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LAM > LAM 3 Midterm 1 > Flashcards

LAM 3 Midterm 1 Flashcards

1
Q

What feedlot changes lead to lameness?

A

high energy diet + substrate changes - lameness

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1
Q

Where does 90% of dairy cow lameness occur?

A

rear limb lateral claw

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1
Q

What is the most common lesion associated with sheep lameness?

A

interdigital space lesions

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1
Q

How will cattle stand if they have lameness in their lateral digit?

A

base wide stance

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1
Q

How will cattle stand when they have medial claw lameness?

A

base narrow or limbs are crossed

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2
Q

What are the 3 synovial structures in the ruminant foot

A

Distan Inter tarsal Joint
Navicular Bursa
Flexor tendon sheath

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3
Q

What is graveling?

A

deep foot infection has to migrate to release the pressure at which tends to occur at the soft tissue planes

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4
Q

What is the role of the Periolic coria?

A

it is a moisture barrier to underlying coria

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5
Q

What spirochete is responsible for 50-70% of bovine lameness in the U.S?

A

Treponema

they live deep in the epidermis and create inflammation

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6
Q

What is considered the dirtiest foot zone + why

A

zone 0 because spray cleaners don’t reach between the claws

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7
Q

What are clinical signs of mild irritation of the interdigital skin (zone 0)?

A

small, red ulcers
mild swelling + pain
undermine heel: seperate perioplic corium from the underlying horn of the bulb

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8
Q

What do the cs related to mild irritation of the interdigital skin lead to?

A

overgrowth of the heel resulting in increased heel weight-bearing + concussive injury = rusterholz ulcer

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9
Q

What is the proper term that is commonly referred to as “foot rot”?

A

interdigital dermatitis

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10
Q

What bacteria are commonly involved in interdigital dermatitis?

A

Fuscobacterium +/- dichelobacter or porphoromonas

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11
Q

Define the pathology found in interdigital dermatitis

A

skin break caused by deep necrosis

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12
Q

What is super foot rot?

A

necrotizing, penicillin resistant necrobacillosis of the foot

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13
Q

What is the name of the disease condition associate with 80% of all lameness in sheep?

A

interdigital dermatitis (foot rot)

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14
Q

What are some cs + findings of interdigital dermatitis in sheep?

A

often malodorous
walk on their carpi (if forelimb disease)

Fuscobacterium + Dichelobacter

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15
Q

What are the 3 phases of digital dermatitis

A

heel ulcers
strawberry foot rot
hairy heel warts or “mortellaro”

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16
Q

Describe the “heel ulcer” phase of digital dermatitis

A

circumscribed erosion/ulcer on border of plantar commissure, or at skin horn jxn, near the declaws (zone 10) or interdigital space

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17
Q

Describe the strawberry foot rot phase of digital dermatitis

A

ulcer fills in with granulation tissue

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18
Q

Describe the hairy heel wart phase of digital dermatitis

A

papillomatous growth
As chronicity increases, granulation tissue toughens up + frong like growths can occur

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19
Q

What microbe is responsible for causing digital dermatitis

A

Tremonema spp.

spirochete in the skin leads to irritation then erythema and inflammation + skin breaks resulting in ulcers

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20
Q

What happens when tremonema enters a herd?

A

epizootics of foot problems and after the adult cows develop partial immunity + mild lesions but if new heifers are introduced they still get severe disease

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21
Q

Describe the progression of Contagious ovine digital dermatitis when it spreads through a herd

A

it starts at the coronary band and leads to underrunning and sloughing of hooves

Treponema related, spreads via new additions to flocks

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22
Q

What is interdigital hyperplasia + what are the lay terms for it

A

chronic irritation leads to hyperplastic tissue growth which may become ulcerated
usually secondary to another lesion

lay terms: fibroma or corn

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23
Q

What is interdigital hyperplasia an indicator of?

