Brainscape's Knowledge GenomeTM

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


See full index

GI2 > Equine 5 > Flashcards

Equine 5 Flashcards

1
Q

What broad age groups are horses classed into

A

neonatal foals <1mo
older foals and weanlings 1-9mo
adults >9mo

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

list the differentials for diarrhoea in foals

A
  • foal heat diarrhoea
  • necrotising enterocolitis
  • neonatal sepsis
  • viral diarrhoea (rotavirus)
  • bacterial diarrhoea (clostridia)
  • parasitic diarrhoea (s. westeri)
  • cryptosporidium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the presentation of foal heat diarrhoea

A

5-14 days old
mild, self limiting diarrhoea
foal remains bright and suckling
normothermic (mean 38.3 degrees)

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

what is the pathogenesis of foal heat diarrhoea

A

likely a change in GI function or diet

unlikely that it is due to changes in dam’s milk

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

what is the diagnosis and treatment of foal heat diarrhoea

A

diagnosed on history and clinical signs

no treatment required

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

which foals are affected by rotavirus

A

all (highly infectious, common cause of diarrhoea). especially those housed in large groups with their dams
usually 7-28days old

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

what is the pathogenesis of rotavirus

A

invade epithelial cells lining the intestinal villi
cell death and blunting of villi
maldigestion through loss of intestinal enzymes
malabsorption through loss of surface area

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

what are the clinical signs of rotavirus

A
  • anorexia
  • depression
  • profuse, watery diarrhoea
  • hypovolaemia (not all)
  • electrolyte derangements (not all)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how is rotavirus diagnosed

A

faeces - PCR, EM, ELISA

all low sensitivity, virus will be diluted if faeces is largely water

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

how is rotavirus treated

A 
vaccination of mares 
supportive therapy
- IVFT (sometimes oral) 
- PPN
- sucralfate 
- vaseline/sudocreme around perineum 
- plasma and antibodies in young foals to prevent secondary infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how is rotavirus prevented

A

colostrum - use a SNAP test to check IgG concentrations in outbreak scenario

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

what are the most common bacterial causes of diarrhoea in foals and adults

A

Clostridium perfringens and difficile

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

what are the clinical signs of bacterial diarrhoea in foals

A 
colic 
hypovolaemia 
profuse, smelly, watery diarrhoea - sometimes red-tinged, haemorrhagic diarrhoea particularly with C perfringens A --> hypovolaemia and hypoproteinaemia 
anorexia 
depression 
SIRS
ventral oedema eventually due to low protein 
low Na, K and Cl 
metabolic acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how is bacterial diarrhoea diagnosed

A

in foals <7 days always rule out sepsis with blood culture
faecal ELISA or PCR for toxin (bacteria is ubiquitous)
ultrasound of SI

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

how is bacterial diarrhoea in foals treated

A

IVFT
broad spectrum parenteral antibiotics (IV TMPS/oxytet/penicillin)
hospitalisation
vaseline around perineum
occasional - whole blood transfusion or plasma if lots of protein lost through GIT
faecal transfaunation - anecdotally effective
steroids if no improvement in diarrhoea

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

what percentage of sick foals with diarrhoea will be septic

A

50% - always assume they are

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

other than clostridia, what other bacterial agent causes diarrhoea in foals

A

E coli - not as important as in farm animals and hard to know if pathogenic or commensal

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

describe a Strongyloides westeri infection in foals

A

transmammary transmission close to birth
signs at 8-12 days old
mild, self-limiting diarrhoea
often ignore
responds to deworming with BZ or avermectins but unnecessary

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

list the differentials for diarrhoea in weanlings

A

Lawsonia intracellularis
Rhodococcus equi
strongylus vulgaris
all adult diseases

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

how does lawsonia intracellularis (proliferative enteropathy) present in weanlings

A 
2-8months old 
depression 
rapid and significant weight loss 
subcutaneous oedema 
diarrhoea 
colic 
poor hair coat 
pot-belly 
severe hypoalbuminaemia 
increased WBCs
anaemia of chronic disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

describe the diagnosis of lawsonia intracellularis

A

difficult to get a definitive diagnosis
clinical signs, low albumin, rule out other causes
marked SI thickening on abdominal US
faecal PCR is insensitive

