Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Equine Med > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Large Stongyles; Species, Pathophysiology, Pre-patent period

A

Species
• Strongylus vulgaris
• Strongylus edentates
• Strongylus equinus

Pathophysiology
• L4 larvae migrate through abdominal blood vessels (verminous arteritis) -> thromboembolism

Prepatent period
• 5.5-12 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Small Strongyles; Pathophysiology, Treatment

A

Pathophyisology
• L3 larvae invade mucosa of large colon and become “encysted”
• Emergence of encysted L4 can cause colic, diarrhea, weight loss, colic, rough hair coat
• Encysted forms may last 2 years or longer!

Treatment
• Limited anthelminthic choices for encysted forms
• fenbendazole, moxidectin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Ascarids; Species, Pathophysiology, Treatment, Pre-patent period

A

Species
• Parascaris equorum

Pathophyisology
• Very hardy eggs migrate through lungs
• after approximately 1 week – cough, respiratory disease
• Horses < 2 years of age. Weight loss, ill thrift, impactions in foals.

Treatment
• Be careful w/ antithelmentics
• Moxidectin, ivermectin

Pre-patent period
• 10-15wks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Cestodes; Species, Pathophysiology, Treatment, Pre-patent period

A

Species
• Anoplocephala perfoliate
• Anoplocephala magna
• Anoplocephaloides mamillana

Pathophyisology
• Transmitted by oribatid mites
• Adult parasites at ileocecal valve area.
• Colic, impaction, intussusceptions, ill thrift, weight loss.

Treatment
• Praziquantel only

Pre-patent period
• 6-16wks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Botfly; Species, Pathophysiology, Treatment

A

Species
• Gasterophilus spp.

Pathophyisology
• Only larval forms in horses
• Some oral irritation with larval migration
• disease due to stomach bots is rare
• Botfly larvae remain in stomach for many months -> Pass into manure -> pupate -> emerge as adult flies

Treatment
• Treat in late summer or fall w/ ivermectin or moxidectin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Benzimidazoles; MOA, drug, use

A

MOA
• Interfere with energy metabolism by binding to beta tubulin and preventing polymerization to microtubules.
• Does NOT induce rapid paralysis or death

Drug
• Fenbendazole

Use
• Double dose recommended for ascarids
• Five days of treatment for encysted cyathostomins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Tetrahydropyrimidines

A

o Can cause irreversible rigid paralysis
o Only treats adult parasites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Macrocyclic Lactones; MOA, drug, use

A

Drug
o Moxidectin, ivermectin

MOA
o Act on glutamate gated chloride channels
o Can cause flaccid paralysis

Use
• Can kill external parasites
• Effective for migrating & encysted cyathostomin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Isoquinolones; drug, use

A

Drug
• Praziquantel

Use
• Tapeworms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Use of Quantitative Fecal Egg Count

A

o Determine shedding status of adults
o Horse w/ low FEC is a low contaminator
o Provides info on ascarids (foals) & strongyles
o Determine if parasites are resistant to an anthelmintic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How to do Quantitative Fecal Egg Count

A

o Collect a sample for FEC prior to deworming.
o Collect a second sample 10 – 14 days after treatment.
o Calculate the percent reduction for each horse.
o Calculate the mean reduction for all horses as an indicator of farm resistance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Limitations of Quantitative Fecal Egg Count

A

o Does not show total strongyle/ascarid burden
o Does not detect larval stages
o Do not show tapeworm infections or pinworms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Parasite Control in Adults Vs Foals

A

Parasite Control
o Two annual ivermectin or moxidectin w/ praziquantel
o Additional treatments to target horses w/ FEC >200EPG
o Treat during spring & fall

Parasite Control in Foals
o 4 treatments in 1st year
o Fenbendazole @ 2-3MO
o 2nd treatment before weaning w/ drug based on FEC
o 3rd & 4th treatment @ 9 & 12MO & include praziquantel
o yearlings – 2YO treated 3-4 times yearly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Hospital Biosecurity Plan

