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VetMed Year 3-Term 2 > w/c 24-Feb-14 > Flashcards

w/c 24-Feb-14 Flashcards

1
Q

When is ACP contraindicated as a sedative in horses?

A

ACP is a phenothiazine. It is hypotensive and therefore contraindicated when there is hypovolemia/toxic colic.
Stallions = Priapism

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2
Q

Xylazine, Detomidine, Romifidine are used extensively in equine sedation. Why might they be combined with a low dose opiod?

A

These are alpha 2 agonists.
They provide deep sedation but can still respond to touch i.e. can still kick.
Adding low dose opiod removes response to touch

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3
Q

What are the most notiable side effects of alpha 2 use in horses?

A

Bradycardia, fall in cardiac output, biphastic blood pressure change (up then back) due to balance between vaso-contriction and cardiac output.

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4
Q

Considerations when using ketamine as an induction agent in the horse

A

Ketamine is a convultant and MUST NEVER BE GIVEN ALONE.
Ketamine is normally given with alpha 2 agonists e.g. Xylazine, Detmoidine, Romifidine)
GIVE ALPHA 2 FIRST!!

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5
Q

What is the function of Guiaphenesin (GG, GGE)?

A

Guiaphenesin is a centrally acting muscle relaxant and is NOT an anaesthetic. Always used in conjucation with anaesthetic agent.

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6
Q

Which is the only volatile anaesthetic agent licenced for use in the horse>

A

Isoflurane is the only licenced volatile anaesthetic agent.

Sevoflurane is used off licence

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7
Q

Which is more respiratory depressive; isoflurane of halothane?

A

Isoflurane is more respiratory depressive than Halothane.

Hypotension is also worse with isoflurane BUT IT IS LESS CARDIAC DEPRESSIVE!= Cardiac Output is well maintained

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8
Q

You have premedicated a horse with atropine 30 minutes into the operation the horses blood pressure falls to <40mmHg. What do you do?

A

-Reduce volatile agents (supplement analgesia by injectable agents
-Use large volumes of fluid
-Ensure horse that is recieveing IPPV is NOT Hypocarbic. Hypercarbia is great circulatory stimulant.
DO NOT USE INOTROPIC AGENTS SUCH AS DOBUTAMINE as this will cause Tachycardia in the horse premedicated with an atropine (anti-cholinergic)

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9
Q

You endoscope a horse and suspect it has a guttural pouch mycosis. What do you do?

A

Withdraw endoscope carefully and refer! If its affected carotid artery = fatal haemorrage.
Don’t stress horse!

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10
Q

A horse with unilateral epistasis has a visible yellow mass in its frontal sinus. What is the most likely diagnosis?

A

Ethmoid haematoma. Causes unilateral epistaxis with intermittent bleeding.

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11
Q

Why might a horse be given atropine pre op?

A

Atropine is a anti-cholinergic drug which reduces salivation and therefore reduces the risk of aspiration pneumonia

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12
Q

Hypoxemia in the horse is thought to come about due to

A

Marked ventilation/perfusion mismatching in the lungs leading to shunting of blood. Due to dorsal recumbancy
The deoxygenating effects of shunts are worsened by the low cardiac output.
Larger the horse= bigger problem.

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13
Q

Why is salivation a problem in ruminant anaesthesia?

A

Saliva is stimulated further by use of ketamine.
Can lead to electrolyte imbalances, also contains collaginases therefore if aspirated can damage lung.,
Or lead to aspiration pneumonia
Can also cause corneal ulcers

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14
Q

Why is bloat a consideration when a cow is anaesthertised?

A

Animals cannot eructate therefore if in lateral recumbancy the cardia is blocked = bloat.
Reduces venous return.

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15
Q

Horses are prone to hypotension. What blood pressure issues to ruminants tend to have>

A

Hypertension! Adult bulls and cattle often >200mmHG.
Due to changeover from para to sympathetic?
Or Hypoventilation therefore increased PaCO2 (but probably not)

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16
Q

Why do ruminants hypoventilate? What are the consequences of this?

A

Hypoventilate due to drug induced respiratory depression, large rumen.
Increased Co2 levels, decreased 02. ippv often used to manage but CARE as ruminants have less fibrous tissue therefore more prone to airway damage

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17
Q

Which sedative needs to be used with CARE in the pregnant animal?

A

The a2 agonist, xyalazine contracts smooth muscle therefore its use in pregnant animals is contraindicated.
Sheeps and Goats are VERY SENSITIVE to a2’s

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18
Q

Which drugs are most commonly used for induction in ruminants?

A

Ketamine (causes some muscle rigididity, laryngeal reflex remain) and Thiopentone (MUST GO IV!!!), Prolonged recoveries, not in thin animals

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19
Q

Which two NSAID’s are licened for use in ruminants and have no milk withdrawek time?

