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1. Specialty - Reading List > Things To Know > Flashcards

Things To Know Flashcards

1
Q

most common murmur in horses

A

aortic regurg associated with degenerative valve disease

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2
Q

anemia, neutrophilia, increased globulins, SAA, fibrinogen, +/- liver enzymes

ventricular hyperkinesis and chamber enlargement on echo

ragged edges of one valve appreciated

A

bacterial endocarditis

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3
Q

prognosis of TR in horses

A

Negative indicators include TR associated with:
1. structural valve lesions (endocarditis, flail leaflets, ruptured chordae tendinae)
2. clinical signs of right sided CHF
3. severe MR or pulmonary hypertension

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4
Q

in horses, degenerative valve disease affects which valve most frequently

A

aortic

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5
Q

what is the cause of TV endocarditis in horses

A

IVC infections

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6
Q

endocarditis mostly affects what valve in horses

A

aortic and mitral equally

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7
Q

bacterial endocarditis most commonly affects what valve in cattle

A

tricuspid

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8
Q

abnormal systolic jugular venous pulsations occur with

A

tricuspid regurg

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9
Q

bounding arterial pulse quality indicates what in horses with AR

A

severity and left ventricular volume overload

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10
Q

AR in horses

A

L sided diastolic
descrescendo, musical

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11
Q

what category of murmurs are most common in large animals

A

diastolic, regurgitation

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12
Q

what can help distinguish v-tachycardia from other tachy-arrythmias?

A

jugular pulses
bruit de cannon
rapid regular rhythm

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13
Q

drugs for v tach treatment

A

lido
quinidine
procainamide
mag sulfate

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14
Q

Treatment for V-tach is indicated when?

A
  1. HR >120 horses, >140 cattle
  2. clinical signs of CHF or CV collapse
  3. multifocal origin for VPD’s
  4. torsades des pointes (wide VT)
  5. “R on T”
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15
Q

coumarin-derived anticoagulant

A

warfarin

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16
Q

how does warfarin act

A

competitive inhibition of vitamin K

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17
Q

vit K dependent clotting factors

A

2, 7, 9, 10

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18
Q

CS of warfarin toxicosis

A

hematomas, ecchymoses of mms, epistaxis, hematuria

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19
Q

lab indication of warfarin tox

A

prolonged PT
because the plasma half life of factor 7 is shorter than the others

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20
Q

diagnosis of warfarin tox

A

history
signs of large vessel hemorragic diathesis
history of exposure
prolonged PT, +/- PTT
no other clotting abnormalities
!!

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21
Q

treatment of warfarin tox

A

give Vit K1 .5-1mg/kg (SC or IM) q6h until PT is normal again

DO NOT GIVE K3 - highly nephrotoxic

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22
Q

CS: spontaneous bleeding, intermittent epistaxis unrelated to exercise, petechial and ecchymotic hemorrhages, hematomas, prolonged bleeding after sx or needle sticks

Platelets have normal morphology, coag parameters, and FDPs

A

Glanzmann’s thrombasthenia

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23
Q

Glanzmann’s thrombasthenia gene

A

ITGA2B

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24
Q

glanzmann’s thrombasthenia

A

platelets are unable to aggregate in response to collagen or ADP blood forms loose clots with limited serum separation and deceased tensile strength

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25
Q

atypical equine thrombasthenia

A

TB’s

-platelets form normal clots and aggregate normally in response to ADP
-significantly reduced fibrinogen binding
-limited prothrombinase activity
-give amicar at sx

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26
Q

equine anemia
-edema, fever, etc.
-morulae observed in the cytoplasm on neutrophils

A

anaplasma phagocytophila

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27
Q

diagnosis of anaplasma

A
  • morula within the cytoplasm of neutrophils and eos (difficult to find though!!
    )
    -positive PCR on blood (buffy coat)
    -paired serology
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28
Q

tx of anaplasma

A

oxytet / doxy

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29
Q

-appear within mature erythrocytes
-non pigmente, paired, pair shaped bodied joined at an acute angle

A

Babesia bigemina

big boy

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30
Q

-small, pleomorphic
-single round or pear shape
-joined at an obtuse angle within mature erythrocyte

A

babesia bovis

little b

the most virulent of the 2

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31
Q

what tick spreads babesia

A

one-host, infected transovarially

boophilus

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32
Q

how does babesia cause anemia

A

-intraerythrocytic reproduction, then the escaping merozoites destroy cells intravascularly
-massive osmotic lysis
-immune mediated removal of damaged and healthy RBCs

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33
Q

diagnosis of babesia

A

-identification on Giemsa-stained blood smears
-serology
-PCR

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34
Q

prognosis of babesia tx

A

better if PCV >12%
poor if PCV <10%

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35
Q

maltese cross

A

-thileria equi
-intraerythrocytic parasite of the horse
-divides into four cells
-treat with imidocarb

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36
Q

QH gelding with blood at the end of urination - most likely cause

A

urethral hemorrhage
-tear / fistula formation along the dorsocaudal aspect of the ischial arch
- Dx on scope
-rest, can give TMS, Sx correct if persistent prob

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37
Q

according to smith, what gent dose is require for nephrotoxicity in the healthy horse?