A

o Prevent intro of pathogens
o Contain pathogens that may be present
o Surveillance for potential pathogens
o Response to introduction of a pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Targeted Testing for Pathogens based on clinical signs to prevent spread of dz

A

Colic
* Salmonella

Surgical wound infections
* MRSA

Catheter site infection
* MRSA
* MDR

Unexplained fever
* EHV

Respiratory Signs
* EHV
* EIV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Primary Vs Secondary Perimeter in Biosecurity

A

Primary
* All suspected infected animals and the animals in immediate contact

Secondary
* All animals at facility that are free of infection but at increased risk of exposure
* Should be monitored

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Preventing Outbreaks at Boarding Facilities

A

o Require specific dz testing
o Require specific Vx
o Quarantine new arrivals
o History and physical exam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Preventing Outbreaks at Horse Shows & Events

A

o Use your own trailer
o Avoid nose-nose contact w/ other horses
o Don’t share equipment
o Don’t put shared hose in water bucket
o Don’t graze in areas where other horses have recently grazed
o Avoid communal areas
o Wash hands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Calculi; who, cause, treatment

A

o Adults
o Usually geldings
o Complete or partial obstruction

Cause
* Ca carbonate due to alfalfa diets

Treatment
* Fluid therapy
* Glucose until K+ normal
* TMS
* Anti-inflammatories after hydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Renal Uroliths; Where, Clinical SIgns, Diagnosis, Treatment

A
  • Kidney or ureter
  • Difficult to diagnose

Clinical Signs
* Colic is rare

Diagnosis
* Ultrasound
* Microscopic hematuria

Treatment
* If no azotemia -> remove affected kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Urethral Stones; Clinical Signs, Diagnosis, Treatment

A

Clinical Signs
* Dysuria
* Colic

Diagnosis
* Endoscopy

Treatment
* Remove w/ endoscopy
* Perineal urethrostomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Bladder Stones; Clinical Signs, Diagnosis, Treatment

A

Clinical Signs
* Hematuria post exercise
* Dysuria
* Colic
* Pyruria
* Incontinence

Diagnosis
* Transrectal palpation
* Cystoscopy + sedation + empty bladder

Treatment
* Manual extraction on females
* Perineal urethrostomy on males
* Mechanical lithotripsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Diagnosing Calculi; Transrectal Palpation Vs Ultrasound

A

Transrectal
* Bladder size, thickness, masses, tone
* Calculi in bladder
* Should palpate bladder empty
* Caudal pole of L kidney

Ultrasound
* Bladder urine, masses, rupture, stone
* Kidney size, echogenicity, masses, cysts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Urinalysis

A

o Always Turbid due to Ca carbonate

USG
* Hyposthenuria <1.008
* Isosthenuria = 1.008 – 1.015
* Hypersthenuria >1.015

Dipstick
* pH (should be 7-9)
* glucose
* myoglobin, Hb, RBC (false + due to pH)
* bilirubin
* protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Acute Renal Failure; Clinical Signs, Diagnosis, Treatment

A

Clinical Signs
* Usually no clinical signs
* Oliguria (anuria rare)
* Lethargy

Diagnosis
* Azotemia
* +/- decreased Na & Cl
* +/- increased K
* isosthenuria
* RBCs
* Proteinuria
* Granular casts
* GGT in urine

Treatment
* Fix primary cause
* Fluids 2x maintenance
* Dopamine to increase BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is considered Polyuria

A

o >50ml/kg/d
o ~25L urine/d

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Primary Vs Secondary Polydipsia

A

Primary
* Psychogenic
* Most common
* Hyposthenuria
* Normal physical exam
* Medullary washout

Secondary
* Renal failure -> azotemia
* PPID
* Systemic dz (sepsis)
* Diabetes insipidus (less common)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Polydipsia Diagnosis

A

Water deprivation test (not if dehydrated or azotemic)
* Baseline UA + BUN/creatinine/BW ->
* No water + slow feeder ->
* BW + USG q6hr
* Normal or primary PD = USG >1.025 after 24hr
* Stop test if BW loss >5% or if dehydrated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Chronic Renal Failure; Diagnosis, Clinical SIgns, Treatment

