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82 Cards in this Set

  • Front
  • Back
What does the Vd of drug tell you?
large Vd= the drug is distributed throughtout a variety of tissues and extracellular fluids (does not necessarily mean high intracellular concentration or good membrane penetration)

small Vd= the drug remains primarily in the vasculature
penicillins spectrum, mode of action, Vd, safety
penicillin Na or K, procaine G: strep, most clostridium
ampicillin, amoxycillin: some gram negative, strep, staph
methicillin:strep, staph
ticarillin: P.aeroginosa, strep, expensive so foals or regional therapy only
mode of action: inhibits cell wall synthesis, time dependent killing
small Vd
poorly lipid soluble
renal excreation
wide margin of safety, but is assoicated with anaphylactic shock
3rd generation
Na ceftiofur (ceftazidime)
resistant to many beta lactamases: strep, staph, some gram negative at larger doses, P. aeruginosa
only parenteral administration
half life 2 hrs
Vd: tissue distribution is good, however: poor membrane crossing!
renal excretion
side effects: immune mediated dermatitis
Cl. difficile associated diarrhea
mode of action
gentamicin, amikacin(foals only) neomycin, kanamycin, tobramycin,: gram neg. some staph
inhibits bacterial protein synthesis, cidial
concentration dependent killing
parenteral or topical
synergism with beta lactams
small vd half life 2 hrs, poor membrane cross-over, deactivation in necrotic material or acidic environment
renal excretion and nephrotoxic-time dependent uptake by proximal tubular cells, so dose once daily
mode of action
marbofloxacin, ciprofloxacin
spectrum:gram neg. some staph no anerobes
gyrase inhibitor
concentration dependent killing
parenteral or enteral
large Vd, very good tissue penetration due to lipophilia
does not reach CNS
excreted through bile, kidney, intestine
toxic in cartilage of young growing animals (less than 5 years)
synergism: beta lactams, metronidazole
erythromycin, azithromycin, clarithromycin, lincomycin, clindamycin, spiramycin, tylosin
gram postive and intracellular pathogens
use in combo with rampfin in rhodococcus equi infected foals or lansonia intercelluarsis
large Vd in most fluids and tissues
DO not use in adults- life threatening typhlo-colitis
safe in foals under six months
static, but can be cidal in large doses
(tetracycline) topical
time dependent killing
broad spectrum: rickettsiae(anaplasma, borrelia, ehrlichia risticii aka neorickettsia risticii) good for long term treatment of strep equi abscess
reasonbaleVd reasonable CNS penetration
renal excretion although enerohpeaticcirculation prolonges half life
toxcity: typhlo-colitis in adult horses although rare
liver damage when renal excretion is impaired
do not give if discolored! binds O2 and get nephrotoxcitiy
chloramphenicol (florfenicol)
broad spectrum (anaerobic and rickettsia) static
time dependent
large Vd
good CNS penetration
enteral and parenteral administration
do not give to animals that will be used for humane consumtion
causes aplastic anemia
potentiated sulfonamides
trimethoprim sulpha
broad spectrum, no anaerobes
time dependent killing
enteral parenteral
PABA folate metabolism
some resistance
reasonalbe tissue penetration
CNS penetration
antibiotic-induced colitis in adult horses
immune-mediated disorders?
rhodococcus tx in foals
high intracelluar concentrations
only given in combo with macrolide
clostridium difficile, (bacteroides spp)
How to treat?
Horse with a choke that was just flushed out
increased res rate and effort, and increased respiratory sounds with crackles and wheezes predominantly ventrally t and R more than L
Parenteral by preference
gentamicin and pen or ceftiofur or TMS
phenylbutazone or flunixin meglumine
How to treat?
