

Heifers infected between 1 yr and first calving, cows infected n the parturient period, also maybe calves that survive

110
Q

What environmental conditions kill Salmonella effectively?

A

Direct sun, drying, composting in 115F temp internally, using bleach or virkon or phenylphenolic cleansers

111
Q

Which anatomical structure is believed to be a major source of contamination (with salmonella) for beef?

A

Lymph nodes

112
Q

Which salmonella vaccine(s) offer superior protection?

A

Modified-live virus, genetically altered vaccines vs killed whole cell vaccines . The siderophore vaccine also did not reduce shedding

113
Q

Which antimicrobials are advised to treat calves < 3 weeks vs older, infected with salmonella?

A

Sulfonamides (oral if < 3 wk, injectiable if older), sometimes fluoroquinolones, florfenicol,

114
Q

Next section: pg 910-20

A

make cards

115
Q
A
116
Q
A

Smith LA Medicine (12 decks)

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