A

Diagnosis
* Renal biopsy

Clinical Signs
* Tarter & oral ulcers
* Decreased oncotic P due to decreased albumin
* Endothelium toxicity due to increased urea
* Increased hydrostatic P due to increased renin
* PU/PD
* Anemia
* Uremic odor

Treatment
* No cure
* Provide water always
* Give HCO3 if low
* Don’t breed
* Increase diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Chronic Renal Failure; Congenital Vs Acquired

A

Congenital
* <5yp
* no ARF
* renal agenesis, hypoplasia, dysplasia

Acquired
* Most common
* Previous injury
* Cause may be unknown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Muscle Responses to Injury

A

Rhabdomyolysis
* Muscle breakdown
* High CK
* Muscle pain
* Myoglobinuria

Atrophy
* Focal or generalized decreased muscle fiber diameter

Hypertrophy
* Increased muscle fiber diameter due to training or genetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Exertional Rhabdomyolysis (Tying Up); Clinical SIgns, Diagnosis, Recovery, Treatment

A

Clinical Signs
* Pain, muscle stiffness, reluctance to move

Diagnosis
* High CK & AST
* +/- azotemia
* hyperkalemia
* myoglobinuria
* exercise challenge test (test CK 4-6hr after exercise)
* genetic testing for predisposition
* muscle biopsy to identify cause
* serum Vit E and selenium levels

Recovery
* Mild – rest 2-3d
* Scarring & decreased muscle mass – recover 3-4m
* Monitor kidneys

Treatment
* IV fluids + dextrose
* Butorphanol & ketamine for analgesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Recurrent Exertional Rhabdomyolysis; Signalment, Diagnosis, Management, Treatment

A

Signalment
* Thoroughbreds
* Young
* Fillies
* Nervous

Diagnosis
* Exercise challenge test

Management
* Train first
* Keep calm
* Decrease grain
* Increase fat
* Turn out to pasture
* Decrease stall rest

Treatment
* Dantrolene PO 1hr pre-exercise (48hr withdrawal before competing)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Polysaccharide Storage Myopathy (PSSM1); Pathophysiology, Signalment, Clinical Signs, Diagnosis

A

Pathophysiology
* Mutation in GSY1 gene
* Elevated glycogen synthase activity
* Increased glycogen stored in muscle

Signalment
* Often quarter horses
* Rarely Arabians, thoroughbreds, standardbreds

Clinical Signs
* Exertional rhabdomyolysis 15-20 min post exercise or post resting
* High NSC in diet
* Stretching, back pain, etc

Diagnosis
* Genetic test for GYS1 on hair or blood
* High CK at rest
* CK 3x post exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Polysaccharide Storage Myopathy (PSSM2); Pathophysiology, Signalment, Diagnosis, Management

A

Pathophysiology
* Amylase resistant polysaccharide muscle w/ no mutation

Signalment
* QH w/ chronic exertional rhabdomyolysis
* Warmbloods w/ sore muscles, lameness, CK normal post exercise

Diagnosis
* Semitendinous/membranous biopsy (unreliable)

Management
* Keep them moving regularly
* Turn out to pasture
* Minimize stress
* Prolong warm-up
* Keep hay low in NSC
* Fast 6hr pre exercise
* Increase fat intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Myofibrillar Myopathy (MFM); Clinical signs, Diagnosis, Management

A

Clinical Signs in arabians
* Decline in performance
* Intermittent tying up
* Increase in CK & AST
* +/- dark urine

Clinical Signs in Warmbloods
* Vague
* Poor performance
* Hindlimb lameness

Diagnosis
* Semitendinous/membranous or middle gluteal biopsy
* Shows abnormal aggregates of desmin
* Often false (+) & (-)

Management
* Core strength
* Consistent low intensity exercise w/ prolonged warm-up
* High protein diet
* Coenzyme Q10
* Minerals
* Vit E (if low)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Myosin Heavy Chain Myopathy (MHCM); Pathophysiology, Signalment

A

Pathophysiology
* Mutation in MYH1 gene
* 1 copy enough, 2 copies sever
* triggered by strep equi, Vx, or others