A

that there was a breakdown of the cruciate ligaments that are responsible for keeping the digits together

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24
Q

Describe the general treatment plan for soft tissue lesions

A
  1. clean foot w/ disinfectant scrubs
  2. Debride/resect necrotic or proliferative tissue
    (be conservative around dorsal commissure)
  3. Sterilize open wounds:
    -foot baths, topical disinfectants, +/- topical antibiotics (extralabel use)
    4.) Deep infections- systemic anbx
    5.) consider bandages/ wires
    6.) corrective trimming of contributory hoof lesions
    7.) decreased the 4 M’s
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25
Q

What topical anbx would you consider for treponema?

A

tetracycline
linomycin
spectinomycin

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26
Q

If a patient has a deep infection caused by a soft tissue lesion, what drugs would you consider?

A

penicillins or sulfas for most
if “super foot rot” oxytetracycline
consider tilmicosin for digital dermatitis

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27
Q

What preventative measures can be taken to prevent ST lesions

A

adequate draining or lime absorbants
manure scrapings
straw bedding
even atraumatic surfaces
limit puddles +snoes
decrease udder hosing
foot baths regularly
regularly trim hooves

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28
Q

What are the 3 main areas that excessive horn growth tends to occur?

A

toe, abaxial wall, heel

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29
Q

What sequelae can occur when excessive toe growth is present

A

straining of the flexor tendons
movement of weight to the heel, splayed toes

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30
Q

What sequelae can occur when there is excessive growth at the abaxial wall ?

A

can strain the cruciate ligament and splays the claws

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31
Q

What sequelae can occur when there is excessive growth at the heel?

A

weight is moved to the heel which increases risk of concussive injury
a wide heel traps material in ID space

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32
Q

What can be seen when there is laminitis of the coria that makes up the wall? (coronary coria)

A

the wall will develop horizontal cracks aka “hardship grooves”

exacerbated by long toes
lever action can put pressure on coria

you can determine how long ago the insult occurred based on how far down the hoof wall it is

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33
Q

Describe the lesion that develops secondary to interrupted growth at the sole or heel

A

“Double Sole” : Anerobic pocket for bacteria that develops when the horn stops growing then restarts growing

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34
Q

What does white line seperation secondary to interrupted growth allow for?

A

abscess development

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35
Q

What does interrupted growth at the heel cause?

A

seperation from the skin known as an “underrun heel” that allows bacterial invasion

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36
Q

What changes does laminitis aka pododermatitis aseptica et diffusa cause to the horn when abnormal horn growth has occurred?

A

Horn becomes soft, bloody and mealy
it allows for bacterial invasion
no longer protects the soft tissue

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37
Q

When is the most common time we see hardship grooves in cattle?

A

1-3 months post partum

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38
Q

What are some genetically induced horn lesions in ruminants

A

screw claw

poor hoof confirmation or quality

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39
Q

What is laminitis induced compartment syndrome

A

edema + hemorrhage between hoof + bone

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40
Q

T or false: Horn lesions may promote ST lesions lesions and ST lesions may affect the adjacent corium

A

True! Bad horn lesions can do this

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41
Q

What do most horn problems result from?

A

abnormal production
this is secondary to diseases of of the corium/ laminae = laminitis

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42
Q

Problems of the ____ are most viable but problems on the ___ are most important

A

Wall; sole

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43
Q

Where do abscesses like to commonly occur in beef cows?

A

along the white line
near the toe (zone 1)

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44
Q

Where do abscesses like to occur in dairy cows?

A

along the white line
the lateral wall near the caudal sole

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45
Q

Why is ventral drainage of abscesses so important?

A

no ventral drainage means that infections will travel dorsad and reach vital structures

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46
Q

What is the pathogenesis that leads to a rusterholz ulcer?

A

weak or absent horn (laminitis) + concussive force (overgrowth) lead to injury + increased udder weight

severe injury will destroy the underlying corium and lead to proliferation of granulation tissue

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47
Q

Where do small ruminants tend to get horn overgrowth

A

abaxial wall grows long + curls under in small ruminants

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48
Q

Where do cows tend to have horn overgrowth?

A

the heel, abaxial wall and the toe

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49
Q

When performing corrective shoeing, what are important steps to ensure the foot is being reshaped to correctly bear weight?