A

20mg/kg q8h for several days

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38
Q

leptin and adiponectin come from?

A

they are both adipokines released from fat tissue

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39
Q

adiponectin

A

-anti-inflammatory
-insulin-sensitizing
-decreases with obesity, IR, and laminitis risk

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40
Q

which adipokine is helpful in assessing laminitis risk

A

adiponectin, NOT leptin

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41
Q

if cows are going down 48 hours post calving, what do they need?

A

CALCIUM

add calcium salts IV, SC
manage DCAD

42
Q

prussian blue stain detects

A

hemosiderin
iron stores or deposits

43
Q

Hemochromatosis

A

Deposition of hemosiderin in parenchymal cells -> tissue damage and dysfunction of liver and other tissues

-Described in Salers cattle:
-Increased iron deposits in liver
-Homozygous recessive inappropriate absorption of iron by GI tract, with subsequent hepatic storage and loss of hepatic function

44
Q

CS of hemochromatosis in cattle

A

decreased weight gain, poor BCS, dull hair coat, loss of incisor teeth, diarrhea

Total serum iron, total iron-binding capacity, and saturation of transferrin (>60%) are increased

Liver iron concentration: >5000ug/g on a wet basis

45
Q

CS of hemochromatosis in horses

A

-ALP, GGT, AST elevated, serum total bile acids >40uM/L
-Total serum iron NOT elevated no saturation of the iron-binding capacity
-Total liver iron: as high as 6700 ppm

46
Q

Hemosiderosis

A

iron accumulates in reticuloendothelial system, not hepatocytes

47
Q

hemochromatosis results in

A

accumulation of iron in the LIVER / hepatocytes

48
Q

in horses with hepatic disease, what were specific indicators of non survival?

A
  1. SBA > 20umol/L
  2. histopath score > 2
49
Q

in horses with hepatic disease, serum bile acids were associated with what

A

-inflammation
-fibrosis

suggesting interference with hepatic function

50
Q

Type 1 vagal indigestion

A

gas accumulation - free gas bloat

always failure to eructate not increased production

upper left distention

51
Q

Type 2 vagal indigestion

A

failure of omasal transport - obstruction of the omasal orifice can be either functional or mechanical
rumen distended with feed

fluid accumulation arises from a failure of rumen outflow with continued food and water intake and saliva production

abdomen is distended at the
midflank and dorsally on the left and ventrally on the right

on rectal examination,
the classic finding of an “L”-shaped rumen is felt due to the significant expansion of the ventral sac toward the right flank

52
Q

Type 3 vagal indigestion

A

failure of abomasal outflow

primary or secondary abomasal impaction
1. Primary - dry course feed with limited water.
2. Secondary - disturbances in abomasal motility or pyloric outflow failure.

classic papple shape

causes: TRP, ischemia of the vagus nerve as a sequelae to RDA, mechanical obstruction or neurogenic dysfunction at the level of the pylorus d/t lymphosarcoma

53
Q

Type 4 vagal indigestion

A

failure of pyloric outflow

partial forestomach obstruction common in late pregnancy

less distention than type 2/3

the enlarged uterus displaces the abomasum cranially

54
Q

most common clinical sign seen with lawsonia (EPE)

A

hypoproteinemia

T.P. < 5.0 g/dl with albumin usually < 2.0g/dl.

55
Q

lawsonia testing in foals on farm?

A

rtPCR is most SENSITIVE

56
Q

lawsonia testing in adults

A

Immunoperoxidase monolayer assay is the most SPECIFIC when determining presence of antibodies in adult horses with EPE

57
Q

tx for salmonella in cows

A

TMS or florfenicol or cephalosporins

58
Q

what antibiotic can be used in feedlots to prevent liver abscesses

A

tylosin

59
Q

how long after infection do horses shed coronavirus?

A

up to 24 days

60
Q

what volume of colostrum does a dairy calf need

A

4L with 50gg/L IGG

61
Q

Dx and Px for a 2 month old foal with hypermetria and trouble nursing

A

cerebellar hypoplasia

bad

62
Q

Fell / Dale immunodeficiency syndrome

A

-normal at birth, develops up to 3 months later
-anemia: normocytic normochromic, no hemolysis
-WBCC low, B cells low, T cells normal, neutrophils often high

63
Q

Difference between Fell/Dale immunodeficiency and SCID

A

SCID: No IgM, no B or T cells, lymphopenia

F/DI: low IgM, low B normal T cells, anemia + lymphopenia

64
Q

Tyzzer’s diagnosis

A

-multifocal hepatitis and necrosis
-Intrahepatocellular filamentous bacteria will be present at the periphery of the lesion.
-Silver and Giemsa stains may help facilitate diagnosis.
-PCR for C. piliforme can aid in diagnosis and treatment.