Signalment
* QH, paints, appaloosas
* Immune system attacks type 2 fibers

38
Q

Immune mediated Myositis; Clinical Signs, Diagnosis, Treatment, Management, Prognosis

A

Clinical Signs
* Muscle loos on topline & rump in 1-3d
* Lethargy
* Anorexia
* Stiffness
* Myoglobinuria

Diagnosis
* Genetic testing for MYH1 gene mutation

Treatment
* Corticosteroids
* +/- underlying dz

Management
* High quality protein diet
* Only give Vx absolutely needed

Prognosis
* Heterozygous – 20% resolve
* Homozygous – less likely to recover

39
Q

Non-exertional Rhabdomyolysis; Clinical Signs, Diagnosis, Treatment, Prognosis

A

o Rare

Clinical Signs
* Acute muscle damage
* Tachycardia & tachypnea
* Stiff/muscle swelling
* High CK & AST

Diagnosis
* Genetic testing for MYH1 gene mutation

Treatment
* Corticosteroids
* +/- underlying dz

Prognosis
* Poor if down

40
Q

Glycogen Branching Enzyme Deficiency; Signalment, Clinical Signs, Diagnosis

A

Signalment
* QH
* Related breeds
* Autosomal recessive
* Carriers are subclinical

Clinical signs
* Variable
* Late term abortion or stillbirth
* Weak foals w/ seizures or sudden death
* Foals have low WBC & high CK, AST, GGT

Diagnosis
* Genetic testing of hair
* Abnormal glycogen

41
Q

Acepromazine

A

o Used for tying up horses
o Increase blood flow to muscle
o Decreases anxiety

42
Q

Hyperkalemic Periodic Paralysis; Signalment, Clinical Signs, Bloodwork

A

o Autosomal dominant
o Mutation of voltage Na channel
o QH
o Homozygous most severe

Clinical Signs
* Muscle tremors/twitching
* Prolapsed 3rd eyelid
* Sweating
* Muscle cramping
* High HR & RR
* Arrhythmias
* Conscious paralysis of airway muscles = noisy breathing
* Conscious paralysis of respiratory muscles = death
* dysphagia = choke

Bloodwork
* Hyperkalemia
* High PCV
* Mild hyponatremia

43
Q

Hyperkalemic Periodic Paralysis; Triggers, Diagnosis, Management

A

Triggers
* Feeds high in K
* Stress
* Heavy sedation
* Anesthesia
* Transportation

Diagnosis
* Genetic testing

Management
* Less than 1% K in diet
* No molasses
* No electrolyte supps
* Regular exercise
* Avoid stress

44
Q

Hyperkalemic Periodic Paralysis; Treatment of Mild Vs Severe

A

Mild
* Feed grain or corn syrup -> insulin release -> K into cell
* Light exercise

Severe
* Ca gluconate + dextrose slowly -> move K into cell
* Tracheostomy

45
Q

White Muscle Dz; Cause, Clinical Signs, Diagnosis, Treatment

A

Cause
* Low Selenium

Clinical Signs
* Tongue in foals
* Heart in adults
* Progressive weakness
* Inability to nurse
* Masseteric atrophy
* Dyspnea
* Dysphagia
* Sudden death

Diagnosis
* Serum selenium (can be normal)
* Serum glutathione-peroxidase

Treatment
* Supplement selenium

46
Q

Clostridium myonecrosis; Clinical Signs, Cause, Diagnosis, Treatment

A

Clinical Signs
* Swelling, painful, warm
* Fever
* +/- crepitus
* high HR & RR
* lethargy

Causes
* Flunixin IM
* Any injectable
* Trauma

Diagnosis
* G (+) rods on Cytology
* Culture

Treatment
* Support for SIRS
* 2x dose penicillin or metronidazole
* surgical fenestration