A

Ketoprofen and Carprofen,

NO LICENCED OPIODS IN UK!

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20
Q

Difference in accessing the jugular vein in cattle and horses?

A

Much more superficial in horses.
In cows its deeper.
CARE NOT TO DO INTRACAROTID INJECTION!

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21
Q

Important considerations for recovery of ruminants from anaesthesia?

A

Ideally in sternal recumbancy, allowing head to drop occasionally to drain saliva.
Extubate with cuff inflated. Suction perior to extubation

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22
Q

Sedation of pigs

A

IV access difficult so go IM initially.
Butyrophenone, Azaperone (dopamine antago)
Leave and wait 20 minutes.

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23
Q

Best venous access for pig

A

Warm water to vasodilate then ear vein.

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24
Q

What is malignant hyperthermia (MH)

A

Dominant gene of humans, pigs and horses.
Fault in a gene.
Inhalation agents cause it to trigger and is often fatal.
ATP depletion leading to muscle rigidity. The use of this ATP generates heat (temp >42)
Monitor for K+ to avoid hyperkaelemia from damaged muscle

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25
Q

Treatment of MH in pigs

A 
Active cooling (water, ice, spirit, cooled IV fluids) 
Remove trigger (inhalation agent), bicarbonate to reduce acidosis, DANTROLENE - decrease calcioum release (expensive)
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26
Q

How do ruminant eye positions inform the anaesthatist about the depth?

A

Ruminant eyes tend to roll down with deepening anaesthesia and rotate back to central position when surgically deep

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27
Q

Which pathogens cause respiratory disease in pre-weaned pigs

A
  1. Progressive atrophic rhinitis
  2. Bordetella bronchisepticum
  3. Enzootic pneumonia
  4. PRRS
  5. Glassers disease
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28
Q

Causative pathogen of enzootic pneumonia in pigs

A

Mycoplasma hyopneumoniae.
30-80% of pigs have lesions at slaughter.
Weaned pigs, Increase coughing- esp after exercise, CRANIAL LUNG lobes = low grade but considerable economic importance

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29
Q

Glassers disease causative agent

A

Haemophilus parasuis.

Disease in pre-weaned/ weaners, growers, finishers

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30
Q

Which pathogen causes severe respiratory disease in pigs, it has high morbidity and high mortality and affects weaners, growers and finishers

A

Actinobacilus pleuropneumoniae. Affects caudal lung lobes. ‘gut shot lesion;
c.f. with Mycoplasma hyopneumoniae = cranial lung lobes therefore less severe

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31
Q

Enzoonotic pneumonae affects what age pigs?

A

Mycoplasma hyopneumonaie = enzoonotic pneumoniea. Affects pre-weaned pigs and non-immune adults

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32
Q

Causative agent of atrophic rhinitis in pigs

A

Pasteurella multocida in association with Bordetella bronchiseptica. Damages osteoblasts and enhances osteoclast activity

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33
Q

If lots of 3 week old piglets have died as well as the farm cats. You would be highly suspitious of…

A

Swine herpes virus type 1. akak Aujesky’s disease
<4 weeks = neurological signs.
up to 5 months = neurological and pneumonia
NOTIFIABLE not in UK atm.
DEAD END HOST IS THE FARM CAT
If pigs and cat die = suspitious

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34
Q

Significance of Porcine Circovirus

A

Immunosuppressive.

90% of UK pigs are seropositive. Has a respiratory component. Coughing

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35
Q

Intermediate host for the main pig respiratory parasite

A

Main pig respiratory parasite is Metastrongylus. Earthworm is the intermediate host.

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36
Q

Method for partial depopulation as a control method for respiratory disease in a pig herd

A

Remove all pigs excluding lactating sows (medicate sows)
Wean to offsite location for 12 week period
Rest and disinfect weaner and grower accomodation

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37
Q

Normal body temperature and heart rate of a sheep

A

Temp: 39 +- 0.5

Heart Rate: 80-90

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38
Q

In a flock with a suspected respiratory problem. There is a couple of sheep that have sudden died. What is the most likely pathogen involved?

A

Mannhaemia haemolytica can cause peracute pneumonia = septicaemia

39
Q

Larangeal condritis in sheep is most common in which breeds

A

Texels/ Beltex (compact sheep!)

Necrosis of Larynx

40
Q

Pathogenesis of Ovine Pneumonia in sheep

A

Mannhaemia haemolytica.

Predisposing damage e.g. PI3.

41
Q

Difference in pathogen between enzootic pneumonia and atypical pneumonia

A

Enzootic pneumonia: pi3 damage then colonisation with M.haemolytica
Atypical pneumonia: Mycoplasma ovipneumoniae

42
Q

Sheep lung worm and when is peak larval contamination?

