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H2 Flashcards

1
Q

What are some potential causes of large colon impaction? Where is the most common site for it?
What is the most effective way of managing it?

A
  1. Diet related (High starch/ low fibre; lack of pasture)
  2. Reduced fluid intake
  3. Fibrous/ poor quality feed/ poor dentition
  • Pelvic flexure
  • Enteral fluids (increases luminal fluid and stimulates gastrocolic reflex): 6-8L/ 500kg q. 2 hours+ pain relief
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2
Q

What are some common risk factors for GIT dysmotility?

A
  1. Dietary manipulation (eg. pH, hydration, froth. Want to aim for >70% slowly fermented fibre <30% cereal)
  2. Intensive or no exercise
  3. Parasitism
  4. Stable mngt
  5. Stereotypic behaviour/ stress
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3
Q

What is the proposed cause of gastric ulceration? Are squamous or glandular mucosa ulcers more clinically relevant? Whatare some options for tx/ mngt?

A

High concentrate/ low roughage diet-> acidification of gastric contents-> protective mat of roughage is lost

  • squamous
  • PPI (omeprazole 1x daily) OR H2 antagonists (ranitidine 2-3 x daily) OR sucralfate. Also can increase roughage or grass turnout
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4
Q

What is anterior enteritis? Can it be managed medically?

A

=infl of proximal SI-> hypomotility> fluid accumulation (maybe due to Clostridial or high concentrate feed?). Will see large volumes of reflux soon after the onset of colic. Reflux will relieve pain.

Can be managed medically most of the time (AIs, IV fluid 60L/d, reflux to decompress stomach, +/- metronidazole, monitoring with US, +/- electrolyte supp)

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5
Q

What are some ddx for acute colitis in adult horses? (What are some complications?)

A
  1. Bacterial (Salmonella, Clostridium),
  2. Antibicrobial-associated colitis,
  3. potomac horse fever,
  4. Coronavirus,
  5. cyathostomiasis,
  6. grain overload,
  7. right dorsal colitis

(Laminitis, coagulopathy, hypertriglyceridaemia, rectal prolapse)

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6
Q

What are some potential complications of colic sx?

A 
Post-op ileus
Adhesions
Anastamosis breakdown
Stricture
Colic
Peritonitis, haemorrhage, endotoxaemia
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7
Q

Endotoxaemia is a potential complication follwoing colic surgery. How might you treat it?

A 
IV fluids
CV support
Hyperimmune plasma (?)
Polymixin B
Sole support/ ice boots (to prevent laminitis)
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8
Q

Adhesions occurring after a colic surgery may start to show clinical disease after how long?

A

5 days to many years (minimise handling)

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9
Q

How might you manage ileus post colic surgery?

A

Reflux, Fluids, AIs, monitor with US

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10
Q

How long does it take for the linea alba to reach full strength following colic sx? Based on this how long should you confine horses?

A

12 weeks

Box confinement for 4-6 weeks then a small yard for another 4-6 weeks

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11
Q

What are some potential complications of acute colitis?

A
  1. Laminitis
  2. Coagulopathy (consequence of SIRS)
    (3. Rectal prolapse)
    (4. Hypertriglyceridaemia)
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12
Q

What tx would you provide for a horse with acute colitis?

A

SUPPORTIVE.

  • Isolation
  • IV crystalloid fluids
  • Anti-inflammatories
  • Analgesia
  • Ice boots (prevent laminitis)
  • Anti-diarrhoeals (di-tri-octahedral smectitie)
  • Probiotics? (Saccharomyces boulardii)
  • Anti-endotoxin tx??? (hyperimmune plasma, plymixin B, pentoxyfylline)
  • ABs (only if severely leukopenic, if PHF or if clostridials)
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13
Q

At what age might we expect horses to have a full set of permanent dentition?

A

~5 years of age (premolars and molars grow at 2-3mm per year)

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14
Q

At what age do we expect tooth caps to come off?

A

2-4 years old

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15
Q

What treatment options are there for acute colitis in foals?

A
  • IV fluids (replacement crystalloids)
  • Plasma
  • Systemic ABSs
  • Antidiarrhoeals
  • gastroprotectants (omeprazole?)
  • Allow to nurse vs. withholding from mare
  • Topical barrier tx (minimise scalding)
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16
Q

What are some ddx for chronic diarrhoea in a horse?

