Misc. Notes Flashcards
Increasing SID is
alkalinizing
due to:
decreasing anions
increasing cations (Na K Ca Mg)
Decreasing SID is
acidifying
due to:
increasing anions (Cl protein lactate ketoacids sulfates)
decreasing cations
approx 2/3 of anion gap is due to the charge of what
-ve charge of albumin / protein
AG equation
(Na+ + K+) - (Cl- + HCO3-)
SIG simplified equation
Na+ + K+ - Cl-
Met Acidosis
dec / -BE
dec HCO3
dec TCO2
Met Alkalosis
inc BE, HCO3, TCO2
FE of x equation
(Serum cr X Urine x) / (Urine cr / Serum x) X 100
Major crossmatch
Donor RBC, Recipient serum
Minor crossmatch
Recipient RBC, donor serum
total blood vol horse
8% BW - 40L
safe to remove how much blood
20% of blood
8% of BW
approx 8L
blood txfn equation
BW x 0.08 x [(desired - actual PCV)/donor PCV]
black leg
c. chauvei
black disease
c. novyi type B
bacillary hemoglobinuria
c. novyi type D
malignant edema
clostridium septicum
clostridia affecting feedlot cattle
c. sordeli
yellow lamb dz
c. perf type A
alpha toxin
lambs - hemolysis
calves - abomasa tympani and ulcers
cattle - hemorrhagic enteritis
enterotoxemia
c. perf type B
alpha, beta, epsilon toxin
enteritis, enterotoxemia, lamb dysentery
necrotic enteritis
c. perf type C
alpha, beta toxin
+/- enterotoxemia
any neonates affected
pulpy kidney
c. perf type D
alpha, epsilon toxin
+/- enterotoxemia
sudden death
sheep affected more than goats/cattle
*focal symmetric encephalomalacia and glycosuria due to hyperglycemia
c. perf type E
abomasal ulcers in calves
Type I error
rejected null hypothesis when it was true
-no real difference existed
-the study did find a difference
Type II error
failed to reject the null hypothesis when it was false
-a true difference existed
-the study failed to detect that difference
under-powered study
source of type II error
-sample size
-variability among subjects
-difference between group means
-a-level
when does CK peak
4-6hrs
when does AST peak
24 hrs
what level of AST would indicate rhabdo vs. travel, etx
> 4000u/l
what changes when muscle cells are injured
K, PO4, and Mg leak OUT
Na, Cl, and Ca leak IN
causes and Dx of exertional rhabdo
RER - exercise test
MH - RYR1 gene (aut dom)
PSSM1 - GYS1 gene (aut dom)
PSSM2 (mus biopsy)
MYM (mus biopsy)
causes and Dx of NON-exertional rhabdo
GBED - GBE1 (aut rec)
NMD - selenium / vitE
MMM - acute master atrophy
Hypoglycin A -
RER treatment
limit NSCs
controlled daily exercise
dantrolene prior to exercise
amylase resistant glycogen is a feature of what dz
PSSM1
amylase sensitive glycogen is a feature of what dz
PSSM2
myofibrillar myopathy (MYM)
likely heritable dz of WBs and arabs
intermittent increases in CK, exertional rhabdo
large design and alpha beta crystallin aggregates
systemic calcinosis
sudden onset epaxial/gluteal muscle atrophy, incr. AST and CK in QHs <9YO
biopsy shows dystrophic calcifications
can also affect other organs ex. lung and GIT
otobuis mogini
spinous ear tick
causes painful muscle contractions - Myotonia
remove and should recover in 36 hours
inherited myotonias
congenita, dystrophia, or HYPP
SCN4A gene
HYPP
58% of QHs
autosomal co-dominant
HYPP
-Na closer to threshold, channels don’t inactivate, K efflux / Na influx
-Triggers: GA, transport, stress, cold, diet high in K
-exercise is NOT a trigger
-CK is usually normal
-Tx: drive K intracellular w/ dextrose, bicarb, calcium; acetazolamide
most common serogroup of Pasturella Multocida in ruminant respiratory disease
A
(5 groups)
most common pathologic serogroups of Man. Hemolytica
A1, A6
(A2 normal flora in cattle, pathologic in SR’s)
most common pneumonia agent in dairy calves
pasturella
causes of fibrinous pleuritis
-mannheimia hemolytica
-also histophilus somni