A

Dictyocaulus filaria.
Peak pasture contamination: Autumn and Winter
Lambs up to 1 year infected

43
Q

Maedi-Visna transmission

A

Lentivirus
Causes wasting and mastitis
Spread mainly by vertical transmission (colostrum and milk) SOME horizontal transmission

44
Q

Treatment for Maedi-Visna

A

NO TREATMENT. Prevent introduction.
Control: Cull clinical cases, cull ewes when 4-5 years old. Cull offspring from infected ewes.
DIAGNOSIS: Grossly the lung feels solid. Histopathology

45
Q

Clinical signs of Maedi-Visna

A

Affected animals normally 3+ (hence control includes culling 4-5yrs), Slow progression of signs, Emaciation, Development of severe respiratory disease, MASTITIS, ARTHRITIS

46
Q

Significance of Sheep Pulmonary Adenomatosis (SPA)

A

Herpes virus and Retrovirus = slowly progressive lung adenocarcinoma (common contagious tumour)
Long incubation.
Transmission: Respiratory route and Vertical

47
Q

Diagnosis of SPA

A 
Sheep Pulmonary Adenomatosis.
Wheelbarrow test= fluid out of nostrils.
Tumour in lungs
Histopathology. 
Can occur with maedi visna 
Introduction to flock with purchased sheep
48
Q

Diagnosis of Strangles

A

Strp equi.equi. NOT A NORMAL INHABITANT.

Nasopharangeal swabs testing +ve are always pathogenic. Doesn’t require prior viral infection.

49
Q

How long does Strep. equi equi stay in environment?

A

1-3 days
Spread by horizontal transmission; nasal secretions/ LN discharge.
Foals born to immune mares resistant for 3 months

50
Q

How long after infection with Strep equi equi do a) clinical signs and b) nasal shedding occur?

A

Strangles

a) Incubation period: 2-6 days
b) Nasal shedding: 3-6 weeks

51
Q

Clinical signs of atypical strangles. SIGNIFICANCE of atypical strangles

A

Mild inflammation of URT, slight nasal discharge, cough, fever, self limiting lymphdenopathy.
Significance: DANGEROUS as doesn’t look like strangels but equally as pathogenic and can cause CLASSICAL strangles in other animals

52
Q

Complications of strangles

A

Purpura haemorrgaica, Lymph node abscessation, Laryngeal hemipegia, Horners syndrome

53
Q

Purpura haemorrgaica pathogenesis

A

Generalised vasculitis caused by type III hypersentitivity reaction.
Thrombosis of small arteries can occur –> Skin and muscle necrosis
Ventral oedema.
Death due to pneumonia, cardiac arrhytmia,

54
Q

Diagnosis of Purpura haemorragica

A

Based on clinical signs.
Leucocytosis/ hyperfibrinogenaemia.
Isolation of S.equi from LN

55
Q

How to determine when strangles infection has been RESOLVED?

A

THREE CLEAR NASOPHARANGEAL SWABS

One negative lavage

56
Q

Treatment of Purpura haemorrgaica

A

type III hypersensitivity therefore treatment involves corticosteroids.Dextamethasone/ Prednisalone

57
Q

Rhodococcus equi

A

Gram +ve widespread in environment. Causes diseases in foals from 1 month to 6months of age

58
Q

Environmental survival time of Rhodococcus equi

A

12 months in warm dry soil. More common in USA, Australia and Ireland.

59
Q

Pathogenesis of Rhodococcus equi

A

Foals infected within first few days after birth.Clinical signs occur later.
Inhalation of R.equi, scaverened by alveolar macrophages but NOT killed.
= progranulomatous response
Pneumonia with abcess formation

60
Q

Two forms of R. equi in foals <6months

A

Respiratory form: Alvolar macrophages but NOT KILLED

Intestinal form: Ulcerative entercolitis, mesenteric lymphadentis DUE TO SWALLOWED SPUTUM

61
Q

Treatment of R. equi

A

Diagnosis: Neutropillia, hyperfibrinogemia, thrombocytosis.
TREATMENT: Erythmocycin and Rifampin (Major differential is alo covered)

62
Q

Horse presents with fever, limb and periorbital oedema, ‘pink eye’- conjuctivitis, nasal and lacrimal discharge. It also is coughing. The mare was covered 4 weeks ago. Likely diagnosis

A

EVA - Stallions = reservoir of infection.
Oedema: arteritis (inflamm of arteries)
Infects macrophages then travels to local LN

63
Q

Before vaccinating a stallion for EVA. You must…

A

Pre vacc blood test and NOTE STATUS IN PASSPORT.

Otherwise can’t tell if horse is EVA carrier because will be seropositive post vacc anyway

64
Q

Difference between stertor and stridor?

