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Exam 3 Flashcards

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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

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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

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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

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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

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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

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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

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7
Q

Tetrahydropyrimidines

A

o Can cause irreversible rigid paralysis
o Only treats adult parasites

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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

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9
Q

Isoquinolones; drug, use

A

Drug
• Praziquantel

Use
• Tapeworms

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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

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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.

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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

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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

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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

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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

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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

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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

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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

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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

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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

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21
Q

Urethral Stones; Clinical Signs, Diagnosis, Treatment

A

Clinical Signs
* Dysuria
* Colic

Diagnosis
* Endoscopy

Treatment
* Remove w/ endoscopy
* Perineal urethrostomy

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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

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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

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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

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25
Acute Renal Failure; Clinical Signs, Diagnosis, Treatment
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
26
What is considered Polyuria
o >50ml/kg/d o ~25L urine/d
27
Primary Vs Secondary Polydipsia
Primary * Psychogenic * Most common * Hyposthenuria * Normal physical exam * Medullary washout Secondary * Renal failure -> azotemia * PPID * Systemic dz (sepsis) * Diabetes insipidus (less common)
28
Polydipsia Diagnosis
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
29
Chronic Renal Failure; Diagnosis, Clinical SIgns, Treatment
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
30
Chronic Renal Failure; Congenital Vs Acquired
Congenital * <5yp * no ARF * renal agenesis, hypoplasia, dysplasia Acquired * Most common * Previous injury * Cause may be unknown
31
Muscle Responses to Injury
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
32
Exertional Rhabdomyolysis (Tying Up); Clinical SIgns, Diagnosis, Recovery, Treatment
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
33
Recurrent Exertional Rhabdomyolysis; Signalment, Diagnosis, Management, Treatment
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)
34
Polysaccharide Storage Myopathy (PSSM1); Pathophysiology, Signalment, Clinical Signs, Diagnosis
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
35
Polysaccharide Storage Myopathy (PSSM2); Pathophysiology, Signalment, Diagnosis, Management
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
36
Myofibrillar Myopathy (MFM); Clinical signs, Diagnosis, Management
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)
37
Myosin Heavy Chain Myopathy (MHCM); Pathophysiology, Signalment
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
Immune mediated Myositis; Clinical Signs, Diagnosis, Treatment, Management, Prognosis
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
Non-exertional Rhabdomyolysis; Clinical Signs, Diagnosis, Treatment, Prognosis
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
Glycogen Branching Enzyme Deficiency; Signalment, Clinical Signs, Diagnosis
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
Acepromazine
o Used for tying up horses o Increase blood flow to muscle o Decreases anxiety
42
Hyperkalemic Periodic Paralysis; Signalment, Clinical Signs, Bloodwork
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
Hyperkalemic Periodic Paralysis; Triggers, Diagnosis, Management
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
Hyperkalemic Periodic Paralysis; Treatment of Mild Vs Severe
Mild * Feed grain or corn syrup -> insulin release -> K into cell * Light exercise Severe * Ca gluconate + dextrose slowly -> move K into cell * Tracheostomy
45
White Muscle Dz; Cause, Clinical Signs, Diagnosis, Treatment
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