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

how is lawsonia intracellularis treated

A

oxytetracycline IV BID
if brighter and diarrhoea not as severe can use doxycycline PO BID
other - erythromycin, clarithromycin, azithromycin PO +/- rifampin to intracellularise antibiotic
colloidal support - plasma

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

describe the presentation of strongylus vulgaris in weanlings

A

6mo and over (lifecycle = 6-9m)
rare due to avermectin use
signs due to L4 migration through arterioles of caecum and descending colon - colic, SIRS, sick horse

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

how is strongylus vulgaris diagnosed and treated

A

difficult unless taken to surgery
clinical exam, history clinical pathology, FEC (but can’t rule out if negative)
treatment = avermectins when foals start to be exposed to eggs

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

how does rhodococcus equi present in weanlings

A

2-4mo
enteric infection - fever and diarrhoea
intra-abdominal abscess (bastard form) - fever and colic
respiratory form (more common) - high RR, cough, ill-thrift

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

describe the lifecycle of rhodococcus equi

A

excreted in dam’s faeces
build up on pasture in warm, dry or wet conditions
ingested by weanling
colonises white blood cells intracellularly
abscessation occurs primarily in the lungs

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

how is rhodococcus equi treated and what are the side effects

A 
rifampin PO plus macrolide 
or 
erythromycin estolate PO 
side effects 
- hyperthermia (erythromycin)
- diarrhoea in dam (macrolides cause severe C difficile infection in adults)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what are the differentials for acute diarrhoea in adult horses

A 
larval cyathastomosis 
clostridial diarrhoea 
right dorsal colitis secondary to NSAIDs 
grain overload 
idiopathic 
dietary changes 
rare 
- salmonellosis 
- antibiotic induced 
- peritonitis 
- sand colic 
- strongylosis 
- duodenitis - proximal jejunitis 
- congestive heart failure 
- liver disease (hyperlipaemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is the most prevalent and severe equine parasitic disease and what are its signs

A

cyathostominosis (80% prevalence)

severe acute or chronic diarrhoea and colic

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

describe the life cycle of cyasthastomes

A

direct cycle:

  • adults adhere to mucosa of caecum and colon
  • pre-patent period 6-14 weeks if no hypobiosis
  • eggs produced and excreted

hypobiosis

  • larvae encyst and development arrested in large intestinal mucosa unaffected by any anthelmintic
  • emerge in spring
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what percentage of a cyasthastome population do larvae make up

A

90%

50% encysted

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

what is the epidemiology of cyathastominosis

A

all ages affected, more commonin young or unexposed horses
egg shedding highest in spring
re-infection in june-sept/oct if not too dry
larvae at maximum number in horse in autumn

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

how is cyathastominosis diagnosed

A

FEC allows you to rule in but not out
history and clinical signs (young, poor worming history, sudden change)
larvae in faeces/on glove after rectal if acute
clinical pathology - neutrophilia, hypoalbuminaemia, hyperglobulinaemia

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

what are the clinical signs of cyathastominosis

A 
spring syndrome (mucosal damage due to L3 emergence)
- colic 
- weight loss 
- ventral oedema 
- diarrhoea (acute usually and chronic) 
- wasting
- death 
- secondary neurological signs 
autumn syndrome (larvae entering intestinal wall) 
- colic (milder) 
- diarrhoea (less severe)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

how is cyathostominosis treated

A

intensive care if acute

  • IVFT
  • parenteral antibiotics depending on age
  • colloidal support (plasma)
  • foot supports
  • polymixin B
  • dobutamine infusion
  • NSAIDs
  • other analgesia (lidocaine, ketamine drip)
  • pre-treatment with steroids before anthelmintics to reduce inflammation
  • moxidectin is larvicidal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

how is cyathostominosis prevented

A 
moxidectin during spring/autumn 
pick up faeces 
keep different ages of horses separate 
avoid overgrazing 
rotate pastures 
(harrowing if hot weather - not effective in England)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is the prognosis for cyathostominosis

