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Equine Disease (ANEQ 346) > Exam 1 - Colic, Parasites, Endotoxemia > Flashcards

Exam 1 - Colic, Parasites, Endotoxemia Flashcards

1
Q

Susceptibility to colic

A

Any horse susceptible, older horses more so
Geographic/regional differences (soft sandy soils/climatic stress)

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2
Q

Risk factors for colic

A

Concentrates (feeding large concentrates of grain causes death to bacteria that breaks down forages, and slowing down of the breakdown)
Rapid changes in concentrates and hay

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3
Q

Anatomical causes of colic

A

Large to small spaces (cecum, small intestinal loops, flexures)
Stomach is smaller then intestine (small/large intestine rather large)
Horses can not throw up (90 degree angle into stomach)

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4
Q

Visceral Pain (gut pain)

A

Intestinal spasms
Mucosal irritations
Distension (stretching)
Tension on mesentary (displacement)
Ischemia (restriction of blood flow)
Injury to peritoneum

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5
Q

Mild colic

A

Pawing
Laying down/getting up
Looking at stomach
Reluctance to eat/drink
Increased HR (50-60)
Increase/decrese in gut sounds

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6
Q

Severe colic

A

Violent kicking at abdomen
Increase in HR and Respiratory (sweating, 70 or higher bpm)
Alter MM and CRT
Distressed/Depressed (sitting like a dog, stretching out)
Sweating
Self Trauma

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7
Q

Causation factors (colic)

A

Concentrates
Sudden access to high soluble CHO (grain, fructans - can’t digest)
Inadequate fiber
Poor quality food

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8
Q

Risk factors (colic)

A

Stabling (not as much movement, can eat irritants (bedding)
Internal parasites (obstructions)
Stress (not eating/drinking)
Management (quick changes, no access to water, lack of routine)
Poor dental care (can’t adequately chew)

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9
Q

Habitat factors (colic)

A

Box stall (bedding impactions)
Pasture (too much ingestion of fructans, can cause colic)
Sandy soils
Weather changes (not drinking enough water)

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10
Q

Vices factors (colic)

A

Cribbing, windsucking, eating too quickly

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11
Q

Clinical signs

A

Pulse rate, respiratory rate, rectal temperatures, color of MM, moisness of MM, CRT

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12
Q

Communication to vet

A

Behavioral signs
Digestive noises (lack there of)
Bowel movements (color, consistency, frequency)
Changes in management (deworming)
Past episodes of abdominal pain
Breeding history

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13
Q

What to do (colic)

A

Keep horse calm/comfortable (let horse lie down - rolling wont cause twist)
Horse rolling/violent - walk calmly
Do not administer drugs unless told to
Follow vet advice until arrival

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14
Q

Vet approach to colic

A

Obtain full history
Do thorough physical
pass stomach tube - relieve gas
Perform rectal exam
May….
- Abdominocentesis (colic is severe)
- Blood Sample
- Refer

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15
Q

Treatments (Colic)

A

NSAIDs (non-steroidal anti-inflammatory)
Sedatives/sedation
Fecal softener (water)
IV fluids, oral fluids
Fluid therapy (aggressive)

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16
Q

Refering due to colic

A

Pain unresponsive to analgesics, recurrence of pain
HR >60 consistently
Gastric reflux >2L
Positive findings on rectal
Deterioration of MM color
Progressive reduction in gut motility, and abdominal distension

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17
Q

Prevention (colic)

A

Daily feeding/exercise routine
High quality diet, mainly roughage
Avoid feeding excessive grain/energy
1.5% BW of DMI should be supplied through hay
Divide daily concentrates
Regular parasite control
Exercise/turnout daily
Fresh water
Avoid feeding on ground
Gradual feed changes
Reduce stress
Maintaining records

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18
Q

Endotoxemia

A

systemic disorder that originates from the host reponse to gram - bacteria, causing host to absorb endotoxins of dead cell

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19
Q

Body defense

A

1st line - epithelial cell wall
2nd line - phagocytic cells, lymphocytes, humoral (IG, complement/acute phase reactants)

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20
Q

Causes of endotoxemia

A

Grain overload (Gram + bacteria multiply, cause death of gram - bacteria)
Obstruction
parasites
Enteritis colitis
ulcers
Local systemic infections

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21
Q

Absorbtion of endotoxins

A

damage to intestinal walls causes mucosa to be weakened and allow toxins to enter blood stream
- Grain + : kills gram - and cell endotoxin released from cell wall

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22
Q

Gram - infection

A

Retained placentas, enteritis (salmonella), peritonitis, foal septicemia

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23
Q

Invasive enteric pathogens

A

Causes direct mucosal legions, allowing for endotoxins to enter blood stream
- salmonella and clostridium (produce exotoxins)
Canthardian beetles (alfalfa)
Black oak
Heavy metals
NSAIDs
Anti-microbial agents

24
Q

Clinical signs (endotoxemia)

A

Depression
Tachycardia/tachypnea
Perfusion deficit
Toxic line and altered color of MM (bright red)
Pyrexia
Colic/Diarrhea
Dehydration, anorexia
Laminitis