65
Q

cause of head tilt in a calf

A

mycoplasma bovis otitis
treat with oxytet or tulathromycin

66
Q

The EPM SAG2, 4/3 ELISA indicates a serum positive for exposure at

A

> 1:250

67
Q

The EPM SAG2, 4/3 ELISA Serum:CSF ratio is predictive of EPM if

A

< 100

68
Q

The EPM SAG2, 4/3 ELISA correlates well with EPM if the CSF value is

A

> 1:40

69
Q

which biovar causes more cases of EHM?

A

EHV-1 D752 (n is more abortions)

70
Q

CSF in EHM

A

xanthrochromia
increased protein
+/- monocytic pleocytosis

71
Q

Scrapie transmission

A

PrPsc occurs at very high concentrations in placental tissue and fluids and is also shed in colostrum and milk, making the periparturient period the riskiest time for the transmission of classical scrapie. Most animals are thought to be infected from their dam at or near birth. Horizontal transmission to other members of the herd or flock that contact fetal membranes and fluids increases during this time as well. Evidence for in utero transmission has been documented. In one study of experimentally infected pregnant ewes, even delivering lambs via cesarean section and removing them immediately from the dam did not break the transmission cycle.

72
Q

WNV and viremia

A

level of viremia directly correlates with the probability of neuroinvasion

73
Q

CAEV diagnosis in a goat kid

A

ELISA is sensitive
AGID is specific
PCR is specific

kids may be transiently positive on serology with MDA - but PCR should be true

74
Q

D, L tryptophan

A
  • lush forage in autumn
  • causes AIP
  • converted to 3-methylindole in the rumen
75
Q

AIP signs

A

pulmonary emphysema
edema
hyaline membrane formation
alveolar epithelial cell and intersitial tissue hyperplasia

76
Q

furasium solani

A

moldy sweet potatoes

4-ipomeanol is the pulmonary toxin

77
Q

perilla frutescens

A
  • cause of AIP
  • perilla ketone
  • high morbidity and case fatality
78
Q

primary ruminal tympany

A

frothy bloat
-pasture: legumes, alfalfa hay
-feedlot: finely ground grain

79
Q

bloat safe legumes

A

digested more slowly

80
Q

preventing feedlot bloat

A
  • rations should contain 10-15% roughage, chopped and mixed in
  • use cereal grain straw or grass hay
  • NO ALFALFA
  • NO FINE GRAINS OR PELLETS
  • rolled or cracked
  • can add tallow or salt
81
Q

strangles SeM titres

1:200-400

A

Weak

  • very recent exposure
  • vaccinated a long time ago
  • rec repeat test in a week
82
Q

strangles SeM titres

1:800-1600

A

Moderate

  • 2-3 weeks post exposure
  • 6mos - 2yrs post infection
83
Q

strangles SeM titres

1:3200 - 6400

A

High

  • 4-12 weeks after infection
  • 2 weeks post vaccination
  • DO NO VAX
84
Q

strangles SeM titres

> 1:12,800

A

Very high

  • diagnostic for abscess or purpura
85
Q

After sx and ventilation, what pneumonia should be suspected? What prognosis?

A

-Klebsiella
-pleuropneumonia
-47% survival

86
Q

“rattles”

A

watery mouth
-e coli endotoxemia and FPT
-NO DIARRHEA
-dull weak cold bloated

87
Q

SCID foal presents with pneumonia

A
  • DX pneumocystis carii
  • TX TMS
88
Q

D-penicilamine

A

binds excess copper

89
Q

What changes can you expect with Vitamin D supplementation in camelids?

A

-increased Ca/Mg
-calcinosis
-increased P?

90
Q

chronic sorghum ingestion causes what

A

-ataxia, hopping gait of both hind limbs
-urine dribbling, flaccid bladder
-abortion, arthrogryposis, neuro defects

91
Q

best antioxidants for cows

A

feed selenium and VitE at NRC guidelines

minimize NEB!

92
Q

lead poisoning in cows

A

-CNS derangement
-ataxia, fasciculation, cortical blindness, running, bellowing
-frothing and GI signs

93
Q

lead poisoning in horses

A

weight loss, incoordination, laryngeal paralysis, CP deficits, loss anal tone, facial paralysis, dysphagia

94
Q

DX lead poisoning

A
  • heparinized blood will not chelate lead
  • level in liver / kidney / bone
95
Q

TX lead poisoning

A

calcium disodium EDTA chelation

sx removal from GIT

96
Q

vitamin a deficiency occurs in

A

growing feedlot cattle
-short term protection by ability to accumulate in the liver
-poor dry forage and grains

97
Q

CS of Vit a deficiency

A

-ill thrift, diarrhea, blindness, pneumonia
-star gazing and seizures in adults

98
Q

which influenza vaccine is recommended to use in an outbreak

A

Flu-Avert intranasal single dose

induces protection within 7 days

99
Q

apolipoproteins upregulated in inflammation
-induced proteins that chemotactically recruit neutrophils

A

SAA

100
Q

which type of pain medication stops nerve transmission?

A

local / lido etc

101
Q

EVA

A

-fever, anorexia, orbital edema / conjunctivitis / lacrimation
- edema and urticaria
- abortion
- aerosol spread or venereal

102
Q

what abc are approved for mastitis

A

NO systemic
7 IMM formulas

1. Specialty - Reading List (9 decks)

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