Amphotericin B
binds ergosterol = cell destruction
Benzimidazole Derivatives
-azoles
inhibit ergosterol biosynthesis
Itraconazole
60% bioavailability
-histo, blasto, and aspergillus
-no adverse effects at 5mg/kg SID
Ketoconazole
poor bioavailability PO
Fluconazole
good plasma, CSF, synovial, aq humor, urine concentrations at 5mg/kg PO SID
-NOT active against fusarium or aspergillus
Vorizonacole
increased volume of distribution w/ systemic administration 4mg/kg PO SID
-choice for aspergillus, crypto, fusarium, candida, bipolaris, sedosporium
conidiobolomycosis coronatus
-granulomatus, URT, increased Eos on histo
-thin walled hyphae, septet, irregular branching
-Tx: topical or intralesional amphotericin B
cryptococcus neoformans
-saphrophytic round non staining capsule
-Tx: amphotericin B IV q24h, fluconazole PO long term, or Vori
-pneumonia, abortion,meningitis, or rhinitis
pseudollescheria boydii
-nasal mycosis
-Tx: topical miconazole
-cant diff on cytology from aspergillus or fusarium
Aspergillus spp
-broad septet hyphae, acute angle branching
-GI or lung opportunistic invasion
-Tx: amphotericin B or itraconazole or Vori if there is rhinitis / sinusitis + topicals
Blastomycosis
-suceptible to amphotericin B, itraconazole, and fluconazole
Histoplasma capsulatum
-suceptible to amphotericin B, intaconazole, or fluconazole
coccioides immites
-inhaled
-causes lung granulomas
-Tx: itraconazole or fluconazole
candida albicans
-fluconazole is first choice
-c. krusei –> vori or amph. B
pneumocystis cannii
-lacks ergosterol
-exists as ameboid yeast
common in SCID foals
-Dx: BAL/TW cytology, can’t culture
-Tx: TMS
one of the following general conditions must be met before you can legally prescribe an approved human or animal drug for an extra-label use:
–There is no animal drug approved for the intended use; or
–There is an animal drug approved for the intended use, but the approved drug does not contain the active ingredient you need to use; or
–There is an animal drug approved for the intended use, but the approved drug is not in the required dosage form (for example, you need a liquid dosage form, but the approved drug is only available as a tablet dosage form); or
–There is an animal drug approved for the intended use, but the approved drug is not in the required concentration (for example, you need 5 mg, but the approved drug is only available at 50 mg); or
–You have found, in the context of a valid veterinarian-client-patient relationship, that the approved drug is clinically ineffective when used as labeled.
For production animals, FDA’s requirements for extra-label drug use
*prohibit or allow?
you from prescribing an approved human drug if there’s a drug approved for food-producing animals that you can prescribe instead.
PROHIBIT
For example, if a drug approved for chickens is available, you must first use that drug to treat a sick cow before reaching for a drug approved for people.
Drugs Prohibited from Extra-Label Uses in all food-producing animals, including horses intended for human food:
Chloramphenicol
Clenbuterol
Diethylstilbestrol (DES)
Dimetridazole
Ipronidazole and other nitroimidazoles
Furazolidone and nitrofurazone
Sulfonamide drugs in lactating dairy cattle, except for the approved use of sulfadimethoxine, sulfabromomethazine, and sulfaethoxypyridazine
Fluoroquinolones
Glycopeptides
Phenylbutazone in female dairy cattle 20 months of age or older
Cephalosporins (not including cephapirin) in cattle, swine, chickens, or turkeys:
-For disease prevention purposes;
-At unapproved doses, frequencies, durations, or routes of administration; or
-If the drug is not approved for that species and production class.