A

guarded, around 30-40% survive without treatment. may take months to re-gain weight as colonic wall takes time to heal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is the prognosis for clostridial diarrhoea

A

30-50%
first losses occur due to the client running out of money to fund IVFT
second bout of losses often due to severe and fatal laminitis (after horse producing normal faeces)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

where is antibiotic induced diarrhoea common and which drugs are indicated

A 
uncommon in UK, common in USA
penicillin 
ceftiofur 
TMPS 
doxycycline 
oxytetracycline 
(any antibitotic which targets gram negative or anaerobic bacteria) 
erythromycin in mares which ingest drug from foal's faeces
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what are the clinical signs of antibiotic induced diarrhoea

A
  • variable
  • mild transient diarrhoea with no systemic effects
  • severe fulminant enterocolitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

how is antibiotic induced diarrhoea diagnosed

A

history

faecal ELISA or PCR for clostridial perfringens enterotoxin and C difficile toxins A and B

42
Q

how is antibiotic induced diarrhoea treated

A

stop antibiotics
faecal transfaunation
metronidazole - rarely used now
if severe - treat as for clostridiosis

43
Q

describe the pathogenesis of grain overload diarrhoea

A

horse gains access to large quantity of hard feed
SI digestion overwhelmed and soluble CHO enters LI
rapid fermentation by lactic acid producing bacteria lowers pH
gram negative enterobacteriaceae die, other bacteria overgrow, gull wall is compromised and bacteria enter the circulation

44
Q

what are the clinical signs and diagnosis of grain overload diarrhoea

A

SIRS
osmotic diarrhoea due to lactic acid being poorly absorbed
severe, often fatal laminitis
diagnosis based on history

45
Q

how is grain overload diarrhoea treated

A 
IVFT
analgesia 
broad spectrum parenteral antibiotcs 
oral laxatives - liquid paraffin coats what is eaten to allow it to pass through the LI 
anti-endotoxic agents - polymixin B
frog supports, ice feet 
PPN to rest gut 
surgery if severe to decontaminate GIT before they get too sick
46
Q

describe the pathogenesis of right dorsal colitis

A

secondary to NSAIDs often if higher than licensed doses administered (not always).
ponies more susceptible to horses.
changes in GI blood flow affects protective mechanisms

47
Q

what are the clinical signs of right dorsal colitis

A 
anorexia 
lethargy/depression 
colic 
diarrhoea 
fever 
SIRS
if chronic 
- weight loss 
- intermittent colic 
- depression 
- anorexia 
- ventral oedema 
- soft/less formed faeces
48
Q

what clinical pathology is seen in right dorsal colitis

A 
hypoproteinaemia 
hypovolaemia 
electrolyte abnormalities 
neutropenia 
occasional anaemia 
increased creatinine
49
Q

how is right dorsal colitis diagnosed

A

presumptive based on history
more common with oral phenylbutazone (and suxibuzone) use, possibly less common with more COX2 selective drugs
transabdominal ultrasound - thickening of RDC wall

50
Q

how is right dorsal colitis treated

A

stop NSAIDS (use paracetamol if analgesia needed)
supportive care
PGE2 analogue - misoprostol to increase GI blood flow and protective factors but has side effects

51
Q

describe idiopathic diarrhoea in horses

A 
persistent diarrhoea
remains normovolaemic 
bright demeanour 
can become hypoproteinaemic over time 
possibly caused by dietary intolerance e.g. haylage
52
Q

how is idiopathic diarrhoea diagnosed

A 
rule everything else out 
history 
FEC
faecal culture (3 over 1 week) 
toxin ELISA
exclusion diet for 4-6 weeks
53
Q

how is idiopathic diarrhoea treated

A

if exclusion diet doesn’t work, codeine phosphate PO BID to reduce LI motility

54
Q

describe salmonellosis diarrhoea in horses

A 
rare cause in UK 
syndromes 
- acute fulminant diarrhoea 
- sepsis in foals 
- depression, fever, anorexia 
- small colon impaction 
can get latent/carrier state
55
Q

how is salmonellosis diagnosed

A

bacterial culture.
3 negative to rule out
5 negative to declare no longer infected after positive