A

we want a flat sole to spread weight evenly
remove extra toe, abaxial wall and heel
ensure there is good balance
avoid damaging the periople
dig out onfected tracks + cracks
remove double soles
trim back granulation tissue
place block on the sound claw if the other claw is very sore
check for infection of deeper structures

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50
Q

What can producers do to help prevent hoof lesions?

A

keep cows healthy - slow adaption to enviornments + diets, good hygiene, good bedding + stalls
exercise without too much standing around
softer substrates
regular hoof trims (2x a yr), foot baths, genetics

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51
Q

T or F donkies + horses have the same pain thresh hold

A

False, a dull donkey = a thrashing horse! Donkies are extremely stoic.

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52
Q

What causes wind-up pain in horses?

A

severe colitis, laminitis

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53
Q

What are some examples of patients that aren’t good NSAID candadites

A

pregnant, hypovolemic, hx of kidney disease,

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54
Q

What NSAIDs impact both the COX-1 and COX-2 pathways?

A

ketoprofen, meloxicam. flunixin meglumate (banamine), phenybutasone (bute),

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55
Q

What NSAID only targets the COX-2 pathway?

A

Firoxib

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56
Q

What are we taking away from the patient when we block productive prostaglandin synthesis?

A

pregnancy maintenance, liver, kidney, GI mucosa, blood clotting

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57
Q

What are indications of NSAIDs ?

A

pain, inflammation, pyrexia, anti-endotoxemia

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58
Q

Contraindications for NSAID administration

A

received a full dose less than 12 hours ago
renal compromise (elevated creatinine)
hepatic impairement
NSAID toxicity: right dorsal colitis
gastric ulcers
pregnancy/lactating
neonates
clotting disorder, thrombocytopenia

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59
Q

What q’s about NSAID use must I always ask?

A

how much is given, how frequently and the last dose given

60
Q

What is the onset of flunixin meglumine?

A

2 hours

61
Q

What type of pain is flunixin meglumine best for?

A

visceral, laminitis pain and ocular pain

62
Q

Why is IM injection of flunixin meglumine always contraindicated in equids?

A

IM injection leads to clostridial myonecrosis and death

63
Q

T or F phenylbutazone is easily reversible from COX

A

False! It irreversibly binds to COX and is slowly eliminated so overdosing disproportionately increases plasma concentration therefore there is a greater toxicity risk

64
Q

What is the dosage of phenylbutazone if it is being chronically used?

A

EOD

65
Q

How is phenylbutazone metabolized?

A

hepatic metabolism

66
Q

T or F phenylbutazone use can cause T4 suppression

A

True!

67
Q

Y or N, can pregnant or lactating animals receive phenylbutazone?

A

NO

68
Q

T or F: Flunixin meglumine has a anti-endotoxic effect

A

True!

69
Q

What type of pain is Firocoxib best for?

A

musculoskeletal pain
many OA horses take it daily

70
Q

Describe the elimination of Firocoxib

A

slow; 2 days

71
Q

T or F: Firocoxib is metabolized through the kidneys

A

False! Hepatic clearance

72
Q

What are the adverse effects that can occur with NSAID use?

A

clostridial infection if flunixin meglumine is given IM
nephrotoxicity: renal papillary necrosis
Right dorsal colitis (TS +/or albumin will decrease; diarrhea, gastric ulcers, impaired clotting, teratogenic

73
Q

What are medical options for pyrexia control in an adult horse?

A

Dipyrone
Acetominophen

74
Q

T or F: acetominophen + flunixin meglumine can’t be given together because they are both NSAIDS

A

False! acetominophen is a weak prostaglandin inhibitor and isn’t considered a “true” NSAID so you can give them both together!

75
Q

What drug is a central target for pyrexia?

A

Dipyrone
causes smooth muscle relaxation, some analgesia
do NOT give to patients with coagulopathies

76
Q

What is the MOA of lidocaine?