AA critical in maintaining GI mucosal integrity and immune function
glutamine
AA precursor of synthesis of nitric oxide and upregulates immune function
arginine
RER for 500kg horse
~11.5 Mcal/d (48.1 MJ)
refeeding syndrome
Refeeding w CHO causes an incr in insulin secretion, stimulating glycolysis, fat and protein synthesis, processes which require phosphate (for phosphorylation and adenosine triphosphate synthesis), magnesium, K and cofactors such as thiamine
Additionally, insulin also stimulates the flux of K into cells
During fasting, whilst serum levels of electrolytes remain normal, intracellular levels are severely depleted
Feeding-induced abrupt intracellular shift of these electrolytes and minerals results in acute hypoP, hypoK, hypoMg and reduced thiamine
Hallmark blood biochemical feature of refeeding syndrome, hypophosphataemia, was present in all horses refed under experimental conditions regardless of diet
Clinical manifestations of refeeding syndrome (respiratory failure, circulatory collapse, neuro signs, GI disturbances) can be avoided by recognition of its possible occurrence prior to the intro of feed, gradual reintro to nutritional support and close monitoring of serum conc of these electrolytes w supplementation based on measured levels
Routine supplementation of K (eg 0.1 g/kg bwt/d)
Phosphate can be supplemented through inclusion of phosphorus-rich bran, mineral dense alfalfa hay, or calcium/sodium phosphate
Thiamine supplementation also recommended – oral supplementation (1000 mg/d) can be achieved w commercial powder or paste formulations or the addition of supplements w a high thiamine content (eg brewer’s yeast)
hyperlipaemia
Hyperlipaemia occurs when rate of lipolysis from adipose stores exceeds rate of removal of TG from plasma
Insulin resistance (IR) is important feature of affected animals
-Insulin: highly anabolic hormone promoting storage of E as fat and glycogen – facilitation of lipolysis and glycogenolysis are inherent features of IR status
Procatabolic status of IR may be esp hazardous when facilitation of lipolysis combined w excessive amounts of substrate (ie adipose stores) in obese animals
Dz resulting from excessive mobilisation of TG stores st plasma clearance processes become overwhelmed à increased plasma [TG] (>5.6 mmol/L), visibly cloudy plasma and a sick anorexic or hyporexic subject follows
Pathological exaggeration of the normal process by which fat deposits are mobilised in the face of a negative E balance –> sick individual w multiorgan compromise demonstrating opacity of plasma owing to high circulating concentrations of abnormal lipoproteins
Major route for NEFAs and glycerol after uptake into liver is
re-esterification back into TG
hyperlipemia diagnosis
1) plasma TG (within VLDL) is > 5.6 mmol/L
(2) plasma or serum grossly cloudy/milky
(3) affected animal overtly sick as a consequence of the lipaemia
CSx: nonspecific, poor to absent appetite, dullness
hyperlipemia tx
-IV AAs and glucose
-insulin - but they are IR
-heparin:Known to stimulate lipoprotein lipase activity in plasma, which may aid clearance of excessive VLDL
Has been used in hyperlipaemia cases at 40-250 iu/kg q 12 h
Heparin therapy might be applied most logically in the presence of inflammatory disease in which cytokines such as TNF-a and GMCSF might be inhibiting lipoprotein lipase
Possible risks of coagulopathy should be monitored
-Alpha-2-adrenergic agonists
Shown to be potent inhibitors of lipolysis – safe to use for sedation in cases.
ketamine
Antagonism of ketamine on the N-methyl-D-aspartate (NMDA) receptors was demonstrated to be responsible for most of the anaesthetic, analgesic, psychomimetic and neuroprotective effects of the drug
Give cautiously to horses w hepatic or renal dysfunction
acorn tox
tannins metabolized to pyrogallol and gallic acid
effect protein binding (salivary, endothelial cells, microbial proteins, alter GI flora)
gastroenteritis and nephrotoxicity
Mares with post partum colic had what measurable changes prior to the colic episode?
higher NEFA (14 day pre - 4 day post foaling)
lower iCa (15-28 days post foaling)
complications of eq coronavirus
associated w disruption GI barrier: endotoxaemia, septicaemia and hyperammonaemia-associated encephalopathy
Doxapram in CPR
don’t use! Increases cerebral oxygen demand
transient bacteremia after tooth extraction - what is usually isolated?