47
Q

Normal Gestation & Parturition

A

o 320 – 365 days

Stage 1
* 1-4hrs
* fetal positioning

Stage 2
* “water breaks”
* 20-30 mins
* active labor

Stage 3
* <3hrs
* passing of placenta

48
Q

Normal Timing for Foals

A

123 rule
* foal standing in 1 hour
* foal suckling in 2hrs
* placenta passed in 3hrs

o righting & suckling reflex in 5 mins
o attempt to stand 30 mins
o stands 1-2hr
o suckles 1-3hr
o meconium passed & colt urination in 6hrs
o filly urination in 12hrs

49
Q

Signs of Immaturity or Dysmaturity

A

o Low birth weight
o Domed forehead
o Short silky hair
o Pliant ears and soft lips
o Flexible limbs

50
Q

Foal Vitals

A

o T = 100-102
o HR >60BPM at birth, 70-100 in first hour
o RR = 60-80 at birth, 20-40 later

51
Q

Colostrum

A

o Produced in last 2-4wks of gestation
o Contains IgG and other
o Replaced by milk in 12-24hrs
o Critically important for immunity

52
Q

Failure of Passive Transfer & IgG Testing

A

o <200mg/dL = very high risk & needs therapy
o 200-400mg/dL = increased risk & needs therapy
o 400-800mg/dL = not ideal, may need therapy
o >800 usually adequate

53
Q

Was there failure of passive transfer?

A

o Test all foals at 18-36hrs
o Look for IgG > 800
o Partial failure = 400-800
o Complete Failure <400

54
Q

Plasma Transfer Due to Failure of Passive Transfer

A

o Give 25 – 50 ml over 15 – 20 min ->
o watch for adverse reactions 
->
o Finish transfusion at faster rate 

o Can give 1 liter over 20-30 min in a 
healthy foal 
(Slower if sick)
o Monitor closely 

o At least 2 L required for most complete FPT foals 

o Recheck IgG after 12 – 24 hours

55
Q

Plasma Transfer Due to Failure of Passive Transfer; Adverse Reactions

A
  • Muscle fasiculations
  • Tachycardia
  • Tachypnea
  • Pyrexia
  • colic
56
Q

Nursing Behavior & Amount of Milk Needed

A

o 20-25% BW milk per day
o should gain 1-3lbs/day

1st wk
* 6times/hr

1-4wks
* 3times/hr

4-24wks
* <1time/hr

57
Q

Umbilical Care

A

o Preferably allow break on its own
o Disinfect umbilical stump 2 or more times per day
o 0.5 chlorhex or 2% iodine, or 1% providine

58
Q

Umbilical Remnant Infection; Structures involved, Diagnosis, Treatment

A

Structures
* umbilical artery, vein, stump, & urachus

Diagnosis
* Ultrasound
* May be normal externally

Treatment
* Medical or surgical
* Treat concurrent bacteremia/sepsis
* Usually gram (-) antibiotics
* Monitor joints daily

59
Q

Umbilical Hernias

A

o Small hernias are common! 

o little or no treatment 

o Occasionally require surgery 

o Ultrasound if suspicion of bowel entrapment and colic

60
Q

Patent Urachus; Basics, Treatment

A

o Present at birth or re-opens after a day or two 

o Not uncommon in sick, recumbent foals 

o May precede umbilical infection
o Watch for urine scald! 


Treatment
* usually medical but may require surgery 

* Local umbilical treatment preferred 

* Antimicrobials MAY be indicated

61
Q

Biochemistry Panel for Foals & Abnormal Elevations

A

o ALP higher than adult
o Bilirubin higher than adult
o Phosphorous present

Abnormal Elevation
* Creatinine – placental insufficiency
* BUN – protein catabolism from starvation in utero
* Lactate – problems w/ perfusion

62
Q

Neonatal Septicemia; Pathophysiology, Routes of Infection, Risk Factors

A

Pathophsiology
* Bacteremia ->
* SIRS ->
* Septic shock ->
* Multiple organ dysfunction ->
* Death

Routes of Infection
* In utero
* Ingestion
* Inhalation
* Umbilicus

Risk Factors
* FPT or partial FPT
* Perinatal stress
* In utero hypoxia
* Placentitis
* Prematurity
* Poor management

63
Q

Neonatal Septicemia; Common Bacteria, Diagnosis, Treatment

A

o Organsisms
* E. coli (most common)
* Actinobaccilus equi
* Salmonella
* Staph
* Strep
* Clostridium

Diagnosis
* Noxic neutrophils
* Increased lactate
* Hypoglycemia
* Sepsis score
* Blood culture (often negative)
* Culture & histo on necropsy
* Culture of joints

Treatment
* Prevent hypothermia! 