56
Q

how is salmonellosis treated and prevented

A

supportive care as for cyathostominosis
antibiotics to manage bacteraemia rather than kill salmonella
isolation - personnel and equipment
phenolics and fumigation of environment

57
Q

when should horses/foals be isolated

A

two out of
- pyrexia
- neutropenia
- diarrhoea
– (except when 24-48 hours after LCV surgery)
neurological disease - decreased tail tone and dog sitting (EHV1)
suspected strangles

58
Q

what are the aims of investigating acute diarrhoea

A

determine

  • likely cause
  • need for specific therapy
  • need for supportive therapy
  • risk to in-contact horses and personnel
59
Q

how is the likely cause of diarrhoea and need for specific therapy determined

A 
history
physical exam 
haematology and biochemistry 
FEC
Faecal PCR/ELISA
faecal culture and sensitivity
60
Q

how is the need for suppportive therapy determined

A 
major body system assessment 
basic bloodwork 
- PCV/TP
- lactate 
- blood gas and electrolytes 
- clotting profiles
61
Q

what does supportive therapy consist of for diarrhoea

A 
IVFT
plasma 
dobutamine infusions - haemodynamic support 
analgesia 
lidocaine infusions 
polymixin B - anti-endotoxic drug 
antibiotics (controversial) 
foot supports/ice 
monitor jugular veins 
ensure eating or consider PPN within 48 hours of anorexia 
steroids (controversial) 
transfaunation
62
Q

list the causes of weight loss

A 
dental disease 
intestinal disease 
parasites 
liver disease 
renal disease 
neoplasia 
GI infection 
chronic systemic infection 
malnutrition
63
Q

why may a horse have reduced feed intake

A

malnutrition due to owner
competition for feed
dental disorders
anorexia due to pain or dysphagia

64
Q

what may lead to reduced digestion, absorption or assimilation of nutrients

A

dental disorders
malabsorption syndromes specific to the intestine
- parasitic disease
- idiopathic
- infiltrative bowel disease (inflammtory or neoplastic)
liver disease

65
Q

what may cause increased loss of nutrients

A

PLE
PLN
squestration to body cavity - peritonitis or pleuritis

66
Q

what may cause a horse’s energy requirements to increase

A 
pregnancy 
lactation 
sepsis 
neoplasia 
other systemic disease
67
Q

what factors may be associated with liver disease in horses

A 
maldigestion (rare) 
anorexia 
hypoalbuminaemia (rare)
increased energy consumption 
infection/sepsis
68
Q

how is liver damage evaluated in horses

A 
damage 
- serum enzyme activities 
- SDH/GLDH - hepatocellular 
- GGT - biliary 
function 
- bilirubin (mild increase with anorexia)
- bile acids (pre vs post prandial doesn't really change)
- ammonia
69
Q

describe renal disease in horses

A 
rare 
PLN may occur
assess using 
- serum creatinine 
- urine SG 
BUN not helpful
70
Q

what may lead to primary peritonitis in horses

A 
haematogenous 
- strep equi 
- actinobacillus 
- R equi 
migrating parasites
71
Q

what may cause secondary peritonitis in horses

A 
sepsis 
- rupture of GI tract 
- uterine tear 
reactive 
- abscess 
- neoplasia 
- ruptured bladder
72
Q

what are the clinical signs of sepsis in horses

A 
pyrexia 
depression 
ileus +/- reflux 
pain on walking 
anorexia
73
Q

how is peritonitis diagnosed in horses

A

abdominocentesis

  • copious volumes of fluid
  • cloudy sample
  • high numbers of degenerate neutrophils
74
Q

what is the prognosis for peritonitis in horses

A

depends on cause

75
Q

may may chronic diarrhoea occur with malabsorption/protein losing enteropathies

A
  • primary large colon dysfunction

- abnormal energy substrates to hind gut flora

76
Q

what are the potential aetiologies of infiltrative bowel disease

A
  • parasites (no direct link)
  • genetic
  • food allergy
  • mycobacterium spp
  • histoplasma
77
Q