Streptococcus spp, Actinomyces spp, Fusobacterium spp, and Prevotella spp were most commonly found. Bacterial genera isolated from swab samples of extracted teeth largely corresponded w those identified in blood cultures
deworming foals <2 months old
only if they have clinical signs of strongyloides westeri enteritis
Strongyloides westeri
Transmammary (lactogenic) route of transmission L3, ingestion of infective larvae from environment, percutaneous from moist environments
Adults: SI, eggs in faeces foals as young as 5 d
Gen not severe pathogen, csx diarrhoea, lethargy, reduced weight gain
Tx if clinical signs enteritis – ivermectin (200 mg/kg), moxidectin (400 mg/kg), oxibendazole 10 mg/kg (label is 15 mg/kg), FBZ
Parascaris spp
Predom equine ascarid sp is P univalens and not P equorum, as commonly assumed
Even foals of youngest age group likely to ingest ascarid eggs as they suckle mare and explore env
Ingestion of eggs à larvae hatch in SI and travel in lymphatics to liver à wander in hepatic parenchyma for 1-2 weeks à enter systemic circulation, carried through R heart and into pulmonary vasculature bed à L3s break out of pulmonary venules/capillaries and enter the alveoli à migrate proximally up the airway or are propelled by coughing into pharynx à swallowed and return to gut where moult to L4 and L5 and begin maturation
PPP 75 – 90 d
Anthelmintic tx of foals < 2mo not recommended – this age: ascarid popn comprised of L4 and immature adults, and anthelmintic efficacy oft suboptimal against immature nematodes
OBZ 10 mg/kg efficacy against patent infections
When to deworm foals for ascarids?
after 60 days
early neuroimmune response to WNV infection in the horse
data show WNV-challenged horses recruit a mixed T cell population at the onset of neuro disease (CD3/4/8+)
equine herpesvirus-associated myeloencephalopathy is the result of
endothelial cell infection of the spinal cord vasculature w EHV-1 during cell-associated viraemia
contact btwn infected peripheral blood mononuclear and endothelial cells
Inflammation generated during viraemia likely upregulates adhesion molecule expression on both cell types increasing contact and facilitating endothelial cell infection
anti-inflammatory drugs decrease infection of endothelial cells likely by reducing contact between EHV-1 infected PBMC and endothelial cells in vitro. The role of adhesion molecules in this process needs further investigation. In vitro results suggest anti-inflammatory drug therapy during EHV-1 infection and viraemia in horses could be clinically relevant.
Corynebacterium pseudoTB produces various ____? that play a role in virulence
extracellular endotoxins
– most studied is phospholipase D (PLD); contributes to tissue pathology and host recognition of PLD can be used diagnostically
-causes hydrolysis and degradation of sphingomyelin in endothelial cell membranes, increasing vascular permeability and facilitating spread and persistence of the bacteria in the host
-PLD toxin produces the pain and edema at infection site
SHI Test
The synergistic activity of Cp exotoxins w the exotoxins of R equi in lysing rbc in agar forms the basis for the synergistic haemolysis inhibition test
SHI detects IgG Ab to Cp and can be used as an aid to dx internal infection – can get titres from being exposed to contaminated env or external infection also
when are abx indicated for pigeon fever
ulcerative lymphangitis, msk infections, internal abscesses, immune compromise – typically 30 d +
Abx may be justified w signs systemic illness (fever, depression, anorexia) or extensive cellulitis present, also consider for horses w deep IM abscesses that are lanced and draining through healthy tissue
might need IV or addition of rifampin
a-fib might be heritable in
STBs
male - pacers
how does asthma affect the heart
Even in remission, asthmatic horses showed a thicker RV wall, an increased LV end-systolic eccentricity index at chordal level and decreased RV longitudinal strain cf controls
CONC: pulmonary obstruction in asthmatic horses induces pulmonary hypertension w RV structural and functional changes
presence of R-on-T phenomenon
VT: ectopic beat occurs during the T wave of preceding QRS, while the ventricle is still repolarising and in its vulnerable period
Torsades de pointes
particular form of wide complex polymorphic VT where the QRS complexes and T waves twist around the baseline of the ECG
ideal asthma tx
long term, inhaled corticosteroids and beta 2 agonists
rifampicin
10mg/kg PO SID
does powdered alpha tocopherol supplementation increase CSF levels?