* Check blood glucose and supplement if needed! 

* Control seizures (diazepam)! 

* Possible bolus IV fluids to increase perfusion 

* Antibiotics
* Enteral nutrition via NG tube
* Fluid therapy
* O2

64
Q

Neonatal Septicemia; Clinical Signs

A

<7 days old
* Decreased suckle reflex & lethargy
* Maybe febrile or hypothermic
* Dehydration
* Toxic MMs, injected sclera, petechial
* Cold extremities & poor pulse quality

Older
* Pneumonia
* Diarrhea / colic
* Distended, hot, painful joints
* Umbilical infection
* Neurologic

65
Q

Cleft Palate; Basics & Treatment

A

o Clefts in soft palate are most common but always digitally palpate hard palate
o Often causes pneumonia

Treatment
* Surgery or euthanasia

66
Q

Diagnostic Approach to Colic in Neonatal Foal

A

o Look for evidence of sepsis
o Nasogastric intubation
o Digital rectal exam
o Ultrasound!!
o Rads
o Abdomenocentesis

67
Q

Most Common Cause of Colic in Neonates; What? Clinical Signs, Diagnosis, Treatment

A

o Meconium impaction

Clinical SIgns
* w/in 12-24hrs of birth
* decreased suckling & depression
* variable pain & abdominal distension

Diagnosis
* Digital rectal exam
* Gas distended colon
* Presumptive

Treatment
* Warm soapy enema (best)
* Acetylcysteine retention enemas
* Repeated enemas may be needed
* Oral laxatives and/or fluids
* Intravenous fluids
* Pain control; flunixin (1/day) or butophanol

68
Q

What is Meconium

A
  • First feces passed by the foal 

  • Composed of bile, mucus, epithelial cells 

  • Dark brown to black in color 

  • Colostrum has a laxative effect that can help with meconium passage 

69
Q

Lethal White Syndrome; Cause, Clinical Signs, Treatment

A

Cause
* Autosomal recessive 

* Mutation in endothelin B receptor gene 

* Lack of submucosal and myenteric ganglia 

* Both parents are frame overo pattern 


Clinical signs
* Foal is all white
* Colic soon after birth

Treatment
* None

70
Q

Clostridium Perfringens Type A Vs Type C

A

Type A
* Present in feces of normal foals by 6 days 

* Clinical relevance is questionable 

* Produces alpha toxin 

* Isolates expressing enterotoxin
* netF toxin may be associated with necrotizing enterocolitis 


Type C
* Uncommon in feces of normal, healthy foals 

* Produces beta toxin -> Inflammation, necrosis, increased 
capillary permeability 

* Enterotoxin and beta-2 toxin may be associated with more severe disease 


71
Q

Clostridium Perfringens Type C Pathogenesis

A
  • Beta toxin is trypsin sensitive 
->
  • Antiprotease activity in colostrum/milk may prevent inactivation of toxin 
->
  • Disease may be more prevalent in foals with good passive transfer 

72
Q

Clostridium Difficile in Foals

A

o Produces at least 5 toxins
o Toxin A (enterotoxin) – increases permeability
o B (cytotoxin) – cytotoxic to mucosal epithelium & exacerbates inflammatory response
o Uncommon in feces of normal foals

73
Q

Foal Infectious Ds; Diagnosis, Treatment

A

Diagnosis Foal Ds
o Consider sepsis & offer referral
o PCR panel for foal Ds pathogens detects organisms & toxins
o CBC Chem
o Abdominal ultrasound
o Hemorrhagic diarrhea (poor prognosis)

Treatment
o Refer!
o Broad-spectrum antimicrobials
o Metronidazole if clostridiosis suspected 

o Fluid, electrolyte, acid-base support 

o Colloids – e.g., plasma 

o Biosponge – smectite clay 

o Nutritional management
o Diaper rash ointment

74
Q

Foal Heat Diarrhea; Basics, Mechanism

A

o Most Common Cause of Diarrhea in Foals 

o Normal physiologic phenomenon 

o Occurs 7-12 days post partum 

o Same time as mare’s post foaling estrus 

o Occurs in orphan foals as well 

o Self limiting, foal remains systemically healthy! 