25
Q

Toxins in circulation

A

Activation of inflammatory response
Inadequate tissue perfusions (circulation of fluid through circulatory and lymphatic system)
Multisystem organ failure
- cardiovasular collapse
- acute renal failure
- Ileus ( lack of muscle contration in intestine)
- Laminitis

26
Q

End stage endotoxemia

A

Endotoxic shock
- multi-organ failure
- Renal failure
- Heart failure
- Death

27
Q

Secondary problems to endotoxemia

A

If they survive >24 hours: subcutaneous edema, laminitis, diarrhea, septic thromboembolism

28
Q

Treatment (endotoxemia)

A

Fluids, treatment acidosis, glucose, anti-biotics, hyperimmune plasma, polymixin B, NSAIDs, Dimethyl sulfoxide (DMSO)

29
Q

Peritonitis

A

Inflammation of the peritoneum

30
Q

Peritoneum

A

Single layer of mesothelial cells that lines abdominal cavity and viscera
- Produces peritoneal fluid (lubricants, production and clearance, macrophages)

31
Q

Diffuse peritonitis

A

Intra-abdominal infection extending beyond transverse colon (towards rectum)

32
Q

Localized peritonitis

A

Only affects one area of peritoneum/one organ

33
Q

Acute peritonitis

A

Occurs as a secondary complication to traumatic injuries involving adbominal cavity, rupture of bowel, abdominal surgery

34
Q

Chronic perionitis

A

Rupture within the abdominal wall

35
Q

Causes of peritonitis

A

Iatrogenic (rectal tear, castration complication)
septic (abdominal abscess)
Traumatic ( breeding and parturition injuries)
Parasitic

36
Q

Clinical signs (peritonitis)

A

Depression, colic, inappetence, pyrexia, congested MM, tachycardia/tachypnea, reduced gut sounds, reduced fecal output, diarrhea, sweating, muscle fasciculations, reluctance to move, pain urinating/defacating

37
Q

Diagnosis (peritonitis)

A

Clinical signs
Rectal exam
Abdominocentesis
Blood work

38
Q

Treatment (peritonitis)

A

Antibiotics
Fluid therapy
Peritoneal lavage
Analgesic and anti-inflammatory
Heparin
Surgical exploration
Nasogastric exploration
Dewormer (if parasites involved)

39
Q

Large strongyles (clinical)

A

Migration through walls of arteries (mesentery - spasmodic colic)
Diarrhea
Poor condition, unthriftiness

40
Q

Diagnosis (large S.)

A

Microscope examination of feces

41
Q

Treatment (Large S.)

A

L3 - travel to small intestine, cecum, right ventral colon and then to liver. Migrates either through hepatic cavity or across peritoneal cavity to liver, and then back to intestine in order to reproduce/molt

42
Q

Small stronglyes

A

Non-migratory red worms
Most important in adults horses
- Live in large intestines, eggs pass in feces

43
Q

Life cycle (Small S.)

A

L3 (infective) develop and eaten
In hindgut, they enter walls of mucosa and form cysts, and then develop into L4 when they will break out of cysts.

44
Q

Clinical signs (Small S.)

A

Profuse diarrhea, rapid weight loss, normal appetitie

45
Q

Treatment (Small/Large S.))

A

Drugs to treat encysted/migratory forms
Dewormer
- Febendazole
- Obendazole
- ivermectin

46
Q

Ascarids

A

Large roundworms, small intestine of suckling and weanling foals mainly to 2 years

47
Q

Ascarids (clinical )

A

Coughing, mucous exudates (lung migration)
Reduced gut motility
Rupture
Unthriftiness, poor growth, pot belly, rough hair coat, loss of appetitie

48
Q

Life cycle (ascarids)

A

L2 - migrate through wall of small intestine to liver heptic portal system and into the via then to lung via pulmonary arteries

49
Q

Pinworm (clinical signs)

A

Anal itching
Erosions on colon mucuosa, no signs

50
Q

Diagnosis of pinworms

A

Find with adhesive tape on anus

51
Q

Treatment (Pinworms)

A

Routine anti-parasitic compounds
Sanitation of stable, paddock fixures
Washing of perineal area

52
Q

Bots (clincal signs)

A

Annoyed with female flies
Periodontal ulceration (1st, 2nd stage)
Stomach legions (2nd, 3rd stage)

53
Q

Strongyloids

A

Intestinal thread worms found in young foals due to transmission through milk
Common signs
- Diarrhea with high fecal count

54
Q

tapeworms

A

Live around ileocecal junction, causing obstructions
Common
2-4.5 cm long
Clinical signs - colic

55
Q

Hambonema

A

Eaten by horses on river beds and can cause stomach legions and ulcers

56
Q

Parasite control

A

Hygienic care of stables, protection of water from fecal contamination
Spread bedding on crop land (1 yr after)
Avoid overstocking
Chain harrow and clipping (spreads parasites, allow for period to kill parasites)
Anthelmintic

Equine Disease (ANEQ 346) (3 decks)

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