NO
does oral prednisolone increase incidence of acute laminitis
NO
data suggest that plant extracts A dracunculus, M pulegium, and Z multiflora havepotential to be used as what?
anthelmintic for the control of ascariasis in equid host
what is the treatment for extrapyramidal effects associated with metaclopramide?
diphenhydramine or anti-histamines
most common causes of pleural effusion in horses
neoplastic (older horse, low TNCC and TP<40g/L)
2ry to bacterial pneumonia (younger, febrile, smaller fluid volume, increased fibrinogen and SAA)
Grade 4 EIPH is associated with racing performance how?
significantly more likely to have a lower finishing position and finish further behind the winner
less likely to place in the first 3 positions and collect race earnings
collected less earnings per race start and were slower over the last 600 m of the race than horses without EIPH (grade 0)
Clinical factors associated w reduced survival in cases of atypical myopathy
Hypothermia (OR 0.18)
Bladder distension (OR 0.11)
Tachycardia (OR 0.97)
Serum CK >100,000 IU/L (OR 0.17)
Recumbency (only factor retained in multivariable analysis, OR = 0.19)
Administration of vitamins during the disease was associated with survival (OR 3.75)
a neurological disease clinically characterised by knuckling of metatarsophalangeal joints, has been described in numerous Nordic horses during last 20 years
acquired equine polyneuropathy
most survivors will recover and return to minimum previous level of athletic performance.
Some horses display residual clinical signs, but often without negative effect on performance and relapse of disease is rare
acquired equine polyneuropathy
histopath findings
peripheral nerves: large fibre predominant neuropathy w conspicuous inclusion body schwannopathy and demyelinating inflammation, supporting ubiquitous histopath features
acquired equine polyneuropathy
CS and etiology
CS: knuckling in fetlock joints of pelvic limbs, horses otherwise BAR
– Unknown aetiology, but seasonal pattern w most cases in winter and spring; most affected horses have been fed wrapped forage, suggesting an environmental, possibly feed-related trigger
– AEP often affects more than one horse at a farm (but prev studies concluded no indication of infectious aetiology)
– Severity ranges from intermittent knuckling (often worsened by stress) to recumbency
– Many horses recover w/ months of rest, some become recumbent and euthanized
sCD14 molecule
soluble CD14:
–amplified early in response to inflammatory signals, including bacterial LPS
–released primarily in response to LPS-induced signalling through TLR4 and magnifies the early inflammatory response to bacterial LPS
–studied as a biomarker for clinical endotoxemia
–higher in horses classified as clinically endotoxaemic
–> poor predictor for clinical endotoxemia
4% modified fluid gelatin
can be used instead of 6% hydroxy ethyl starch for volume expansion and oncotic support
–no adverse effects on hemostasis or renal parameters
main factors affecting outcome in equine neonates admitted to hospital at UGA from 80s-2000s
primary disorders, sepsis, temperature, acid base status, and neutropenia
odd of survival for equine neonates in 00’s vs 80’s
increased by 3.4X
Equine laryngeal dysplasia
a congenital disorder caused by hypoplasia or aplasia of the structures derived from the fourth and possibly sixth branchial arches
–very rare, esp in a foal
–usual presentation abnormal noise during exercise and poor performance
–foal: severe resp distress and weakness
Can a critical number of intestinal progenitor cells predict tissue viability and survival to discharge of large colon volvulus (LCV) cases?