Mechanism:
* hypersecretion into small intestine 
overwhelms absorptive capacity of immature colon 

* Most likely due to changing of microbiome

75
Q

Uroperitoneum; Causes, Pathogenesis, Clinical Signs, Diagnosis

A

Causes
* Ruptured urinary bladder
* Ruptured urachus

* Ruptured ureter

* Ruptured urethra

Pathogenesis
* Rupture during parturition – often dorsal bladder

* Necrosis and rupture after parturition – anywhere!

Clincal Signs
* Free peritoneal fluid
* Collapsed bladder
* Hyponatremia
* Hypochloridemia
* Hyperkalemia

Diagnosis
* Fluid:serum creatinine ratio >2

76
Q

Signs of Generalized Vs Partial/Focal Seizures

A

Generalized
* Opisthotonus
* Paddling
* Extensor rigidity

Focal
* “chewing gum”
* muscle tremors/twitches
* may remain standing

77
Q

Perinatal Asphyxia Syndrome; Pre-partum causes, Parturition Causes, Foal Clinical Signs

A

Pre partum Causes
* Reduced maternal O2 (cardiopulmonary disease or anemia)
* Reduced uterine blood flow (hypotension, systemic illness)
* Placental disease (placentitis, twins)
* Reduced umbilical blood flow

Parturition Causes
* Dystocia
* Premature placental separation
* Induced labor
* C-section
* Prolonged stage 2 labor
* Premature rupture of the umbilical cord

Foal Clinical Signs
* Prematurity/dysmaturity
* Prolonged recumbency
* Thoracic disease
* Sepsis

* Anemia
* Cardiovascular disease
* Neuro signs
* Basically anything

78
Q

Perinatal Asphyxia Syndrome; Type 1 & 2, Diagnosis, Treatment

A

Type 1 & 2
* 1 – born normal; signs w/in 48hrs
* 2 – born abnormal

Diagnosis
* Clinical signs
* Usually septic as well

Treatment
* Diazepam for acute seizures!
* Nutritional/fluid support
* CNS support
* Tissue oxygenation
* Seizure control
* Prevention of sepsis
* Nursing care for decubital ulcers, corneal ulcers, aspiration pneumonia, self-injury

79
Q

Bacterial Meningitis; Clinical Signs, Diagnosis, Treatment, Prognosis

A

Clinical Signs
* Often in septic foals
* Cerebral or spinal signs w/ pain
* Rapidly progress to seizures

Diagnosis
* CSF analysis

Treatment
* Broad spectrum antibiotics

Prognosis
* Poor

80
Q

Metabolic Neurologic Dysfunction in Foals

A

Hyponatremia (< 120 mEq/dL)
* Cerebral edema

Hypernatremia (> 160 mEq/dL)
* Cerebral dehydration

Hypocalcemia / hypomagnesemia
* Tetany, rigidity

Hypoglycemia
* Obtunded, seizures

Metabolic acidosis

81
Q

Congenital Hypothyroidism Dysmaturity; Clinical Signs, Risk Factors, Treatment, Prognosis

A

Clinical Signs
* Prolonged gestation
* Mandibular prognathism (underbite)
* Contracted tendons
 +/- ruptured extensor tendons
* Delayed ossification of cuboidal bones
* Hernias, poor muscle development