horse with pleuropneumonia
fever, reluctance to walk, horizontal percussion line with dorsally increased sounds with crackles and wheezes
venterally silence totale
parenteral by preference
chest drainage
gentamicin, pen, metronidazole
or enrofloxacin, pen, meetronidazole
or chloramphenicol, preferably at later stage
flunixin meglumine
strongyles dewormers
moxidectin (do not give to foals less than 4mon)
large killed at any stage with IVM or MXD
only late L3 are killed by MXD in small
early L3 are killed by fenbendazole
strongyloides westeri dewormers
parascaris dewormers
moxidectin (not less than 4m)
careful in weaned hores that have never been wormed before, common for obstruction
tapeworms dewormers
praziquantel, pyrantel (2-3x)
bots treatment
NSAID properties
anti inflammatory
side effects
gastro-intestinal hemorrhage and nephropathy
aspirin use
only to decrease platelet aggregation cox-1 inhibitor
the one and only dose for phenylbutazon
2.2mg/kg every 12 hr
(1g Q12hr in a 450kg(1000lb) horse
NSAID toxicity
decreased renal blood flow
decreased mucosal blood flow with right dorsal colon most intensely affected
-protein loss
common causes of colic in young horses(less than3yr)
intussusception;ascarid impactions; gastric ulcers;foreign body obstruction/fecoliths
common causes of colic in middle age horses (7-10yr)
cecal impaction;epiploic formen entrapment; enterolithiasis
common causes of colic in old horses(greater than 10yr)
enterolithiasis; pedunculated lipoma; other neoplasia; fecoliths
common causes of colic in american miniatures
fecoliths and enteroliths
common causes of colic in STBD's and belgians
inguinal hernias
common causes of colic in arabians and morgans
common causes of colic in stallions
inguinal hernias
common causes of colic in mares
large colon volvulus and uterine torsion granulosa cell tumor
alfalfa hay causes what type of colic
bermuda grass hay common feed in what type of colic
ileal impactions
abdominal distention in adult verus foal
adult-most likely cecum or large colon
foal-SI, cecum, large colon
colic conditions causesing increased temperature
sand colic (normal to 102.5)
endotoxemia- rupture
infectious- abscess, viral, ect
common causes of decreased temperature
artifactual from pneumorectum;
transrectal palpation palpable structures
pelvic flexure
parts of ventral and dorsal colon
cecum w/ventral band and rarely duodenum
mesenteric root in smaller horses
lliac arteries and desecending aorta
small colon
left kidney
nephrosplenic space
SI not palpable unless distended or thickened
uterus ovaries
internal inguinal ring
capacity of stomach
first change observed is an increase in fluid volume
normal:TP less than 2; WBC less than 5000
L.I. surgical obstruction TP greater than 2 WBC variable
S.I. strangulating obstruction TP greater than 4, WBC variable
avoid when high risk of enterocentesis or severe pain
normals for Na K Mg pH and HCO3
normal daily oral intake of fluids
30-60ml/kg/day or 1L/hr/500kg
primary ICF cation:
primary ICF anions:
Primary ECF cation:
Primary ECF anions:
primary ICF cation:K(higher than other speices)
primary ICF anions:phosphate and proteins
Primary ECF cation:Na
Primary ECF anions:Cl and HCO3
sodium is a key player in maintenance of effective circulating volume
calculating dosage of HCO3 from BD
BD x BWT(kg) x 0.3
only treat if acidosis is not responsive to fluids
begin with replacing 1/4 of the deficit and repeat blood gas measurement
expected abnormalities in the colic
Na and Cl generally WNL
Ca low
K variable, low with anorexia, high with azotemia
Mg low(50%) with concurrent low Ca or increased wigh MgSO4 therapy
HCO3 usually low
anion gap
(Na+K)-(HCO3+Cl)= AG
AG greater than 25 is a poor prognostic indicator
central venous pressure
estimates perload and approximates the ratio of blood volume to blood volume capacity
useful for
1.monitoring propensity for edema in at risk patients urine production w/diuresis
3.hypo-oncotic states
4.right heart failure
normal adult=7-12cm H2O
Colloid oncotic pressure
measure in patients that are hypoproteinemic and receiving crystalloid fluids or horses receiving synthetic colloids (not detectable by refractometery)
normal adult urine production
adhesion prevention
abdominal lavage
most common clinical sign for choke
nasal discharge
equine esophageal clinical anatomy
crainal 2/3 straited muscle
common carotid, vagosympathetic trunk, and recurrent laryngeal n. course w/ esophagus dorsolaterally within the deep fascia of the neck.
poorly developed vomiting reflex
treatment of choke non surgical
remove all access to feed and water
spontaneous resolution w/ or w/out sedation
gental lavage with stomach tube, cuffed nasotracheal tube to prevent aspiration
higher chokes more likely to aspirate
choke treatment surgical
only when absolutely necessary
esophageal lavage under general anesthesia, cuffed endotracheal tube placed in esophagus and nasogastric tube sealed inside to create pressure
esophagotomy- when sticture present
clinical anatomy of SI
duodenum not accessible to visualization
jejunum 70% can be exteriorized, long mesentery
Ileum 50% can be exteriorized
antimesenteric band (ileocecal band)
functional obstruction of SI
proximal jejunitis/anterior enteritis
clinical signs:
-pain responsive to NG decompression, then depression
-leukocytosis with toxic left shift
-orange discolored or foul-smelling reflux
-abdominocentesis:increased TP; normal WBC
treatment: supportive care and gastric decompression
strangulating obstruction of SI most common site
distal jejunum and ileum
epiploic foramen entrapement
can be left to right or right to left, left to right most common
mean age 9.8 years
geldings and thoroughbreds overrepresented and cribbing horses
Ileum most common segment involved
factors affecting success of small intestinal surgery
1.ID and correction of primary problem
2.intra-op decompression of distended SI
3.resection of all compromised intestine
4.preservation of anatomic and physiologic continuity of intestine
5.rapid completion of surgery with minimal trauma
6.early return of intestinal function to normal use
7.appropriate post-operative support
sequence of events for SI resection/anastomomosis
1.reduce incarceration and decompress if possible
2.ligate vasculature
3.luminal occlusion
4.transect and suture mesentery
5.resect bowel at distal end(at an angle to maximize luminal diameter and preserve blood flow to antimesenteric border)
6.decompress(if not done earlier)
7.perform anastomosis
large colon anatomy
attached only at right colon
right ventral-sternal flexure-left ventral-pelvic flexure-left dorsal-diaphragmatic flexure-right dorsal-transverse colon.