phosphor-histone H3 (PHH3)
<2.1 PHH3 positive cells per crypt were 96.6 times more likely to die; correctly predicted death w 100% Se and 84.62% Sp
Clinical presentation of strongylus vulgaris non-strangulating intestinal infarction
mild colic >24 h duration without signs of shock or strangulated intestine
increased peritoneal fluid WBC (>5 x 109/L)
increased [SAA] and a positive s. vulgaris-specific Ab titre
Survival of s. vulgaris non-strangulating intestinal infarction is possible in cases where
surgical intervention w resection of the infarcted intestine is feasible
–Infarctions may occur in segments of the intestinal wall when arteries or arterioles are occluded by thrombi produced as a consequence of larval migration in the main branches of the cranial mesenteric artery
–May have pyrexia, peritonitis and palpation per rectum of a painful and thickened mesenteric root in horses w S vulgaris-associated colic
long term survival reported after esophageal disorders
66%
Prevalence of oesophageal disorders was significantly higher in what group of horses
up tp 4 years of age
suggested etiology of EOTRH
contribution of initial biomechanical stresses and strains, followed by secondary involvement of micro-organisms
concurrent administration with rifampin affects clarithromycin bioavailability how?
actually DECREASES IT!
–Despite the profound decrease in clarithromycin bioavailability caused by concurrent admin w rifampin, concentrations of clarithromycin in PELF and BAL cells are well in excess of the MIC for at least 90% of R equi isolates (0.06 mg/mL) and even the concentration of clarithromycin that prevents emergence of resistant mutants (0.24 mg/mL when combined w rifampin)
–Combination of a macrolide w rifampin remains the recommended treatment of choice
WHAT has replaced erythromycin in the combination w rifampin for treatment of R. equi?
WHY?
Azithromycin and clarithromycin have replaced erythromycin in the combination w rifampin because of their higher oral bioavailabilities and considerably higher concentrations in pulmonary epithelial lining fluid and bronchoalveolar cells
When infection w a macrolide-resistant isolate of R. equipment is confirmed, limited effective alternatives exist.
Recommendations are:
IV or nebulised gentamicin (6.6 mg/kg bwt q 24). Use of vancomycin, imipenem, or linezolid in foals should be restricted to life-threatening R equi isolates caused by isolates confirmed to be resistant to all other possible alternatives
Anaemia with autoagglutination is consistent with
IMHA
Host-adapted leptospiral serovars are characterised by
lack of clinical disease, minimal Ab response and persistence of leptospires in the proximal renal tubules of maintenance hosts which allows for contamination of the env to infect both incidental and host-adapted species
Leptospires cause pathology by
penetrating mucous membranes or abraded skin and induce endothelial damage
Diseases associated w leptospirosis in horses
reproductive failure (abortion and hydrallantois), ERU, renal failure, resp disease, and foetal hepatic disease
common isolates in equine metritis
MIXED infections
–G- and enterococci oft assoc’d w resistance to most frequently used amx
–Potentiated sulphonamides not an appropriate 1st choice eq metritis
–Pen + amikacin or enro better than pen + gent
which corynebacterium causes abscesses in horses
c. pesudotuberculosis
NITRATE REDUCING BIOVAR
definitive diagnosis of c. pseudoTB
culture or synergistic haemolysis inhibition
(SHI) titres >1:512
CS of hypoPhosphatemia
obtundation, anorexia, tachycardia, tachypnoea, and generalised muscle fasciculations
Hyperlipaemia
TG >5.7 mmol/L (500 mg/dL), lipaemic plasma, csx present
well-described in minis that enter negative E balance, dt high hepatic efficiency of this species in the synthesis and release
Severe hypertriglyeridaemia