A

Stertor: Tissue vibration
Stridor: Narrow airway
Both abnormal respiratory sounds

65
Q

Describe the examination of the upper respiratory tract

A

Examination: Nasal discharge, Facial symmetry, Airflow (rebreathing test exacerbates)
Palpation
Percussion - paranasal sinus

66
Q

How to characterise nasal discharge

A

Character: Serous,mucoid, purulent, necrotic
Unilateral/Bilateral
Odor: No odor/ foal odo

67
Q

Ddx for nasal discharge with foal odour

A

Dental disease, neoplasia, necrotising LRT disease

68
Q

When radiographing the sinus, what are we looking for?

A

Fliod lines = parallel straight lines = radiographically pathoneumonic

69
Q

Causes of sinusitis

A

Dental disease (09,10,11 or M1, M2 M3), bacterial infection, fungal infection, neoplasia,

70
Q

Rostral Medial Sinus portal risks

A

Sinoscopy risks damages teeth

71
Q

Types of guttural pouch disease

A

GP empyema (most common)- bact infec
GP catarrah - excessive mucus
GP mycosis
GP neoplasm

72
Q

Where is the associated swelling with guttural pouch disease

A

Viborg’s triangle

73
Q

How do diagnose guttural pouch empyema?

A

Endoscopy/ radiography (fluid line),, chondroids

74
Q

What are chondroids?

A

Inspissated pus

75
Q

Treatment of GP empyema?

A

Pouch lavage (penicillin in 5% gelatin)
REMOVE CHONDRIOIDS before lavage
Surgical: Virborg’s triangle approach for drainage

76
Q

Which bone divides the guttural pouch into medial and lateral sections?

A

Stylohyoid bone

77
Q

Common bacterial isolate from sinusitis in horse

A

Strep. zooepidemicus

beta haemolytic

78
Q

Frontal sinus communicates with the ____ sinus via the __

A

Frontal sinus communicates with the CAUDAL MAXILLARY sinus via the Frontomaxillary opening.

79
Q

Which two sinus does the Caudal maxillary sinus communicate with?

A

Sphenopalatine and Middle conchal sinus’

Also the caudal maxillary communicates with the frontal sinus via the frontomaxillary opening

80
Q

Why are respiratory noises so significant in the horse racing industry>

A

Gait and respiration are linked 1:1 at the gallop.
Therefore if horses breathing is delayed length gait.
Resistance inversely proportional to the 4th power of radius of airway

81
Q

DDx of Stertor

A

Stertor: Tissue vibration
DDSP (also dynamic)
Nostril problems

82
Q

Ddx of Stridor

A

Airway narrowing.

RLN, Chondritis, Mass lesions

83
Q

Which phase of the respiratory cycle would you expect to hear abnormal noise for a horse with DDSP

A

DDSP: Dynamic. Stertor (tissue vibration)

EXPIRATORY

84
Q

Example of disorder that causes dynamic, stridor in INSPIRATORY phase of breathing cycle

A

Stridor: Narrowing of airway. In Inspiration

RLN (Recurrent laryngeal neuropathy)

85
Q

Signs of Recurrent laryngeal neuropathy?

A

RLN. ‘Roaring’ Inspiratory Stridor: Narrow airway

86
Q

Which parts of the URT are affected by a) DDSP b) RLN?

A

a) DDSP: Pharynx

b) RLN: Larynx ‘roaring’-inpiratory stridor

87
Q

Clinical signs of DDSP? Including structural changes

A

Expiratory noise, decreased performance, mouth breathing (pathopneumonic) due to free border of palate DORSAL to epiglottis

88
Q

Treatment for DDSP (Conservative and Surgical)

A

Conservative: Tongue tie, Cornell collar (mimic function of TH muscle), keep mouth closed
Surgical: Trim edge of palate (Staphylectomy), thermal palatoplasty, Laryngeal tie forward (mimic thyrohyoideus muscle)

89
Q

Which muscle is involved in DDSP?

A

Expiratory stertor (vibration) Thyrohyoideus dissection leads to DDSP therefore tie forward mimics function of TH

90
Q

Pathogenesis of RLN?

A

Due to degenerative axonopathy or recurrent laryngeal nerve. LEFT SIDE affected. Result is impairement of cricoarytenoideus dorsalis muscle (primary adductor of arytenoid cartilage)
Therefore if impaired collapse of lumen = stridor

91
Q

Normal position of the free border of the palate relative to the epiglottis?

A

NORMALLY. Horse = obligate nasal breather

Free border of the palate is UNDER the epiglottis.

92
Q

A horse has a sudden decrease in performance and a noted expiratory stridor. What could be causing this?

A

Epiglottic entrapment.
More common in horses with epiglottic hypoplasia or deformity.
On endoscope don’t see dorsal epiglottic vessels (they are covered by tissue)

93
Q

Which two conditions does epiglottic hypoplasia predispose to?

A

DDSP and Epiglottic entrapment

VetMed Year 3-Term 2 (11 decks)

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