A

sodium channel blocker at neuron synapses

77
Q

When is lidocaine administration indicated

A

As an anti-arrhythmic (v tach or digoxin)
For use as as propulsive motility promotor of GIT (for ileus, enteritis, refluxing), as an analgesic

78
Q

What adverse reactions can be seen in horses with lidocaine sensitivity or accidently received a bolus?

A

seizures, muscle fasiculations, excitability

79
Q

Why should we be cautious when giving horses lidocaine with a highly protein bound drug?

A

lidocaine is moderately protein bound in plasma so there is more free drug in the plasma putting the animal at a greater toxicity risk

80
Q

Why should we be cautious when using an alpha 2 while sedating a patient?

A

it reduces GI motility
avoid use in animals with arrhythmia’s, neonates,
It alters blood glucose

81
Q

If a pyrexic horse is given an alpha 2 as part of a sedation protocol and develops tachypnia then what does that tell us ?

A

the patient has a true fever

82
Q

What impact does torb administration have on future morphine, pethidine or fentanyl given up to 8 hours after?

A

torb is a partial k an u agonsit and antagonist
because it is a partial antagonist it will reduce the efficacy of the drugs it proceeds

83
Q

If a client wants to stop giving their patient steroids, what do you tell them?

A

NEVER stop a course of steroids abruptly! Taper steroids off according to clinical improvement, then reduce by 20% of your dose every few days

84
Q

When can procaine pen g cause fatal reactions?

A

If it if accidently given IV! MUST be given IM route

85
Q

Why is it important to give penicillin (usually K pen) slowly?

A

it stimulates GI motility which looses manure and can cause patient to expel loose manure and be crampy + colicky

86
Q

What is the MOA of Penicillin?

A

beta-lactam
bactericidal, time-dependent, inhibits cell wall synthesis, hydrophilic

87
Q

when is penicillin (usually K pen) indicated?

A

gram positive organisms, some anerobes (clostridium), has poor gram negative coverage
it is commonly a part of broad spectrum therapy

88
Q

What is the MOA of gentamicin

A

Aminoglycoside that is synergistic with beta lactams

inhibits protein synthesis, bactericidal, hydrophilic, concentration dependent

89
Q

Indications for gentamicin use

A

gram negatives

90
Q

What do foals often receive instead of gentamicin + why?

A

Foals get amikacin because it is less nephrotoxic, higher dose for foals

91
Q

Contrainidications of gentamicin use

A

concentrates in renal tubular cells (nephrotoxic potental)
not for dehydrated, azotemic, renal-compromised patients

92
Q

MOA of oxytetracycline

A

Tetracycline, broad spectrum, inhibits protein synthesis
Bacteriostatic, time-dependent, lipophilic
Good for intracellular pathogens and penetrating tissues
Does not cover enterococcus (not good for foal sepsis)

93
Q

When is oxytetracycline indicated?

A

Neorickettsia risticci aka Potomac Horse Fever
Tick-borne disease (anaplasma)
At supratherapeutic doses, for foal flexural limb deformities

94
Q

What are contraindications of oxytetracycline use

A

Nephrotoxic (see gentamicin warning)

95
Q

Why should I avoid rapid oxytetracycline administration?

A

they will collapse
Given slowly IV, diluted in isotonic fluids because binds calcium

96
Q

If a patient was receiving IV oxytetracycline in hospital, what drugs will we consider sending them home on?

A

go home on oral doxycyline or minocycline

97
Q

MOA of potentiated sulfonamides (TMS), Equisul

A

Broad spectrum (gram negative and positive, protozoa), nucleotide synthesis inhibition at two points (trimethoprim and sulfadiazine or sulfamethoxazole)
Bactericidal, time-dependent

98
Q

What drug should be avoided for pseudomonas or bacterioides?

A

potentiated sulfonamides (TMS) , Equisul

99
Q

What are indications for potentiated sulfonamides (TMS), Equisul

A

Good first-line, used frequently for wounds
Strangles
Equine protozoal meningoencephalitis (EPM)
Mild pneumonia
NOT for sepsis

100
Q

What are contraindications of potentiated sulfonamides (TMS), Equisul

A

Poorly active in abscesses, purulent material
Must give 2 hours apart from antacids (sucralfate)
May cause diarrhea → stop if noticed

101
Q

What is the difference berween TMS and Equisul?