A
  1. RDC
  2. Sand enteropathy
  3. Cyathostomiasis
  4. IBD
  5. Alimentary lymphosarcoma
  6. Equine proliferative enteropathy
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17
Q

What are the 4 recognised types of IBD in horses?

A
  1. Granulomatous enteritis
  2. Lymphocytic-plasmacytic enterocolitis
  3. Eosiniophilic enterocolitis
  4. Multisystemic eosinophilic epitheliotropic disorder
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18
Q

When do we see mass emergence of small strongyles (Cyathostomins) in horses?

A

Late winter to early spring

Late summer to early autumn

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19
Q

Where do cestodes normally attach in the horse?

A

Ileocaecal valve

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20
Q

What are the main pathogenic worms in equids?

A

Small strongyles (cyathostomins)
Ascarids (Parascaris)
Tapeworms (anoplocephalans)

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21
Q

What are some limitations of FECs in horses?

A
  • not reflective of encysted larvae population
  • don’t correlate with numbers of adults
  • egg shedding may be intermittent
  • detection limit of technique
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22
Q

What is the difference between BZs and MLs mechanism of action on worms?

A

MLs- paralytics (no use on encysted larvae)

BZ- interferes with metabolism

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23
Q

What are the goals of selective deworming?

A

Prevent parasitic disease by:
1. minimising pasture contamination (through reducing the numbers of eggs laid by adult worms, and
also where possible removal of faeces before eggs develop to infective L3 larvae)
2. preservation of the refugia.

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24
Q

What are some criteria indicative of blood transfusion in horses?

A

Acute anaemia PCV <12%
Chronic anaemia PCV <8-10%
PCV drop to 18-24% in 24 hr period or less

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25
Q

What are some treatment options for urogenital haemorrhage in a mare post foaling? What are some DDx for post foaling colic?

A

Analgesia
IV fluids (isotonic crystalloids 40-80 ml/kg and hypertonic fluids 4-6 ml/kg)
BS antibiotics (?)
Keep mare quiet
Anti-fibrinolytics (tranexamic acid, formalin)

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26
Q

What is the difference between a major and minor cross-match?

A

Major: donor RBCs and recipient serum

Minor vice versa

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27
Q

What are some potential adverse reactions to blood transfusion?

A

Potential for disease transmission
Potential fatal (blood type polymorphism)
recipients rapidly develop Abs to transfused RBSc
Impairs bone marrow response to anaemia by blunting pdn of EPO

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28
Q

What is the most common cause of liver disease in horses?

A

PA toxicity (senecio spp and echium)

29
Q

What events may lead to a mare being classified as high risk? (think about historical, pre-partum and peri-partum events)

A

Historical events:

  • Repeated breeding or previous premature termination of pregnancy
  • Previous dystocia
  • Prolonged pregnancy
  • Premature placental separation or placentitis
  • Previous sick foals

Pre-partum events:

  • Premature lactation
  • Recurrent colic or disease during lactation
  • Excessive abdo enlargement
  • Prolonged gestation

Peri-partum events:

  • Dystocia
  • Meconium staining of the foetus
  • Premature placental separation
  • Delivery without adequate udder dvpt
  • Abnormalities of the placenta
30
Q

What might persistent bradycardia in the neonate be due to? How about persistent tachycardia?

A

Hypothermia, hypoglycaemia or hypoxaemia

Congenital cardiac defect

31
Q

How does acute resuscitative fluid therapy work?

A

Give 20ml/kg as bolus over 30-60mins IV
Assess vascular volume and tissue perfusion. Can repeat bolus 3-4 times (up to 60-80ml/kg). After this, if vascular volume is adequate but tissue perfusion isn’t, may need to consider inotrope or vasopressor therapy

32
Q

What are potential complications of fluid therapy in a foal?

A
  1. Catheter site infections and thrombophlebitis
  2. Electrolyte derangements (replacement fluids provide more Na and less K than needed)
  3. Neurologic consequences? (Na concentrations should not be changed by more than 10-12mmol/L over 24hours)
  4. Pulmonary oedema
33
Q

What is the most common bacterium isolated from blood cultures of septic foals?

A

E. coli

34
Q

By what time point should meconium be passed in the foal? What is meconium? What are some risk factors?