how is infiltrative bowel disease diagnosed

A
  • rectal biopsy
  • duodenal biopsy
  • laparoscopy
78
Q

how is infiltrative bowel disease treated

A
  • anti-inflammatory doses of steroids
  • anthelmintics if parasites may be a factor
  • diet of highly digestible foods and high fibre
79
Q

how is infiltrative bowel disease classified

A
  • granulomatous enteritis
  • lymphocytic-plasmocytic enteritis
  • multisystemic eosinophilic epitheliotrophic disease
  • eosinophilic enteritis
80
Q

name the types of equine lymphoma

A 
alimentary - 2-5yo and aged horses 
generalised - aged horses
solitary - any age 
cranial mediastinal - any age 
cutaneous - any age
81
Q

what paraneoplastic syndromes may occur with equine lymphoma

A
  • hypercalcaemia

- haemolytic anaemia

82
Q

name the types of malabsorption in horses

A
  • anthelmintic responsive
  • steroid responsive
  • non-steroid responsive
83
Q

how dose right dorsal colitis usually present

A

protein losing enteropathy
hypovolaemia
alongside NSAID administration

84
Q

how is right dorsal colitis diagnosed and treated

A

ultrasound - thickened RDC >5mm
stop NSAIDs
supportive care
misoprostol to increase intestinal blood flow

85
Q

what obvious causes of weight loss should be ruled out when taking a history

A

diet

parasites

86
Q

what should be looked for on clinical exam when investigating weight loss

A 
BCS - is weight loss genuine 
jaundice 
oedema - PLE
fever 
oral/dental exam 
rectal exam - thickening/mass
87
Q

what further tests should be used when investigating weight loss

A

liver, renal and inflammatory markers
repeat blood tests
abdominocentesis
FEC (won’t find tapeworm)

88
Q

what non-specific changes may be seen on H&B when investigating weight loss

A

leucocytosis - peritonitis/cyathastominosis
neutrophilia - peritonitis
eosinophilia (sometimes parasites but uncommon in horses)
anaemia of chronic disease
increased liver enzymes

89
Q

how may total protein be altered with weight loss

A

decrease

may be masked by concurrent hypovolaemia

90
Q

how may hypoalbuminaemia be interpreted

A

GI loss more common than renal
peritoneal/pleural effusions
liver disease (rare)

91
Q

how may hypoglobulinaemia or hyperglobulinaemia be interpreted

A

hypo - GI loss

hyper - chronic inflammatory disease (cyathostominosis)

92
Q

how may hyperfibrinoginaemia be interpreted

A

infection
inflammation
neoplasia

93
Q

when does serum amyloid A increase

A

inflammatory response

94
Q

describe the interpretation of serum protein electrophoresis

A

a - infection, inflammation, neoplsaia (acute phase protiens)
b - parasitism, chronic infection, neoplasia (C reactive protein)
g
- polyclonal - chronic infection, abscesses, neoplasia
- monoclonal - tumours of reticuloendothelial system

95
Q

what may oral glucose tolerance test be used for

A

test if there is an issue with sugar absorption

96
Q

what are the issues with an oral glucose tolerance test

A
  • only assesses sugars (not proteins or fats)
  • doesn’t only assess SI function
  • D-xylose absorption test more reliable but expensive
97
Q

what may paritial malabsorption in the oral glucose tolerance test indicate

A

parasitism
localised lesions
rapid GI transit

98
Q

what may a delayed flat curve on an oral glucose tolerance test indicate

A

delayed gastric emptying

poor starvation

99
Q

what can be assessed on intestinal ultrasonography

A

wall thickness (should be 2-3mm)
lumen diameter
motility
anatomy

100
Q

what methods may be used for GI biopsy in the horse

A

midline exploratory celiotomy UGA
flank laparotomy - reduced recovery time
laparoscopy - further reduced recovery time
rectal mucosal biopsy using uterine biopsy instrument
duodenal biopsy via gastroscopy

GI2 (27 decks)

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