Clostridium myonecrosis; Clinical Signs, Cause, Diagnosis, Treatment
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
Normal Gestation & Parturition
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
Normal Timing for Foals
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
Signs of Immaturity or Dysmaturity
o Low birth weight o Domed forehead o Short silky hair o Pliant ears and soft lips o Flexible limbs
50
Foal Vitals
o T = 100-102 o HR >60BPM at birth, 70-100 in first hour o RR = 60-80 at birth, 20-40 later
51
Colostrum
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
Failure of Passive Transfer & IgG Testing
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
Was there failure of passive transfer?
o Test all foals at 18-36hrs o Look for IgG > 800 o Partial failure = 400-800 o Complete Failure <400
54
Plasma Transfer Due to Failure of Passive Transfer
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
Plasma Transfer Due to Failure of Passive Transfer; Adverse Reactions
* Muscle fasiculations * Tachycardia * Tachypnea * Pyrexia * colic
56
Nursing Behavior & Amount of Milk Needed
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
Umbilical Care
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
Umbilical Remnant Infection; Structures involved, Diagnosis, Treatment
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
Umbilical Hernias
o Small hernias are common! 
 o little or no treatment 
 o Occasionally require surgery 
 o Ultrasound if suspicion of bowel entrapment and colic
60
Patent Urachus; Basics, Treatment
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
Biochemistry Panel for Foals & Abnormal Elevations
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
Neonatal Septicemia; Pathophysiology, Routes of Infection, Risk Factors
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
Neonatal Septicemia; Common Bacteria, Diagnosis, Treatment
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
Neonatal Septicemia; Clinical Signs
<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
Cleft Palate; Basics & Treatment
o Clefts in soft palate are most common but always digitally palpate hard palate o Often causes pneumonia Treatment * Surgery or euthanasia
66
Diagnostic Approach to Colic in Neonatal Foal
o Look for evidence of sepsis o Nasogastric intubation o Digital rectal exam o Ultrasound!! o Rads o Abdomenocentesis
67
Most Common Cause of Colic in Neonates; What? Clinical Signs, Diagnosis, Treatment
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
What is Meconium
* 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
Lethal White Syndrome; Cause, Clinical Signs, Treatment
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
Clostridium Perfringens Type A Vs Type C
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
Clostridium Perfringens Type C Pathogenesis
* 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
Clostridium Difficile in Foals
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
Foal Infectious Ds; Diagnosis, Treatment
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
Foal Heat Diarrhea; Basics, Mechanism
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
Uroperitoneum; Causes, Pathogenesis, Clinical Signs, Diagnosis
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
Signs of Generalized Vs Partial/Focal Seizures
Generalized * Opisthotonus * Paddling * Extensor rigidity Focal * “chewing gum” * muscle tremors/twitches * may remain standing
77
Perinatal Asphyxia Syndrome; Pre-partum causes, Parturition Causes, Foal Clinical Signs
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
Perinatal Asphyxia Syndrome; Type 1 & 2, Diagnosis, Treatment
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
Bacterial Meningitis; Clinical Signs, Diagnosis, Treatment, Prognosis
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
Metabolic Neurologic Dysfunction in Foals
Hyponatremia (< 120 mEq/dL) * Cerebral edema Hypernatremia (> 160 mEq/dL) * Cerebral dehydration Hypocalcemia / hypomagnesemia * Tetany, rigidity Hypoglycemia * Obtunded, seizures Metabolic acidosis
81
Congenital Hypothyroidism Dysmaturity; Clinical Signs, Risk Factors, Treatment, Prognosis
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
Reasons for Increased Bilirubin in Foals
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
Neonatal Isoerythrolysis; Pathophysiology, Clinical Signs, Diagnosis, Treatment
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
PPID; Pathophysiology, Signalment, Clinical Signs, Diagnosis, Treatment, Side Effects of Treatment
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
Thyroid Adenoma
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
Equine Metabolic Syndrome; Pathophysiology, Clinical Signs, Diagnosis
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
Equine Metabolic Syndrome; Management
* 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
Hyperinsulinemia Associated Laminitis Pathophysiology
o Prolonged hyperinsulinemia -> o Chronic laminitis -> o Laminae stretch and damage -> o Hoof rings
89
Monovalent Vs Multivalent Vaccines
Monovalent * Single dz * Less reactions Multivalent * One shot against multiple dzs * More likely to have rxn
90
Common Multivalent Vx in Horses
“Four-way” * Equine influenza * EEV * WEV * Tetanus 
“Five-way” * Above + equine herpesvirus (rhinopneumonitis) 
 “Six-way” or more! * Above + West Nile virus and others
91
Core Equine Vxs
o Tetanus
 o Rabies o West Nile virus o Eastern equine encephalomyelitis o Western equine encephalomyelitis

Equine Med (3 decks)

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