A

Equisul” has a longer half-life than TMS, and improved oral bioavailability
TMS tablets are very inexpensive

102
Q

MOA of ceftiofur

A

Bacerticidal, time-dependent, broad spectrum, gram negative
Poor intracellular penetration, but distributes widely extracellularly
Ceftiofur = 3rd generation.

103
Q

What are the contraindications of ceftiofur use

A

Protected: 3rd generation
Intracellular pathogens

Should reserve this drug for good stewardship

104
Q

Indications of ceftiofur use

A

If nephrotoxicity prohibits aminoglycoside use
Per culture and sensitivity!

105
Q

WHat is considered a complete course of use of: penicillin, oxytetracycline, potentiated sulphonamides

A

IV K Penicillin and gentamicin should be at least 3, ideally 5 days
Oxytetracycline: can start with IV and end with oral doxycycline or minocycline
Potentiated sulphonamides: 5-10 days, or more

106
Q

How should i assess my patient while on antibiotic therapy

A

Evidence of continued clinical signs? (Fever, dumpiness, respiratory signs, purulent wounds)
Recheck labwork: abdominocentesis, complete cell count, inflammatory markers, BAL/TBA
Is the threat gone? Abscess presence, corneal ulcer, exudative surgical site
Not responding to therapy? Culture and sensitivity…

107
Q

MOA of omeprazole

A

proton pump inhibitor

108
Q

Indications of omeprazole

A

gastric ulcers, 28 days, full dose

109
Q

What is the preventative dose of omeprazole

A

1/4 a full dose

110
Q

T or F omeprazole must be given after a meal.

A

False, it needs to be given on an empty stomach

111
Q

MOA of sucralfate

A

anti-acid, binds to exposed mucosa, stimulates mucus & bicarb production.

112
Q

When must you give sucralfate + why?

A

must be given 1-2 hours apart from other medications because it interacts

113
Q

Indications for sucralfate use

A

gastric ulcers, esophageal obstruction (choke), colitis, foals
Withhold for 6 hours before endoscopy

114
Q

Describe the vax protocol for EEE/WEE for a broodmare with unknown vax hx or is previously unvaxxed

A

2 dose series:
receive second dose 4 weeks post first vax and then revax 4-6 weeks pre-partum

115
Q

Vax protocol for WEE/EEE for an adult horse whose never been vaxxed for it or has unknown vax hx

A

2 dose series
receive second dose 4-6 weeks after first dose

116
Q

Vax protocol for a horse over 1 yr that has prev vx hx of WEE/EEE

A

annual revac prior to onset of vector season

117
Q

In what horses should you consider a 6 month revax interval for WEE/EEE

A

horses less than 5 yrs of age
horses residing in endemic regions with extended vector seasons

118
Q

What is the vax protocol for a foal from a mare whose never been vaxxed against WEE/EEE or a foal whose mare has been prev vaxxed against it?

A

3 dose series:
first dose at 4-6 months of age
second dose 4-6 weeks after the first dose
third dose at 10 to 12 months of age

followed by annual vax

119
Q

Why is there a 2 dose series recommendation in foals whose mare was vaxxed in the prepartum period but only a one dose series at 4-6 months of age in a foal of unvaxxed or unknown history?

A

foals from vaxxed mares are recommended a 2 dose interval because we want to address the potential for maternal antibody interference

120
Q

Tetanus dosage interval in foals of mares who were vaxxed in the pre partum period

A

3 dose series:
1st dose at 4-6 months of age
2nd dose at 4 to 6 weeks
third dose at 10 to 12 months of age

annual revax

121
Q

Tetanus dosing interval for foals of unvaxxed mares or lacking vax history

A

first dose at 3-4 months of age
second dose at 4 to 6 weeks after 1st dose
third dose 10 to 12 months of age

annual revax

122
Q

Tetanus dosing interval for broodmares prev vaxxed

A

annual
4-6 weeks pre-partum

123
Q

If a horse over 1 year has no vax history or unknown hx for tetanus what is their dosing interval

A

2 dose series
receive second dose 4-6 weeks after first dose

124
Q

When should you booster tetanus in a horse

A

at time of penetrating injury or before sx if it has been over 6 months since last vax

125
Q

If you have a broodmare with unknown or no hx of WNV vax, what is the dosing interval

A

vax naive mares when open

126
Q

Is WNV a 2 or 3 dose vax series for adults? What about foals?