bands: 4-4-1-3-2 (RVC-LVC-LDC-RDC-small colon)-four on the floor 132.
intercolonic mesentery
large colon impaction and fecaliths
coarse feed, inadequate mastication, insufficient water. fecalith is a hard fecal ball common in young(<1yr) in old horses(>15yr)
clinical findings:
most common site is pelvic flexure-LVC, and junction bt RDC and transverse colon.
mild intermittent colic
HR mild increase
Intestinal sounds usally present and associated with pain
peritonel fluid usually normal or slight increase in TP if prolonged
RDC impactions are often presumptive diagnosis based on persistent mild colic with little or no change in peritoneal fluid parameters in the face of normal rectal findings and lack of fecal production
IV and oral fluids
do not feed until impaction resolved
if unresposive to medical terapy left paralumbar laparotomy under local anesthesia or ventral midline celiotomy under general anesthesia
surgery rarely necessary for simple impactions, but often necessary for fecaliths
sand impaction
cause:horses on pasture in areas with sandy soils, fed off ground
clinical findings:
mild colic or severe acute pain if RDC/transverse colon completely obstructed, or accompanied by a colonic displacement
tends to accumulate in RDC
strech out or spend time laying down
low grade fever
sand in feces
peritoneal fluid often normal, but weight of sand makes enterocentesis likely resulting in peritonitis
ausculted sand in ventral abdomin
radiography is useful diagnostic aid
psyllium and water via stomach tube
oral and IV fluids
large amounts of sand may require surgical removal
form RDC and transverse colon
through an enterotomy in the pelvic flexure
good in most
complications:colonic rupture, severe colitis and endotoxemia
cause: magnesuim and ammonium phosphate crystals around a nidus. most common in SW,CA,FL,IN. Arabians, Morgans, and American miniatures
alfalfa hay
clinical findings:
1/3 history of recurring colic
RDC at junction with transverse colon or small colon. most common site is the proximal small colon
rarely palpable
abdominal radiographs
peritoneal fluid usually normal unless wall ischeimic
surgery to decompress colon and cecum and then remove
enteroliths with one or more flat sides are accompained by more enteroliths
prognosis:very good
large colon volvulus
occurs near the attachment of the colon to the cecum.
often assoicated with parturtion, grass diet and or highly fermentable feeds
most often in broodmares 8yr and within the first 3 months after foaling
clinical findings:
acute colic
mesentery bt dorsal and ventral colon edematous on rectal
severe pain if strangulating
HR increased
marked abdominal distention
may have gastric reflux
recurrance 15% in brood mares
may perform colopexy or resection
good to poor
left dorsal displacement,nephrosplenic entrapment
cause:movement of the pelvic flexure or the entire left colo over nephrosplenic ligament
clinical findings:
mild to moderate pain or intermittent painful episodes
mm normal
HR slightly increased
colon palpated over ligament, bands of LVC running dorsocranially to the left kidney
spleen enlarged and displaced ventral
paracentesis may show blood due to splenic puncture
left kidney behind spleen with colon gas medial to spleen on ultrasound
1.restict feed intake with spontaneous correction
2.IV phenylephrine to encourage spleenic contraction followed by light exercise
3.short term anesthesia, put horse in right lateral recombancey, elevate rear legs, dorsal recombacey with ballottement of abdomen, to left lateral recombancey, recover. concurrent recal palpation may help during roll, midline apporach, spleen is retracted medially, and colon is lifted up to free it, can laparospic ablation of the nephrosplenic space for repeat offenders
right dorsal displacement
cause:pelvic flexure moves laterally around base of cecum and them may lie caudally in the pelvic inlet or continune cranially near the diaphragm, often complicated by 180 degree volvulus near the base of the cecum.