usually reserved to describe [TG] > 5.7 mmol/L in large breed-horses that are typically asymptomatic
Hyperlipidaemia
TG 1.0 – 5.7 mmol/L, plasma clear, csx absent
extracellular phosphate deficit (mmol) can be calculated as:
bwt (kg) x (desired phosphate concentration [mmol/L] – current phosphate concentration [mmol/L]) x 0.3 (the extracellular fluid coefficient)
acquired MADD results in inhibition of various mitochondrial enzymes, leading to diminished b-oxidation of fatty acids and accumulation of toxic acyl-CoAs
Atypical Myopathy
what substance was found to reduce intestinal binding of hypoglycin A
activated charcoal
b-amyloid precursor protein
beta-APP
b-APP is an extensively post-translationally modified and proteolytically cleaved transmembrane protein, assoc’d w synaptic formation and repair, that is present at high concentrations within neurons
Increased b-APP expression is part of the acute phase response to neuronal injury, occurring in acquired diseases, in various neurodegenerative conditions incl Alzheimer’s disease, in Down’s syndrome and tauopathies, and in murine neurodegenerative disease models - expression therefore not specific for EGS
diagnosing eq. grass sickness
–Histo exam of H&E stained rectal biopsies for chromatolytic neurons is insensitive as a diagnostic test for EGS
–authors hypothesised diagnostic accuracy could be improved by immunolabelling for b-amyloid precursor protein (b-APP), which has increased expression in cranial cervical ganglia (CGG) neuronal perikarya in EGS
– b-APP immunoreactivity was increased in neuronal perikaryal and axons in sections of CCG, ileum and rectum from EGS horses cf controls
– Rectal biopsies: mean immunoreactivity grade exceeding 1.1 was 100% Sp and Se for EGS, and the presence of at least one neuron w diffuse labelling of the entire cytoplasms (grade 3) was 95% Se and 100% Sp for EGS
CONC: histo assessment of b-APP immunolabelled rectal biopsies is more sensitive than conventional histo exam in EGS diagnosis
Soltalol
blocks both b1 and b2 receptors and has K channel blocking activity
By blocking outward K channels, sotalol inhibits the delayed rectifier potassium current, thereby slowing the repolarisation phase of the cardiac tissues
Due to its class III anti-arrhythmic effects, sotalol lengthens the QT interval, monophasic action potentials, and effective refractory periods (ERPs) in human and small animal cardiac tissues
does nebulized dex SP suppress HPA axis?
NO! But systemic admin does
does nebulized dex SP decrease BAL neutrophil % in healthy horses?
YES
gamithromycin + rifampicin
the plasma exposure of gamithromycin is significantly increased by co-admin of rifampicin which is most likely caused by inhibition of hepatic elimination
when to use gamithromycin + rifampicin
Abscess score >10 cm, WCC >13,000 cells/mL
Healthy neonatal foal E requirement
approx 20-150 kcal/kg bwt/d
RER critically ill neonatal foal
approx 50 kcal/kg bwt/d (~1/3 E requirement for growing, active normal foals)
Caloric content of 50% dextrose solution
1.7 kcal/g
benazepril treatment in horses with L sided valvular regurg
Relative to baseline, horses tx’d w benazepril had statistically significant reduction in:
–LV internal diameter in systole
–Aortic sinus diameter
–Percentage of the aortic annulus diameter occupied by the base of the AR jet
tx w oral benazepril (1 mg/kg q 12) resulted in statistically significant echocardiographic changes that might indicate reduced cardiac afterload in horses w L-sided valvular regurgitation.
is enalapril PO an effective ACE blocker in horses
NO - low bioavailability
what coag parameters may be affected if blood is drawn via an IVC
AT and D-dimers
What test is more accurate for prognosticating in equine hepatic dz?
biopsy
which coagulation parameter is altered with EHV-1 infection, in vivo and vitro?