A

24-36hours

Glandular secretions from GI tract, amniotic fluid and cellular debris

Hypoglycaemia or sympathomimetics-> hypomotility

35
Q

How might you treat a meconium impaction?

A
  • Fleet enema (or retention enema with acetylcysteine)

- analgesia/ muscle relaxant (diazepam or butorphanol and buscopan)

36
Q

What is lethal white foal syndrome?

A

frame overo dam and sire-> foal with severe irreversible ileus due to lack of myenteric innervation. Colon is narrow or absent

37
Q

Why do ascarids impactions have a poor prognosis?

A 
Ascarids release toxins
inflammation from surgery
Prolonged ileus is common
High risk adhesions
Foals are often unthrifty
38
Q

How might you medically manage an ascarid impaction in a 3-5 month old foal?

A
  1. encourage them to pass via enteral fluids or oil
  2. provide anti-infl (flunixin)
  3. decompressio of fluid build up via NGT
  4. IV fluid support
39
Q

What is a pathognomonic sign of intussusception? Where are most common sites of occurrence?

A

target lesion on ultrasound

Jejunojejunal, ileocaecal or caecocolic

40
Q

What are potential consequences of gastroduodenal ulceration in foals? What are some risk factors?

A

bowel can stricture during healing causing outflow obstruction after the initial ulceration

Risk factors: physiologic stress, hypoxia, illness; long time between feeds; NSAIDs

41
Q

To confirm a uroabdomen in a foal via abdominocentesis, what parameter do you look for?

A

Peritoneal fluid [creatinine] equal to or more than 2x plasma [creatinine]

42
Q

How might you stabilise a foal with urabdomen that has a ohyperkalaemia?

A
  1. IV fluids (dilution)
  2. IV glucose (destrose)-> stimulates endogenous response
  3. Exogenous insulin (+ dextrose infusion)
  4. Sodium bicarbonate (alkalosis-> intracellular K movement)
43
Q

What is the plasma [Na+] and [K+] in horses?

A 
Na= 133-145mmol/L
K= 3-5mmol/L
44
Q

Where is the most common site of bladder rupture in a foal?

A

dorsal bladder wall

45
Q

What are some ECG changes that might suggest that increased K levels are having a significant effect?

A
  1. Widening and lowering of amplitude followed by inversion and final disappearance of the P waves
  2. increase T wave amplitude
  3. Increased in QRS interval with some irregularity in ventricular rate
  4. Periods of cardiac arrst that become terminal or are followed by ventricular fibrillation
46
Q

How do NSAIDs cause Acute renal damage?

A

inhibit PGEs and PGI2-> loss of vasodilation and ischaemic injury-> medullary crest necrosis

47
Q

What are some causes of chronic kidney disease?

A
  1. Prolif glomerulonephritis (type 3 HS)
  2. Chronic interstitial neohritis
  3. Pyelonephritis
  4. Other ( amyloidosis, polycystic kidneys, neoplasia)
48
Q

What clin path findings might you see with CKD? what are the common presenting complaints?

A
  • azotaemia
  • hyperCa
  • +/- hypermagn.
  • Isosthenuria
  • clear urine

weight loss, PU/PD, poor performance (look out for dental tarta and ventral oedema)

49
Q

How might CKD be managed?

A
  • adequate hydration,
  • salt supp
  • diet
  • monitor, maintain appetite
  • ABs if pyeloneph.
50
Q

What are some ddx for gross haematuria?

A
  1. idiopathic renal haematuria (think arabians)
  2. renal calculi
  3. neoplasia
  4. cystic calculi
  5. urethral haemorhhage
51
Q

What is idiopathic renal haematuria ?

A

Dx of exclusion. See signs of blood loss and horse is generally not azotaemic. Arabians

52
Q

What are common neoplasia in kidneys of horses? how about the bladder?

A

Adenocarcinomas, renal cell carcinoma

  • nephroblastoma
  • secondary neoplasia (adenoma, lymphosarc, haemangiosarc, melanoma)

SCC and TCC

53
Q

How might you prevent cystic calculi?

A

Grass hay diet
Urinary acidification
Increase water consumption

54
Q

What are some ddx for urinary incontinence?