clinical findings:
moderate pain
slow development of systemic deterioration as the blood supply to displaced colon is usually maintained
taenia of the colon running transversely across the pelvic inlet, can't fing cecum or pelvic flexure on rectal
distended and tight abdomen
elevation of liver enzymes from twisting of biliary system in chronic cases
surgical intervention to locate pelvic flexure, exteriorize and empty if necessary, rotate left colon cecal base and correct volvulus if present
very good
nonstrangulating infarction
either due to thromboembolism from stronglye larvae-induced damage to the cranial mesenteric artery or one of its branches, or local low blood flow state
clinical findings:
chronic intermittent dull pain without evidence of obstruction
very painful if complete infarction
distended colon
paracentesis-very high WBC COUNT and may RBC
surgical resection of the infarcted tissue
treatment of peritonitis
IV fluids
larvicidal therapy
heparin or aspirin
cecal anatomy
1m in length
mesentery attaches to dorsal body wall
four bands
-dorsal forms ileocecal band
-lateral forms the cecocolic ligament
cecal artery(branch of ileocolic artery)
cecal impaction
fibrous feed
bad teeth
young horses post surgery, other dz, or management change
primary cecal motility disturbance
clinical findings:
off feed
mild abdominal pain
always at risk of cecal rupture
use peritoneal fluid analysis and rectal exam findings to dictate therapy
rectal exam is diagnostic-impaction on right side of abdomen w palpable ventral cecal band
medical-IV and oral fluids
surgery-typhlotomy or complete cecal bypass-ileocolic anastomosis
ileocecal, cecocecal and cecocolic intussesception
cause and clinical findings:
tapeworms(anoplocephala perfoliata) may predispose to the condition
wide variety of presenting clinical signs; acute, severe pain to mild, chronic dz
manual reduction and resction
enterotomy of the RVC with resection
small colon impaction
after diarrhea/colitis suggesting functional impairment leading to ileus and dehydration of ingesta
clinical findings:
pain mild to moderate but may be severe if obstruction complete
rectal palpate of firm tubular impaction in small colon
surgery is indicated if progressive pain results, peritoneal fluid abnormalities,or too firm to resolve medically
pelvic flexure enterotomy and surgically assisted enemas
50% positive for samonella post surgery
intraoperative and post operative treatment with DTO smectite(biosponge)may assist with prevention of post-op diarrhea
general features of small colon dz
clinical signs may be insidious
often associated with endotoxemia
evacuation of the large colon concurrently with relief of SC obstruction recommended
esseential to preserve luminal diameter when performing an eneroromy of the small colon
use strong,longer lasting absorbable suture for the enterotomy since firm digesta passes the site
higher bacterial counts and increased collagenase activity present in the lumen of the small colon compared to the large colon
more predisposed to adhesion formation than the large colon
small colon anatomy
pelvic inlet to anus
classification of rectal tears
gradeI:involve mucosa or mucosa and submucosa only
gradeII:defect in muscularis but mucosa intact
gradeIII:mucosa, submucosa, and muscularis, leaving only serosa (a) or mesentery (b)
gradeIV:all the way through
most common cause of rectal tears is _________ and most are __________
field management of rectal tears
1.recognize and accept responsibility
2.caudal epidural and sedation
3.evacuate rectum
4.evaluate tear(bear arm)
5.pack rectum 3" stockinette with moistend roll cotton,dilute betadine and surgical gel, purse string rectum shut
6.tetanus toxoid and systemic antibiotics
7.ship to referral center
8.promptness of diagnosis and treatment essential
grade I recal tear treatment
put on pasture
fecal softeners
tetanus toxoid
recheck every couple of days
grade III and IV rectal tear treatment
ventral midline celeotomy-evacuate colon/lavage abdomen
primary suture per rectum
repeated manual evacuation
loop colostomy
end colostomy
temp indewelling recatl liner
in periparturient mares, rectal eversion and direct suturing
rectal prolapse types
typeI: rectal mucosa only
typeII: all or part of the rectal ampulla(full thickness of rectal wall)
typeIII: type II plus intussesception
typeIV: rectum and variable length of small colon intussuscept through the anus
If rectal prolapse goes beyond _______ likely have torn mesenteric attachments which results in poor prognosis
perirectal absecess
often unknown
enemmas in foals
feed/thermometer punture
breeding injuries
gravitation of gluteal abscess following IM injection
clinical signs:
low grade colic and depression, anorexia, decreased fecal production, tenesmus and fever
palpation, ultrasound and percutanous or transrectal aspiration of pus
establish drainage either percutaneously, per rectum, or vaginally depending on location. lavage abscess and adminster laxatives, appropriate antibiotics and NSAIDs.
rectal polyps and neoplasia
usually pedunculated
remove by ligation and division
-types: most common are SCC and melanoma, with rectal adenocarcinoma and leiomyosarcoma less common. estimated that 80% of gray horses over 15years have melanomas
dependent on the nature of the lesion. surgical excision, cryo, eletrosurgery, laser surgery, hyperthermia, chemotherapy, radiation therpay, immunotherapy, and combinations of these therapies