EHV-1 infection increased peripheral blood mononuclear cell (PBMC) TF procoagulant activity in vitro and in vivo
In infected horses, this increase was observed during the acute infection and was most marked at the onset and end of viraemia
NSD were observed btwn horses that showed signs of EHM and the horses that did not develop EHM
recently discovered virus reported in case of invasive SCC
Equus caballus papillomavirus 8
the most common cause of fungal infections of the resp tract of horses in the SE US
Conidiobolus coronatus
c. coronatus
- fungal hyphae do not stain with H&E
- do not form large granulomatous masses - just slightly raised regions, pocked, maybe bleeding
the most suitable test currently available for assessing peripheral (tissue) insulin resistance
isulin tolerance test (ITT)
when does cTnI peak in healthy horses
2-6 hours post exercise
cor pulmonale
Development of pulmonary hypertension without a primary cardiac disease, secondary to a severe pulmonary parenchymal disease
This pathologic condition is a consequence of increased pulmonary resistance secondary to pulmonary vascular or parenchymal disease, and is associated w pulmonary arterial hypertension resulting in R ventricular hypertrophy and dilatation, and heart failure
Seen in cattle after living at a high-altitude (>2500 m) leading to hypoxia
cor pulmonale in horses
cardiac remodelling, uncommonly observed in horses, secondary to pulmonary hypertension leading to dilatation and hypertrophy of the right cardiac chambers
A few cases of cor pulmonary secondary to severe and chronic pulmonary diseases such as equine asthma, or granulomatous pneumonia, have previously been reported and these were oft assoc’d w poor prognosis
IgG measurements in foals
reference standard: radial immunodiffusion assay RID <8 g/L
Digital Brix: <7.8%
Optical Refract <44g/L
CONC: the two refractometers exhibit utility as rapid, inexpensive screening tests and have a good sensitivity for assessing FTPI in neonatal foals
eosinophilic keratitis
immune mediated disorder associated w an underlying type I or IV hypersensitivity reaction to parasitic or environment allergens
SUMMER
–blepharospasm, epiphora, conjunctival hyperaemia and corneal ulceration
–Caseous yellow discharge, yellow/whitish infiltrative deposits and/or corneal plaques are probably pathognomonic but only recorded in ~25% of cases
–Any aseptic nonhealing ulcer should be assessed cytologically in order to r/o EK, but false -ves may occur, as eosinophils are more likely to migrate into stroma layers in chronic cases, from where they keep releasing chemotoxic molecules that prevent epith healing
Localised nonprogressive EK
characterised by minimal corneal involvement and ocular pain, usu lesions are located around the third eyelid margin and they are reported as chronic/long standing non-healing ulcers. In some cases, as small, white/cream plaque that quickly detaches from the corneal bed can be see
Progressive extensive EK
characterised by marked ocular pain with extensive lesions that progress rapidly axially, generally from the periphery towards the central cornea. These lesions are more likely to form corneal plaques and get complicated w microbial infections, perhaps dt the extension of the epith impairment, involvement of the stromal layers is possible and should be considered in refractory cases
how does reserpine affect platelets?
reserpine causes significant changes in plt function, most likely dt serotonin release and re-uptake which primes platelets for activation and thromboxane B2 release
these findings suggest that clinicians should harvest blood for biological processing prior to the onset of reserpine administration
Renal Tubular Acidosis
result in a hyperchloremic metabolic acidosis and
clinical signs of depression and anorexia. Tachypnea
may also be present due to the compensatory mechanisms for metabolic acidosis
Type I RTA
occurs with distal tubular dysfunction
is classically described as a failure to excrete hydrogen
ions
A strong ion approach to the mechanism of type I
RTA would suggest that there is insufficient urinary NH4
+ to remove adequate amounts of chloride in the urine.
type II RTA
the proximal tubule fails to resorb adequate
bicarbonate.
A strong ion approach to type II RTA would
be consistent with an inappropriate reabsorption of
chloride.
how to distinguish between type I and II RTA
Evaluation of urine pH has been proposed as a
means for distinguishing between the two types of RTA
in horses, but this may be more complicated given the
normally alkaline urine of horses (Aleman et al., 2001).
Type I RTA would be associated with more alkaline
urine, and type II RTA with relatively more acidic urine.
Potential adverse effects of hypertonic sodium bicarbonate include
hyperosmolality of extracellular fluid, hypokalemia, hypernatremia, hypocalcemia, and paradoxic intracellular and CSF acidosis.
rectal fluid admin
plain fluids at 5ml/kg/hr