A

two for adults
3 for foals

127
Q

T or F protective titers are avaialble for EEE/WEE

A

False

128
Q

How is EEE/WEE spread?

A

Mosquitos, less frequently other insects and nasal secretions
horses, especially those in endemic areas (South, coastal)

129
Q

What regions of the US are at risk for rabies exposure

A

Endemic in every US state (except Hawaii)

130
Q

What is the vaccine protocol to ensure protection against rabies?

A

Inactivated tissue culture-derived products
Single dose with annual revaccination

131
Q

What is the protective titer for rabies

A

definitive titer not established but >0.5IU/ml considered robust but will not protect animal from quarantine/euthanasia

132
Q

How is WNV spread

A

Avian reservoir host, Mosquitos (infrequently by other bloodsucking insects)

133
Q

When is the best time to administer the WNV vax

A

USDA Licensed Vaccines:
(2-inactivated whole, recombinant canarypox, inactivated flavivirus vector

Administer in spring before vector season

134
Q

T or F both horses and humans are dead end hosts for WNV

A

True

135
Q

What regions are at risk for WNV

A

Continental US, most of Mexico and Canada

136
Q

Is there a protective titer established for tetanus

A

titer levels >0.01 IU/ml considered to be protective (Cornell)

137
Q

What exactly is the tetanus vaccine

A

Formalin inactivated, adjuvanted toxoid - alone or in combination with others

138
Q

What risk factors should indicate that a horse should be vaxxed for Rhinopneumitis? (EHV)

A

horses less than 5 yrs of age
horses on breeding farms or in contact with pregnant mares
horses housed at facilities with freq. equine movement on + off premises
performance or show horses in high risk situations

139
Q

What risk factors should indicate that a horse should be vaxxed for strangles?

A

if they live on premises where strangles is a persistent endemic problem

less than 5 years of age

140
Q

What is the fecal egg count reduction test

A

used to determine if strongyles and/or ascarids are resistant to a given antihelminthic

141
Q

Why do we monitor ERPs?

A

has the most practical implication for measuring possible emergence of resistance for common antihelmintics

142
Q

What are common equine nematodes?

A

large strongyles
small strongyles
Pinworms
Ascarids (round) worms

143
Q

T or F Strongyles have intermediate + Paratenic hosts

A

False, they have direct life cycles!

144
Q

Where do cyathostomins (small strongyles) encyst

A

in the mucosal lining of the large intestine

145
Q

What age group do ascarids like to infect + what cs does it cause?

A

foals/ weanlings
weight loss, diarrhea, impaction

146
Q

T or F: most horses develop strong immunity + eventually cease shedding eggs

A

true

147
Q

What is the gold standard for detecting anthelmintic resistance

A

Fecal egg count reduction test

148
Q

When are fecal egg count reduction tests

A

more reliable during grazing season as encysted cyathostomins tend to accumulate during autumn and winter months
Adult female worms shed fewer eggs when it is not grazing season

149
Q

What parasites can be identified with the Baermann technique

A

lungworms and immature cyathostomin infections

150
Q

What are reasons to do a fecal egg count

A

evaluate efficacy of drugs
evaluate and monitor ERP
Determine shedding status of horse
determine parasite burdens in foals and weanlings as round vs strongyle

151
Q

What are limitations of Fecal egg count

A

doesn’t accurately reflect true worm burden
doesn’t detect immature or larval stages of parasites
underestimate tapeworm infections
pinworms (scotch tape test) + gastrophilus don’t shed in feces

152
Q
A

LAM (6 decks)

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