A
  1. cystic calculi
  2. sabulous urolithiasis-> bladder paralysis and incomplete emptying
  3. UTI (urinalysis >20 orgs/ HPF and> 10 WBCs/HPF))
  4. Neurologic causes (LMN lesions, EHV- 1 myelitis, cauda equina neuritis)
  5. Ectopic ureter
55
Q

How might you diagnose and tx sabulous urolithiasis?

A

Dx: palpation per rectum, cystoscopy, US
Tx: bladder catheterisation and lavage; prokinetics (bethanechol)
guarded px.

56
Q

What are some causes of PUPD in horses?

A

Commonly:

  • renal failure
  • PPID
  • Psychogenic PD
  • Iatrogenic

Rare:

  • DM
  • DI
57
Q

What is pergolide mesylate? What may be used as an adjunct treatment?

A

Dopamine antagonist used in the treatment of PPID. Start at 2ug/kg SID

Cyproheptadine (serotonin antagonist)

58
Q

In what ways can you measure insulin dysregulation in horses with equine metabolic syndrome?

A
  1. Basal plasma insulin conc. (likely if >50 uIU/ml. Normal is <20)
  2. Oral (in feed) glucose tolerance test (>80-90 uIU/ml)
  3. Oral sugar test (>45uIU in NA)
  4. Insulin tolerance test (<50% reduction from baseline after glucose admin)
59
Q

What is the difference between hyperlipidaemia and hyperlipaemia?

A

Hyperlipidaemia:

  • increase triglycerides (<500 or 5.5)
  • No gross lipaemia
  • No hepatic lipidosis

Hyperlipaemia:
-Increased triglycerides (>500)
Gross lipaemia
- May head to hepatic lipidosis

60
Q

What are the signs of anyhydrosis?

What are risk factors? What are some management factors?

A

Acute: (no cutaneous signs)

  • Increased HR, RR and temp
  • Fever
  • Panting and nostril fare at rest
  • Lack of sweating
  • Death

Chronic:

  • Poor performance
  • Patchy dry coat after exercise
  • Flaky/scurfy skin (forehead)
  • Hair loss (face, chest) over time
  • PU, PD
  • Poor appetite
  • Loss of condition

Moving from temperate to hot humid climate; horses native to hot country

Management: move to cooler climate, reduce grain/ protein in diet, no strenuous exercise in heat, ensure well hydrated

61
Q

What are clinical signs of EMS?

A
  1. Generalised obesity (7/9 or greater)
  2. Regional adiposity
  3. Cresty neck
  4. Laminitis (+/- founder lines)
62
Q

What are some typical clin path findings of starving horses?

A
  • anaemia
  • lymphopenia
  • decreased TP, albumin, phosphate, magnesium, BUN
  • increased TG, Br, NEFA
63
Q

What are some risk factors of refeeding syndrome?

A
  • BCS of <3.5/9 and an unknown dietary history
  • Faster for > 5-10 days
  • lost >10% body weight over <2months
  • hepatic lipidosis
64
Q

Which breeds are predisposed to congenital ventricular septal defect?

A

Welsh Mountain Ponies
SBs
Arabians

65
Q

What are some arrhythmias that are common in athletic horses and are “normal”?

A

Second degree AV block
Sinus arrhythmia
Sinoatrial block

66
Q

What is quinidine? How does it work? What are CIs?

A

Treatment for atrial fibrillation. Prolongs action potential and lengthens myocardial cell refractory period

CIs: complex VPCs, rapid ventr. rate, CHF

67
Q

What are some PM findings of ionophore toxicosis? What are some tx options?

A

Pale myocardium
Subendocardial haemorrhage
Myocardial necrosis

Tx (supportive):
Activated charcoal
Correct electrolyte abnormalities
DIGOXIN CONTRAINDICATED

68
Q

How do tetanus and botulism toxins differ in their intracellular signalling?

A

Both bind receptors on pre-synaptic membrane of the NMJ. Botulism toxin mostly remains at NMJ. It blocks the release of Ach-> flaccid paralysis.
Tetanospasm (tetanus toxin) is transported to spinal cord. Enters renshaw cells to block release of inhibitory neurotransmitters by that interneuron-> disinhibition of the gamma-motor neuron

69
Q

What are some clinical signs of CN IX and X dysfunction?

A

Dysphonia (snoring and roaring)
Dysphagia
Regurg

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