Abomasal/Intestinal Dzs Flashcards
What electrolyte change would you expect to see on bloodwork of a cow with simple indigestion?
(Hypocalcemia → d/t not eating)
If mastitis is on your list of differentials, how can you rule it out?
(Palpate the udder (should be hard and swollen) and CMT (should be >1mil for clinical))
What are the different levels and associated somatic cell count for the california mastitis test?
(Negative - 0, trace - 300k, CMT 1 - 900k, CMT 2 - 2.7mil, CMT 3 - 8.1mil)
The BHB comes back as 3.3mmol/L on a cow you tested, would you consider her subclinical/clinical/severe (choose)?
(Severe, >3 mmol/L is severe; subclinical is 1.1-1.4 mmol/L)
What are some causes of a displaced abomasum?
(Anything that causes atony of the abomasum → ketosis, hypocalcemia, increased VFAs, endotoxemia)
Whether a DA goes to the left or right depends on what other structure and what characteristic of that structure?
(Rumen, if its large/full → RDA, if small/empty → LDA)
RTAs are a counterclockwise/clockwise rotation of a DA (when viewing the cow from the rear).
(Counterclockwise)
How do you determine where you are going to place your tacks for a roll and tack fix of a displaced abomasum?
(A hand’s breadth lateral to midline and a hand’s breadth caudal to the sternum)
How can you confirm that you have punched into the abomasum in a roll and tack?
(Test with litmus paper, will be greenish to pink)
What are the pros and cons of a roll and tack?
(Pros → cheap, quick, less invasive; cons → entrapment of other stuff, can displace again)
What are the pros and cons of a right side omentopexy?
(Pros → you know its back in place, relatively easy, can check for fatty liver; cons → omental tears in fat cows, risk of peritonitis and wall abscess (can mitigate with abx), and cannot break down adhesions or observe tears/ulcers)
(T/F) A right sided omentopexy can be used to fix a left or right side DA.
(T)
(T/F) Left sided abomasopexy can only fix LDAs.
(T)
(T/F) A right sided paramedian approach can be used to correct both an RDA and LDA.
(T)
If a weaning calf presents for pain in the lower right anterior quadrant of their abdomen, what is likely the issue?
(Abomasal ulcer)
What is the purpose of giving a calf with an abomasal ulcer aluminum hydroxide and magnesium oxide?
(Will neutralize acid)
What is the typical manifestation of a sheep with an abomasal emptying defect?
(Anorexia and weight loss)
What do you expect to see on bloodwork of a sheep with an abomasal emptying defect?
(Hypochloremia, hypokalemia, and metabolic alkalosis)
What is the purpose of administering erythromycin to a sheep with an abomasal emptying defect?
(It is an abomasal stimulant, can also try cathartics and laxatives but nothing is super useful)
A study showed that palpation at what day of gestation has been associated with atresia ani in cattle?
(42)
How do females affected by atresia ani, recti, or coli compensate?
(Form a rectovaginal fistula → can go on and live life, just cannot be bred but still good for slaughter)
What are the treatments for atresia ani, recti, and coli?
(Ani → create an anus, recti and coli → euthanasia)
Why is oral and IM penicillin administered in cases of hemorrhagic bowel syndrome?
(It is thought to be caused by clostridium perfringens type A)
Why is hemorrhagic bowel syndrome typically seen within the first 100 days in milk?
(Bc that is when the most stress occurs and when they are eating the most → sets up the perfect spot for Clostridium perfringens type A)
What are the clinical manifestations of hemorrhage bowel syndrome?
(Off feed, depressed, increase heart and resp rate, progressive abdominal distention, low pitched pings in lower right abdomen (d/t gas in GI tract))
What do you expect to find per rectal palpation in a cow with hemorrhagic bowel syndrome?
(Blood clots/bloody feces and distended small bowel loops)
How do cattle with a cecal dilation/retroflexion/torsion present clinically?
(Anorexic, drop in milk, scant feces (d/t being blocked), and signs of colic (bruxism, looking at flank, and shifting weight))
How is cecal dilation/retroflexion/torsion prevented?
(Increase forage and decrease grain)
What in the clinical presentation of a cow with a suspect cecal pathology will allow you to determine if the cecum is just dilated versus torsed?
(Heart rate → will be much higher with a torsion)
What clinical signs are associated with intussusception in ruminants?
(Colic, depressed, anorexic, abdomen swells over a couple of days, dehydration)
Why is surgery not a great option for correction of intussusceptions?
(It is difficult to get good surgical access to the small intestines → will self correct but prognosis is poor)
What is the clinical manifestation of small intestinal volvulus in cattle and is it usually an acute or chronic progression?
(Clinical manifestation → increased heart and resp rate, painful, and swollen abdomen; acute onset with rapid progression)