Risk Factors
* Mustard plants
* Nitrates
* Lack of mineral sup

Treatment
* Support

Prognosis
* Guarded

82
Q

Reasons for Increased Bilirubin in Foals

A

Pre-hepatic
* Mild is normal in neonates
* Neonatal isoerythrolysis

Hepatic
* Tyzzer’s disease
* Equine herpesvirus I
* Septicemia

* Iron toxicity
* Drug-related
* Asphyxia

Post-hepatic
* Gastroduodenal ulcer disease
* Biliary atresia
* Hepatic abscess

83
Q

Neonatal Isoerythrolysis; Pathophysiology, Clinical Signs, Diagnosis, Treatment

A

Pathophysiology
* 1st pregnancy foal inherits RBC antigen from sire ->
* mare sensitized to antigen & produces Ab ->
* 2nd pregnancy Abs concentrated in colostrum ->
* foal ingest colostrum ->
* Abs coat RBCs ->
* Hemolysis & agglutination
* Mule foals at very highrisk due to “donkey factor”

Clinical Signs
* Decreased suckle
* Tachycardia & tachypnea
* Weakness/lethargy
* Hematuria
* Icterus

Diagnosis
* 1-5d old
* clinical signs
* cross-matching
* jaundice foal agglutination
* blood typing / Ab typing
* Coomb’s test

Treatment
* Support
* Transfusion
* Allow foal to suckle after 12 hours if mare is well stripped

84
Q

PPID; Pathophysiology, Signalment, Clinical Signs, Diagnosis, Treatment, Side Effects of Treatment

A

Pathophysiology
* Degeneration of dopaminergic neurons in hypothalamus
* Slow & progressive

Signalment
* Old horses

Clinical Signs
* Hypertrichosis (hairy)
* Lightening hair coat
* Delayed shedding
* Laminitis
* Increased infections
* Fat
* High FEC/g
* Increased endorphins = chill
* PU/PD
* Neuro signs (less common)
* Abnormal lactation
* Muscle wasting

Diagnosis
* Baseline ACTH (slightly high normally in winter)
* TRH stimulation Test
* Assess insulin

Treatment
* Pergolide - dopamine agonist (Prascend)
* Lifelong dz

Side Effects of Treatment
* Anorexia
* Diarrhea
* Lethargy

85
Q

Thyroid Adenoma

A

o Common in older horses
o Uni or bilateral
o Moveable not painful mass on throat
o Does not produce hormones
o Benign
o Monitor over time

86
Q

Equine Metabolic Syndrome; Pathophysiology, Clinical Signs, Diagnosis

A

Pathophysiology
* Insulin dysregulation
* Hyperinsulinemia

Clinical Signs
* Normal diet w/ Abnormal fat deposition
* Laminitis
* Tachycardia
* Hypertension
* May have preputial/mammary edema, lipoma, subfertility
* Maybe hyperglycemia, hypertriglyceridemia

Diagnosis
* Basal insulin
* Basal glucose
* Oral sugar test (best test)
* Insulin tolerance test (look for <50% decrease glucose)
* Serum leptin

87
Q

Equine Metabolic Syndrome; Management

A
  • No grazing, grain, treats
  • Hay 1.5% BW
  • Slow feeder
  • Hay <10% NSC
  • Soak hay 60 mins
  • Mineral-vitamin low sugar balance
  • Exercise

If no response to diet
* Levothyroxine (gradually discontinue)
* Metformin hydrochloride
* Sodium-glucose co-transporter 2 inhibitors

88
Q

Hyperinsulinemia Associated Laminitis Pathophysiology

A

o Prolonged hyperinsulinemia ->
o Chronic laminitis ->
o Laminae stretch and damage ->
o Hoof rings

89
Q

Monovalent Vs Multivalent Vaccines

A

Monovalent
* Single dz
* Less reactions

Multivalent
* One shot against multiple dzs
* More likely to have rxn

90
Q

Common Multivalent Vx in Horses

A

“Four-way”
* Equine influenza
* EEV
* WEV
* Tetanus


“Five-way”
* Above + equine herpesvirus (rhinopneumonitis) 


“Six-way” or more!
* Above + West Nile virus and others

91
Q

Core Equine Vxs

A

o Tetanus

o Rabies
o West Nile virus
o Eastern equine encephalomyelitis
o Western equine encephalomyelitis

Equine Med (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions