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364 Cards in this Set
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Clinical Signs: Prolapsed third eyelid, elevated serum potassium, sweating, muscle fasiculations, muscular weakness, respiratory distress
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HYPP
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Myopathy that manifests as abnormal skeletal muscle membrane excitability leading to episodes of myotonia, sustained muscle contraction, and/or paralysis
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HYPP
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Definitive diagnosis is the the demonstration of the base-pair sequence substitution (phenylalanine for leucine) in the abnormal segment of the DNA encoding for the alpha subunit of the sodium channel. Submission of hair roots or whole blood (EDTA tubes)
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HYPP
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Why may a tracheostomy be required in the treatment of HYPP?
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Due to the respiratory distress from paralysis of the muscles of the URT and larynx.
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What is the treatment for mild cases of HYPP?
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Mild exercise (hand-walking) to stimulate epinephrine (which stimulates Na/K ATPase activity to mobilize potassium) and drive it intracellularly. Also, feeding grain or KARO syrup to stimulate insulin-mediated movement of potassium across cell-membranes. Avoid molasses!
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What is the treatment for severe cases of HYPP?
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Calcium gluconateto raise the membrane threshold potential which will decrease membrane excitability; IV dextrose +/- bicarbonate can be used to enhance intracellular movement of potassium.
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What dietary and management considerations should be employed in cases of HYPP?
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Avoid alfalfa, molasses, canola oil, and soybean oil. Multiple feedings per day. Regular exercise. Acetazolamide is a K-wasting diuretic that works by increasing renal potassium ATPase activity and stabilizes blood glucose.
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What disease is also known as "thumps" and when does it occur?
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Synchronous diaphragmatic flutter occurs in horses suffering from fluid and electrolyte imbalances.
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What is synchronous diaphragmatic flutter?
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Contraction or twitch in the flank region in synchrony with the heart.
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What is the most consistent metabolic derangement reported in horses with SDF? How does it work?
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Low ionized calcium associated with hypochloremic metabolic alkalosis. Metabolic alkalosis may alter the ratio of free to bound calcium (increasing calcium binding to protein and decreasing ionized calcium)
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How does synchronous diaphragmatic flutter occur?
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In association with atrial depolarization in horses; disruption of normal membrane potential of the phrenic nerve, which passes directly over the atrium and results in nerve discharges at depolarization.
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What are the most likely causes of ARF in the horse?
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Nephrotoxic exposure or due to hypoperfusion/ischemia of the kidney.
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What is the most common pathologic lesion of ARF in horses?
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Acute Tubular Necrosis
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What is the most common cause of acute tubular necrosis in horses?
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Administration of aminoglycoside antibiotics (-mycins)
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What is the most nephrotoxic of the aminoglycosides?
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Neomycin (gentamicin, kanamycin, and amikacin have similar levels of toxicity)
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What is the least nephrotoxic aminoglycoside?
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Streptomycin
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What is the mechanism of aminoglycoside nephrotoxicity?
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Filtration at the glomerulus preceding accumulation within the proximal tubular epithelial cells leading to disruption of the metabolic processes; resulting in cell swelling, death, and sloughing into tubular lumen. Release of lysozymes and accumulation of intracellular calcium are likely involved in cell death.
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How do most cases of aminoglycoside toxicity occur?
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Repeated doses and long-duration of treatment leading to accumulation. NOT due to overdose or use in an azotemic patient. A healthy kidney will tolerate overdose without detrimental effects.
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What is the common history of aminoglycoside nephrotoxicity in the horse?
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Prolonged administration in the absence of monitoring trough concentrations or serum Creatinine levels.
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Which aminoglycosides can be used for >10 days provided adequate hydration and monitoring?
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Amikacin and gentamicin
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What is the lowest increase of serum creatinine concentration that indicates toxicity?
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0.3 mg/dl
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Why are sick foals more prone to aminoglycoside nephrotoxicity?
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Prolonged treatment related to septicemia, not due to functionality of neonatal kidney.
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What electrolyte imbalances can predispose the kidney to ATN related to aminoglycoside use?
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Hypokalemia and hypocalcemia
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Increased urinary fractional excretions of sodium with accompanying fluid diuresis will have what sort of effect on the equine kidneys?
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Protective
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What sort of dosing is recommending to reduce aminoglycoside toxicity?
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Once daily
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Why should the administration of aminoglycosides be delayed in the azotemic patient?
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It shouldn't! The toxicity is due to accumulation in the proximal tubular epithelial cells not the function of the kidney. As long as rehydration is ensured, treatment may be started immediately.
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How does ARF related to ATN usually manifest? What is the prognosis?
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Non-oliguric to polyuric renal failure. The outcome is favorable as long as the duration of ARF is not prolonged and the underlying disease process are corrected.
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True/False: Peritoneal and pleural dialysis, plasmaphoresis, and hemodialysis have proved effective in the horse but are prohibitively expensive.
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False. They don't work.
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What toxic nephropathies should be considered in horses?
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Vasomotor nephropathy, pigment nephropathy, NSAID therapy, Vitamin D toxicity, heavy metal ingestion, acorn poisoning, and leptospirosis.
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What is vasomotor nephropathy? What are risk factors?
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Results from any condition that causes sustained, marked hypotension or relase of endogenous pressor agents (i.e. cortisol). Hemorrhagic shock, severe intravascular volume deficit, septic shock, and coagulopathy are risk factors in horses.
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What muscle condition precedes pigment nephropathy? What hematologic pathology can do it?
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Rhabdomyolysis. Hemolysis.
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What are the renal prostaglandins suppressed by NSAIDs and what do they do?
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PGE2 and PGI2 are vasodilators.
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Where are renal prostaglandins founds in the highest concentrations? So what does this mean at necropsy?
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Medullary tissue. So you'll find the lesions associated with the renal medullary crest.
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What is the most common cause of Vitamin D toxicity?
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Ingestion of plants (i.e Cestrium diurnum aka Day-blooming Jasmine)
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When should leptospirosis be considered in ARF/ATN?
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When vasomotor nephropathy can be ruled out and there is no history of nephrotoxic exposure.
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A horse has a more marked anorexia and depression than should be expected due to the primary disease process, what should be considered as a concurrent disease?
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Acute Renal Failure
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A patient has failed to produce urine for six to 12 hours following initiation of fluid therapy, what disease becomes a concern?
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ARF
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What laboratory values are expected in a horse with ARF?
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Creatinine 5-15 mg/dl; BUN 50-100 mg/dl; BUN/Cr ration < 10:1; hyponatremia, hypochloremia, hyperkalemia, hypocalcemia, hyperphosphatemia, metabolic acidosis.
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What USG values are consistent with ARF?
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Isothenuria (1.008 to 1.012) or a lack of concentrated urine (<1.020) in the face of dehydration/azotemia
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What urinalysis values are consistent with ARF?
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Enzymuria (due to tubular damage), glucosuria, proteinuria (indicates glomerular damage); sediment will reveal casts, RBCs, leukocytes, and decreased calcium carbonate crystals; increased excretion of sodium, chloride, and phosphate are also common.
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When should collect a urine sample?
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Before initiation of fluid therapy or it's useless.
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What is the most accurate assessment of renal function in the horse?
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Measurement of Glomerular Filtration Rate
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How is GFR measured in clinical settings?
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Timed urine collection of inulin and creatinine clearance as well as nuclear scintigraphy.
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When should nuclear scintigraphy definitely be performed in the horse?
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Prior to nephrectomy to determine GFR of kidneys.
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When is renal biopsy most commonly performed?
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To determine glomerular injury and tubular necrosis.May be indicated in cases of ARF when primary disease process is inapparent.
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What is a potential complication of renal biopsy?
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Fatal hemorrhage
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Which kidney is biopsied and how is it located?
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Right kidney is most commonly performed with ultrasonographic guidance.
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What is often the most obvious determinant in assessing degree of renal injury?
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Patient response to therapy.
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What is the first step in ARF therapy?
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Judicious fluid therapy to replace volume deficits and correct electrolyte and acid-base abnormalities.
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What parameters should be monitored during ARF therapy?
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Magnitude of azotemia, serum concentrations of sodium, chloride, and bicarbonate.
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What is typically the fluid therapy of choice in ARF?
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0.9% NaCl, as hyperkalemia is often present.
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Following replacement of volume and correction of electrolyte imbalances, what is the next step in evaluating the ARF patient?
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Determining whether the patient is oliguric or non-oliguric (polyuric). Observe patient for 12-24 hours post-therapy.
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Is the prognosis more favorable for oliguric renal failure or polyuric renal failure?
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Polyuric. And it will be obvious: dry stall vs. wet stall.
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What is a potential sequela of oliguric renal failure that is not seen in polyuric renal failure?
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Edema
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An azotemic patient was treated with fluids and re-evaluated 24 hours later. The degree of azotemia was decreased by ~50%. What is the characterization of the azotemia?
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It is likely a pre-renal azotemia, rather than renal azotemia related to ARF.
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Why monitor blood pressure in severely systemically ill patients with ARF? What medical action might it dictate?
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Blood pressure can confirm restoration of normovolemia, whereas other patients may remain hypotensive with extravascular fluid accumulation as edema. In the latter cases, pressor therapy is indicated. No, that wasn't worded very well, but Chaney's long notes were even worse.
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What is a non-invasive method of monitoring patient response to volume administration?
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Monitoring Central Venous Pressure
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How is CVP measure in the horse?
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Via manometer and IV catheter placed in the jugular vein.
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A patient receiving IV fluids has a CVP =6 cmH2O. Has the patient received adequate volume?
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No, patients with a CVP < 8 cm H2O are considered to have not received adequate volume.
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A patient receiving IV fluids has a CVP = 10 cm H2O. Has the patient received adequate volume replacement?
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Yes, a patient with CVP > 8 cm H2O is likely volume overloaded and is at risk for pulmonary edema.
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What is a non-invasive way to evaluate renal function and deposition of IV fluid administration?
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Body weight.
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How can we measure urinary output in horses?
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Placement of indwelling urinary catheter, only possible in males.
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If a horse remains oliguric after 12-24 hours, what is the next step in treatment?
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Furosemide 1mg/kg q2-4 hours
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What is the mechanism by which furosemide increases renal perfusion, GFR, and tubular flow?
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It doesn't do this effectively in horses with ARF.
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What are additional diuretic therapies in horses with ARF?
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Mannitol (1mg/kg CRI as 10-20% solution) and dopamine (3-7 ug/kg/min)
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Are most cases of ARF polyuric or oliguric?
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Polyuric, so diuretic therapy is unnecessary.
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What is the prognosis for a patient that remain oliguric following administration of furosemide, mannitol, and dopamine?
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Grave.
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How long should a polyuric (or oliguric-to-polyuric) patient receive fluid diuresis?
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Until the creatinine returns to normal or reaches a steady state with improvement in patient appetite and demeanor.
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Why is potassium supplementation relevant in the equine patient?
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Diuresis will promote potassium loss and supplementation may be necessary; provided in the form of TPN or PPN (dextrose CRI) or enteral nutrition in the initial stages of therapy before appetite returns. I have no idea what this means besides "potassium supplementation"
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A horse with a Creatinine of 2-3 mg/dl following treatment for ARF may have what sort of sequelae.
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Creatinine values may return to normal over several months OR it may be possible that the patient sustained permanent loss of renal function.
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What is another sequela of ARF in horses? This is basically a sequela to anything from a sneeze to an amputation in horses.
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Laminitis.
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What is CRF?
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An irreversible disease process characterized by a progressive decline in GFR.
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What are the two categories of CRF in the horse?
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Primary glomerular disease and primary tubulointerstitial disease.
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What is the short- and long-term prognosis of CRF?
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Short: Fair to guarded. Long: Poor.
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What are primary glomerular diseases leading to CRF in horses? (There are four.)
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GN, nonspecific glomerulonephropathy, renal glomerular hypoplasia, and amyloidosis.
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What are primary tubulointerstitial diseases leading to CRF? What is the general term describing these diseases?
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Incomplete recovery from ATN/ARF, pyelonephritis, nephrolithiasis, hydronephrosis, renal dysplasia, and papillary necrosis (rare). Chronic interstitial nephritis.
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What is indicated by proliferative glomerulonephritis?
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Increased cellularity of the glomerular tufts as a result of an influx of inflammatory cells and proliferation of the mesangium.
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What is the inflammatory cellular infiltrate in cases of proliferative glomerulonephritis?
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Deposition of circulating immune complexes along the basement membrane of the glomerulus.
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You've got to ask yourself one question: Do I feel lucky?
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Well, do ya, punk?
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What is the mechanism and type of hypersensitivity that occurs in proliferative glomerulonephritis?
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Type III Hyper Sensitivity: Deposition of immune complexes activates complement and vasculitis ensues.
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What antigens are suggest to trigger proliferative nephropathy?
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Streptococcal and Equine Infectious Anemia antigens.
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True/False: It has been observed that immune-complex deposition along the glomerular basement membrane is unique to clinical cases of proliferative glomerulonephritis.
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False. Immune-complex deposition is observed at a much greater prevalence than indicated by clinical disease. It is rare that PGN is of clinical significance.
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What is the most common cause of CRF in horses?
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Chronic Interstitial Nephritis and Fibrosis.
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How does tubulointerstitial disease develop?
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Typically as a sequela to ATN following nephrotoxic exposure or vasomotor nephropathy. Additional etiologies include drug-induced interstitial nephritis (in junkie horses), urinary obstruction, pyelonephritis, renal hypoplasia/dysplasia, and papillary necrosis.
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What must be considered in horses younger than five years with indications of CRF? What is a clinical indication of CRF?
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Congenital and developmental abnormalities must be considered. (i.e. renal dys-/hypoplasia, polycystic kidney disease). Growth retardation.
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What is the most common clinical sign associated with CRF?
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Weight loss! Followed by a small amount of ventral/pectoral edema.
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Why is PU/PD rarely seen in equine CRF?
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Because it probably goes unnoticed by owners.
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What GI lesions may be observed in equine CRF?
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Dental tartar, frequently on the incisors and canines as well as oral ulcers. Also, melena may be observed.
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What are the clinicopathologic findings in horses with CRF? What can affect the laboratory values?
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Laboratory values may be affected by diet. Azotemia: >5 mg/dl, BUN:Cr ratio >10:1, mild hyperkalemia, hyponatremia, and hypochloremia are most commonly observed. Hypercalcemia.
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To what is is hypercalcemia related in cases of equine CRF? What management effect should this have?
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Dietary intake rather than magnitude of azotemia. Increased grass hay rather than alfalfa hay to decrease dietary calcium.
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What are the expected values of serum proteins in horses with CRF?
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It depends. Glomerular disease? Hypoproteinemia. Immune-mediated disease? Pyelonephritis? Increased globulins.
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What is expected on urinalysis of a horse with CRF?
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It depends on the etiology of the CRF. Typically dilute with deceased crystals and mucus. Isosthenuria is common, but hematuria and pyuria may be present.
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Why is bacterial culture recommended in all CRF patients?
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Because pyuria is not always detected, even in cases of septic pyelonephritis.
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Why is rectal examination important in cases of CRF?
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Stones or dilated ureters may be palpable.
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Ultrasound of an equine patient reveals hydronephrosis and nephroliths; there is also a loss of parenchymal echogenicity and corticomedullary distinction. These are common signs with what disease?
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Chronic Renal Failure.
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Ultrasound examination of an equine patient reveals loss of renal parenchymal echogenicity and decreased corticomedullary distinction. What disease process is suspected?
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Chronic Renal Failure
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You are performing an abdominal ultrasound of a 9-month old foal with ill-thrift and nonspecific disease signs. You find that the image of the left kidney appears distorted and misshapen with variable echogenicity and you cannot find the right kidney at all. Your clinician mocks your ultrasound skill and asks which nephrotoxin is responsible for this. You answer....
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"It's not a toxin, it's a congenital abnormality. Sucka."
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When is cytoscopy indicated?
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For visualization of the distal urinary tract, especially when hematuria or dysuria are present.
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What is the most accurate assessment of renal function?
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GFR
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Why is biopsy not all that useful in CRF patients? When is it indicated?
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Because you may be far removed from the initial etiology that the biopsy findings are nonspecific and unremarkable. It's only indicated if it will alter the treatment and/or prognosis.
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What are the management factors in treating stable CRF in horses?
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Decrease calcium intake (no alfalfa), increase NaCl intake. If metabolic acidosis is present, sodium bicarbonate administration may be warranted.
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How effective is treatment for glomerular disease?
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Not very.
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How effective is immunosuppressive therapy in glomerular disease?
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Limited benefits.
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What should be done in a horse with poor body condition and CRF?
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Increase caloric density and palatability of the diet.
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Why is there a poor prognosis for CRF?
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Irreversible and progressive loss of nephron function.
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A horse in CRF has a Cr = 4mg/dl, BUN:Cr ratio of 12:1 and is in good attitude and body condition. What is the first therapeutic goal?
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Maintenance of body condition.
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What are the most common causes of acute blood loss in horses?
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Trauma, surgery, and guttural pouch mycosis.
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How can acute blood loss result from guttural pouch mycosis?
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Erosion of the carotid artery leading to hemorrhage.
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What are clinical signs of hemoperitoneum?
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Colic signs
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What are clinical signs of hemothorax?
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Dyspnea
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What are clinical signs of hypovolemic shock?
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Tachycardia, tachypnea, cold extremities, pale mucous membranes, muscle weakness and death.
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A horse experienced an episode of acute blood loss four hours ago. What are the expected PCV and TP values?
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Likely normal as there has not been time for redistribution of ECF to compensate for volume loss.
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Besides dehydration, what can mask severity of blood loss?
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Splenic contraction
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How long is the bone marrow regenerative response in horses?
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Three to four days
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In horses, the is mild anisocytosis and a mild to moderate increase in MCV. What does this indicate?
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Erythroid regeneration
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How can hemoperitoneum be visualized? Confirmed?
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Ultrasound exam. Abdominocentesis
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What is the initial treatment goal in cases of acute blood loss?
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Control hemorrhage
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What is the treatment for a controlled hemorrhage and hypovolemic shock?
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Intravenous crystalloid solutions at 40-80 ml/kg.
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What is the fluid, concentration and dosage, used to temporarily reverse shock and provide anti-inflammatory effects in cases of severe trauma?
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Hypertonic saline (7% NaCl) at 4 ml/kg.
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What is the recommended volume to be administered to an equine patient with acute blood loss? Why?
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Three to four times the estimated blood loss as only 25% of crystalloid volume will remain in the vascular space.
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In uncontrolled hemorrhage, why is aggressive fluid therapy not recommending?
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Aggressive therapy is not recommended as it may exacerbate bleeding by increasing blood pressure, disruption of clots, and hemodilution of clotting factors.
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What is the recommended fluid therapy protocol in cases of uncontrolled hemorrage?
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"Controlled hypotension." Low volumes of crystalloids of whole blood to maintain organ vitality without normalizing blood pressures. The goal is an MAP of ~60 mmHg.
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When is whole blood transfusion indicated in horses?
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PCV < 20% has likely depleted RBC reserves in the spleen. If the PCV falls to < 12% in 24-48 hours, then blood transfusion is indicated.
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If a stable patient has a PCV of 14%, is blood transfusion indicated?
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Not necessarily. A PCV of 12-20% in a stable patient may not require a transfusion.
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Besides PCV, what other measurements dictate the need for a whole blood transfusion?
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Heart rate, blood lactate, indirect blood pressure, and colloid oncotic pressure.
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How long will a blood transfusion support oxygen-carrying capacity in the horse?
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Only 2-4 days before being removed by the reticuloendothelial system.
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Why is there a short lifespan of transfused RBCs in the equine patient?
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High degree of blood type polymorphism
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How much blood should be transfused into an equine patient?
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20-40% of estimated blood loss
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If a 500kg equine patient experiences a PCV drop of 36% to 12%, what is the estimated blood lost and what volume of whole blood should be transfused?
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8% of BW = ~40L total blood volume. 67% blood loss = ~27L lost. 5.4-10.8L = Transfusion volume (20-40% of total loss)
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What is the highest recommended rate of administration for colloid fluid or blood products?
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Not greater than 20 ml/kg/hr
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What are clinical signs of a transfusion reaction in the horse?
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Piloerection, increased TPR, muscle fasciculations, defecation, restlessness, or sudden collapse.
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What treatment is indicated in cases of transfusion reaction? Can the transfusion be continued?
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Immediate cessation of transfusion, anti-inflammatory therapy, IV crystalloids. Transfusion can be initiated more slowly at a later point.
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What is guttural pouch mycosis?
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Fungal disease of the medial compartment of the guttural pouch.
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What is the causative agent of guttural pouch mycosis?
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A. nidulans and A. fumigatus have been implicated but the exact etiology is unknown
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What is the most common presenting complaint of guttural pouch mycosis?
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Intermittment epistaxis and dysphagia
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What sort of lesions are expected in cases of guttural pouch mycosis?
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Fungal invasion of neurovascular structures in the medial guttural pouch. Usually unilateral but may be bilateral.
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What causes epistaxis in horses with guttural pouch mycosis?
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Fungal erosion of the wall of the internal carotid artery in the roof of the medial compartment. The external carotid and maxillary arteries may also be affected, but this is less common.
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How is it that epistaxis of GPM may be unilateral or bilateral?
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The pharyngeal openings to the guttural pouch are caudal to the nasal septum.
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How serious is epistaxis in GPM?
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May occur at rest and are often intermittent. Bleeding varies from mild to severe with the possibility of fatality from the first observed episode.
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What is the most effective treatment of GPM?
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Intra-arterial occlusion of the affected vessels is considered most effective. Balloon-tipped catheters and arterial coils have been used.
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In guttural pouch mycosis, why is it necessary to proximally and distally occlude the affected artery?
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In order to prevent collateral circulation from the Circle of Willis from reperfusing the pouch.
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What may it be frustrating to medically manage GPM?
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Variable success of topical fungicides and enzymes. Accompanying neurologic dysfunction (dysphagia, blindness, Horner's Syndrome). Recurrent fungal plaques
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What neurologic dysfunction can accompany GPM?
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Blindness, Dysphagia, Horner's Syndrome
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What's Horner's Syndrome?
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Ptosis, miosis, enopthalamos
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What are potential causes of hemothorax or hemoabdomen?
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Trauma, post-operative abdominal surgical hemorrhage, neoplasia, foaling, pregnancy, organ rupture, mesenteric injury, coagulopathy, ovarian hematoma, systemic amyloidosis, and idiopathic causes.
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What are the most common causes of hemoperitoneum in horses?
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Traumatic rupture of the spleen, reproductive tract, hemorrhages in mares, and neoplasia.
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What is the breed and age correlation in patients with hemoabdomen?
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Arabs and Thoroughbreds, middle-aged to older (>13 years)
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What are the most common clinical signs of hemoabdomen?
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Colic, lethargy, hypovolemic shock, pale MM, prolonged CRT, tachycardia and tachypnea. Additional signs include anorexia, weakness, trembling, cool extremities and abdominal distension.
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A patient present with colic signs, abdominal distension, pale mucus membranes, prolonged CRT, tachycardia and tachypnea. What is included in your differentials?
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Hypovolemic shock brought on by hemoabdomen.
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Why may controlled hypotension may be necessary in the patient with hemoabdomen?
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It may be difficult to localize the source and control the source of the abdominal hemorrhage. Hemostasis should be achieved before initiating aggressive fluid therapy.
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What's the desired MAP in controlled hypotension?
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~60 mmHg
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What drugs may be administered to sedate patients with acute blood loss?
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Acepromazine
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What is the survival rate of equine patients with acute blood loss?
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51-74%
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What is the medical term for equine Cushing's Disease?
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Pituitary Pars Intermedia Dysfunction (PPID)
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A horse present with hirsutism, PU/PD, and hyperglycemia. What is a differential?
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PPID
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What is the breed/age/sex predilection for horses affected with PPID?
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Horses >15 years. No breed/sex predilection.
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In PPID, what leads to clinical signs of disease?
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Loss of dopaminergic inhibition leads to increase of MSH release. This results in secretion of beta-endorphin (B-End), alpha-melanotropin (a-MSH), and ACTH from POMC-polypeptides. Adrenocortical stimulation is secondary to release of these hormones.
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What sequelae are expected from the loss of dopaminergic inhibition?
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Excess circulating glucocorticoids, physical destruction of the pars nervosa due to hyperplasia of pars intermedia, and direct peripheral action of POMC-polypeptides.
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What is the average age of a horse affected with PPID?
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19 years
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What is the most common clinical sign observed in PPID?
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Hirsutism!
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An owner notes the appearance of guard hairs beneath the mandible, along the chin and distal limbs of an equine patient. What disease becomes a concern?
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PPID. Guard hairs often precede hirsutism.
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What is the leading cause of euthanasia in horses with PPID?
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Chronic/recurrent laminitis.
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Why are PU/PD common in PPID?
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Destruction of the pars nervosa by hyperplasia of pars intermedia leads to decreased secretion of AVP (aka ADH). Also, hyperglycemia can cause osmotic diuresis.
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.Why is hyperhidrosis observed in PPID patients?
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Equine sweat glands are under beta-adrenergic control.
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What leukocyte abnormalities may be observed in a horse with PPID?
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Neutrophilia and lymphopenia, effect of glucocorticoids.
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A patient presents with a recurrent laminitis, PU/PD, and hyperhidrosis. What is a differential?
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PPID
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How is PPID definitively diagnosed?
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Low-dose dexamethasone suppression test.
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What is the procedure for a low-dose dexamethasone suppression test?
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Blood draw at 5pm, administer dex, wait 19 hours. Normal values <1ug/dl.
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What is the weakness of a low-dose dexamethasone suppression test?
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While good for screening, season variation (August/September) may yield false positives.
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On necropsy of a euthanized horse, you find diffuse, adenomatous hyperplasia of the pars intermedia. What was the most likely reason for euthanasia?
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Chronic laminitis as the horse likely had PPID.
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What is the treatment for PPID?
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Fastidious management protocols for feeding and husbandry as well as control of secondary complications like infections and laminitis. Pergolide is a long-acting dopaminergic agonist that has shown modestly effective.*
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A horse being treated for PPID presents for diarrhea, colic, and anorexia. What should be evaluated beyond the PE and MDB?
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These are dose-dependent side effects of Pergolide. Evaluate dosage.
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One day in June, you perform a low-dose dex suppression test and find cortisol levels of 3 ug/dl in the patient. Bloodwork reveals a glucose of 180 mg/dl. What can you inform the owner?
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Definitive diagnosis of PPID. Excellent long-term prognosis with appropriate management. Hyperglycemic patients still carry a good prognosis that will improve with control of glucose levels. Severely hyperglycemic patients (>275 mg/dl) have a guarded prognosis.
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What are the expected clinical signs of Equine Metabolic Syndrome?
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Regional adiposity and insulin-resistance. NOT hypertension, abdominal adiposity, or microalbuminemia.
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A horse prsents with a BCS of 8/0 and recurrent laminitis. What is a differential?
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Equine Metabolic Syndrome
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What breeds tend to be more prone to equine metabolic syndrome?
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Ponies > Horses; Morgans > Arabs > Fjords
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What age group is predisposed to EMS?
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Adult horses >5 years
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How is EMS diagnosed?
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Documentation of resting hyperinsulinemia
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Insulin levels of >20 uU/mL suggests what?
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Insulin-resistance
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Insulin levels of >30 uU/mL suggests what?
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Hyperinsulinemia
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If a horse has a resting insulin level of 25 uU/mL, what is the diagnosis?
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Insulin-resistance not hyperinsulinemia (and therefore not EMS)
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Describe the glucose/insulin test.
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Collect baseline blood glucose, administer 150 mg/kg via 50% dextrose IV, follow with 0.10 uU/kg of IV insulin. Documentation of blood glucose levels above baseline for >45 minutes indicates insulin resistance.
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What dietary management approach should be taken with EMS?
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Weight loss: non-structural CHO in hay should be < 12%; pre-soak hay to reduce CHO; Grass hay (1.5-2.0% per day of goal weight). Restrict pasture grazing
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Why may swimming be the ideal exercise in EMS cases?
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Laminitis is common with EMS and makes traditional exercise difficult.
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What pharmaceutical therapy may be prescribed in cases of EMS?
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Levothyroxine may reduce body weight and improve insulin sensitivity. Use until ideal weight is reached, but not for more than six months
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A horse has a history of lethary, exercise intolerance, and muscular problems. What endocrine disease is a differential?
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Hypothyroidism
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How is a diagnosis of hypothyroidism confirmed?
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Measurement of low serum T3/T4 levels, but more definitively diagnosed by TSH stimulation tests.
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Why can thyroid supplementation not be considered diagnostic of hypothyroidism?
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Placebo effect
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What is the effect and mechanism of fescue toxicity in horses?
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Endophyte alkaloids of a symbiotic fungus act as a dopamine agonist which inhibits TSH and lead to hypothyroidism.
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What is the treatment for fescue toxicity?
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Domperidone, a dopamine antagonist.
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In pregnant mares, what are signs of fescue toxicity?
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Prolonged gestation and agalactia
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How do neonatal T3/T4 concentrations differ in the foal from those in an adult horse?
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The normal foal will have T3/T4 concentrations 10-20 times higher than those of an adult.
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What is the most common thyroid disorder in the horse?
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Hyperplastic goiter.
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How does a hyperplastic goiter develop?
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Consumption of excess iodine and/or goitrogenic plants by the mare during gestation
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Besides dysmaturity (prolonged gestation) in the mare, what other syndromes may be seen in neonatal hypothyroidism?
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Mandibular pragnathism and incomplete ossification of the mandible.
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What must be caution be taken in treatment of hypothyroidism in horses?
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Without a confirmed diagnosis, the associated health risks are largely unknown.
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What is the most common indication of a thyroidectomy?
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If the mass becomes large enough to compress the respiratory and/or alimentary tracts. Most thyroid tumors are benign and nonfunctional and can be ignored.
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What endocrine disease is associated with dysfunction of the posterior pituitary?
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Diabetes insipidus
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What endocrine disease is associated with dysfunction of the neurohypophysis?
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Diabetes insipidus
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What is the most common cause of diabetes insipidus?
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Decreased ADH release secondary to destruction of the posterior pituitary by hyperplasia of the pars intermedia. Primary diabetes insipidus is rare.
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What is the most common clinical presentation of diabetes insipidus?
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PU/PD in otherwise normal animal (absence of azotemia!)
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What is the expected USG of a patient with diabetes insipidus?
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< 1.010 and a failure to concentrate with water deprivation test
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Why is polydipsia often unnoticed as a clinical sign?
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Failure to observe and also psychogenic polydipsia is observed as a vice.
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How can you distinguish between a patient with diabetes insipidus and psychogenic polydipsia?
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A psychogenic PD patient will concentrate urine (>1.025) on water deprivation test.
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What are other names for nutritional hyperparathyroidism?
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Big Head Dz, Bran Dz, Miller's Dz
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Why is nutritional secondary hyperparathyroidism no longer the most common cause of hyperPTHism in horses?
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Widespread knowledge of proper equine nutrition
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What leads to the clinical signs of bran disease?
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A relative calcium deficiency secondary to excess dietary phosphorus
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What are clinical signs of Miller's disease?
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Facial bone enlargement, ill-thrift, difficulty of mastication (bone loss), molar fracture, spontaneous long bone fracture, shifting lameness and physitis.
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A patient presents with shifting lameness, apparent difficulty masticating, and an upper airway noise may be heard. What is your tentative diagnosis?
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Nutritional Secondary Hyperparathyroidism
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What electrolyte abnormalities can lead to hyperplasia of the parathyroid gland?
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Hyperphosphatemia and hypocalcemia
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What is the etiology of Big Head Disease?
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PTH secretion inhibits vitamin D synthesis, increasing bone resorption and bone loss (primarily in the facial bones). The bone loss is replaced by un-mineralized connective tissue.
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Why might a Bran Dz patient remain normocalcemic?
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The disease is so slowly progressive that calcium levels are maintained.
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What dietary changes should be applied to a horse with secondary nutritional hyperparathyroidism?
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Elimination of grain from the diet as well as all feeds containing excess oxalates. Supplementation of calcium is warranted, typically in the form of calcium carbonate.
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What is the ideal Ca:P ratio for supplementation therapy in Bran Dz?
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4:1 to 3:1. Continue for several months.
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What electrolyte abnormalities may be expected in hypervitaminosis D? What pathology can be expected?
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Hypercalcemia, normophosphatemia. Calcification of arteries, tendons, and ligaments.
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What plants may cause hypervitaminosis D?
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Cestrum diurnum (day-blooming jasmine)
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What is the prognosis of hypervitaminosis D?
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Poor
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Where is the mitral valve auscultated?
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Left 5th ICS midway between the shoulder and olecranon.
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Where is the aortic valve auscultated?
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Left 3rd to 4th ICS just below the shoulder
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Where is the pulmonic valve auscultated?
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Left 3rd ICS just below aortic valve
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Where is the tricuspid valve auscultated?
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Right 3rd to 4th ICS midway between the shoulder and the olecranon
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What does S1 represent?
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Ventricular contraction, closure of the AV valves, pulse occurs.
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What does S2 represent?
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Semilunar valves close; diastole
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What does S3 represent?
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Sound of rapid ventricular filling
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What does S4 represent?
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Sound of atrial contraction
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Non-pathologic murmurs are most common in what equine patient?
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Neonates
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How common are systolic functional murmurs in horses?
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66% of horses will have one
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What is the normal resting heart rate of a horse?
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24-44 bpm
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What is the most common nonpathologic murmur in horses?
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Second-degree AV block
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What is the most common cause of second degree AV block in horses?
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Increased vagal tone
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What is the only heart sound expected during second-degree AV block?
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S4 (atrial contraction)
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What is the expected heart rate of a horse with a nonpathologic second-degree AV block?
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>24 bpm
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What sound will be absent in a sinus heart block in horses?
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S4, as there is no atrial contraction.
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What causes sinus block in horses?
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Increased vagal tone
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When is a third-degree heart block normal?
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Never
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Edema is most common with what sort of heart failure and where is it found?
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Right heart failure will cause cool/pitting/nonpainful/symmetrical edema in the ventral thorax and abdomen.
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What respiratory signs are expected in a horse with heart disease?
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Tachypnea, coughing, crackles, cyanosis, poor CRT
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What is the most common sequela to rupture of chordae tendinae?
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Pulmonary edema
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What is the most common cardiac cause of pulmonary edema?
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Rupture of chordae tendinae
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And irregularly irregular rhythm is most consistent with what cardiac abnormality?
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Atrial fibrillation
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When are premature atrial or ventricular contractions significant?
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When heart rate is increased or when they occur more frequently that a few per hour
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Murmurs are typically associated with what?
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Valvular abnormalities, shunts, altered contractility, altered blood viscosity
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When does a systolic murmur occur?
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Between S1 and S2
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When does a diastolc murmur occur?
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Between S2 and S1
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What does generalized venous distension indicate?
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Increased pressure
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A horse is observed to have jugular pulsation in the caudal third of the neck. What heart disease in indicated?
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None. This is normal.
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A horse is observed to have jugular pulsation in the middle third of the neck. What heart disease is indicated?
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Tricuspid regurgitation and right heart failure
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Why is it difficult to definitively diagnose jugular pulsation in the horse?
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There is a strong referred pulse from the carotid artery that may obscure the sign.
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Bounding pulses are associated with what cardiac abnormality?
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Aortic valve insufficiency
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What is the most useful tool for cardiac rate and rhythm disturbances in the horse?
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ECG
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Why is ECG so useful in the horse?
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Large heart with extensive Purkinje network
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Where should you put the ECG leads on the horse?
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Negative (right arm) on right jugular groove. Positive (left arm) on left heart apex. Ground lead on site distant. Run on Lead 1
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What is the normal configuration of the P wave in the horse?
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Often bipolar and may change configuration
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What is the normal configuration of the QRS complex in the horse?
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Usually negative and consists most of S-wave
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What is the normal configuration of the T wave in the horse?
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Usually positive
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What is the biggest deflection in the equine ECG?
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QRS complex
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What must follow every QRS complex?
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T wave
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How is an echocardiogram performed in an equine patient?
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2.5 MHz probe with horse standing and on the right side of the chest
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What structural information can be obtained from an echocardiogram?
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Size of the heart, shape of the valves, wall thickness, presence of peri-/endocarditis
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What functional information can be obtained from an echocardiogram?
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Motion of walls and valves, fractional shortening
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What is fractional shortening?
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(LV size in diastole) - (LV size in systole) * 100 = Fractional Shortening
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What is normal fractional shortening in a horse?
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35-45%
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What is indicated by fractional shortening of >45%?
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I have no idea.
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What is indicated by fractional shortening of < 25%?
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Failure
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Where shall I go? What shall I do?
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Frankly, my dear, I don't give a damn.
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Elevated cardiac troponin I may be increased in what heart pathology?
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Myocarditis
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Decreased PaO2 reflects what heart pathology?
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Hypoxemia due to shunts
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How is blood pressure measured in horses?
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Indirect BP measured at coccygeal artery. NOT THE (#*%% VEIN.
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What can be used to detect transient or intermittent arrhythmias?
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Holter monitor or event monitor
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What is the most common congenital abnormality in horses?
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Ventricular septal defect
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Is a VSD an acquired or congenital abnormality?
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Congenital
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What are the common sequela of a VSD?
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Oxygenated blood shunted left-to-right; pulmonary hypertension and left-sided overload. Pulmonary edema may eventually develop.
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Badges?
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We ain't got no badges! We don't need no badges! I don't have to show you any stinking badges!
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When do clinical signs of a VSD manifest?
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Early in life
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What sized defect is thought to distinguish between clinical and subclinical VSD?
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2.5 cm
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VSD will have what sort of murmur?
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Right-sided, >Grade III; A systolic murmur is often present over the mitral or aortic valve
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How is a diagnosis of VSD confirmed?
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2D echocardiogram. With a "bubble" test or color flow doppler to confirm shunt.
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What is the tetralogy of Fallot?
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VSD, dextroaorta, right ventricular hyperplasia, stenotic of the pulmonary artery.
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What is the direction of the shunt in the TOF?
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Right to left flow across VSD due to stenosis of pulmonary artery
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What determines the severity of clinical signs in TOF?
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Degree of stenosis of pulmonary a.
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A left-sided heart base systolic murmur (>III) is indicative of what congenital heart pathology?
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Tetralogy of Fallot
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PDA in horses?
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Subclinical, rare, congenital, not treated. Bam.
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What is the most common cause of acquired heart murmurs?
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Valvular abnormalities
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What lesions are associated with acquired valvular abnormalities?
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Degenerative changes, myocarditis, endocarditis, ruptured chordae tendinae
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What is the most common sequela to valvular abnormalities?
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Insufficiency or leakage is more common than stenosis
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What are the most common acquired valvular insufficiencies?
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Aortic and mitral valves
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Aortic and/or mitral valve insufficiency lead to what?
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Left-sided volume overload and pulmonary hypertension
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When do horses develop pulmonary edema?
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Besides chordae tendinae rupture, when pulmonary hypertension occurs rapidly.
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Left-sided overload and pulmonary hypertension in horses will more likely lead to what?
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Right-sided failure
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What sequela to valvular lesions can predispose a horse to atrial fibrillation?
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Atrial enlargement.
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Atrial enlargement can predispose a horse to what cardiac abnormality?
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Atrial fibrillation
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What murmur is associated with aortic valve dysfunction?
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Diastolic with PMI at 3rd/4th ICS
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What murmur is associated with mitral valve dysfunction?
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Systolic murmur at 5th ICS
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A diastolic murmur at the 3rd/4th ICS on the left is likely due to dysfunction of which valve?
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Aortic
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A systolic murmur at the 5th ICS on the left is likely due to dysfunction of which valve?
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Mitral
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Aortic insufficiency can lead to what sort of pulse abnormality?
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Bounding pulses
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Why is right-sided failure a concern with failure of the tricuspid valve?
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It isn't.
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How can a valvular defect be definitively diagnosed?
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Echocardiogram is useful for diagnosis and prognosis; 2D: Document chamber enlargement, fractional shortening, abnormal valves. Color flow Doppler to evaluate degree of regurgitation
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Aortic/mitral insufficiencies carry a good prognosis in horses if what?
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If the horse is asymptomatic, the regurgitant jet is small, and there is no evidence of left-sided enlargement. So basically the prognosis is good as long as no pathological changes occur. Go figure, eh?
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Your equine patient has a murmur Grade II. On echocardiogram, you find fractional shortening < 30%, the pulmonary artery is larger than the aorta, and the left atrium is 18 cm. What do you tell the owner?
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Something nice and consoling. Be gentle with them. Prognosis is guarded to grave. Yes, even with a quiet murmur.
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Which is more likely to affect performance: Tricuspid or Mitral insufficiency?
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Mitral.
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Which has a worse prognosis: a louder or quieter murmur?
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Neither.
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What is the pathology of endocarditis?
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Acquired defect of the heart follow embolus of focal infection to the heart valves.
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What are the most common causes of endocarditis?
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Pasteurella, Actinobacillus, and Streptococcus
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What valves are most commonly affected by endocarditis?
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Aortic and mitral valves
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Is endocarditis more common in older or younger animals?
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Younger (<4 years)
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What is the most specific diagnosis of endocarditis? What are nonspecific CBC/Chem signs of endocarditis?
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Visualization of abnormal valves on echocardiogram. Inflammatory leukogram, hyperfrinogenemia, hyperglobulinemia
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What is the treatment for endocarditis?
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Long-term antimicrobial therapy based on C&S (4-6 weeks).
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What is the prognosis of endocarditis?
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Fair to good if treated before significant valvular lesions. Poor to grave if lesions cause heart failure
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What is the pathophysiology of myocardial disease?
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Inflammation of cardiac muscle! Caused by endotoxemia/septicemia, viral infection, parasitic migration, bacterial endocarditis, electrolyte abnormalities, GI disease, Toxins, WMD, Lymphosarcoma, Infarcts/Fibrosis
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Cardiac inflammation, degeneration, and/or myocyte electrolyte changes can lead to what?
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Altered conduction, murmurs, and arrhythmias. Reduced myocardial function, chamber dilation, AV valve insufficiency, heart failure
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What are the most common type of murmurs in myocardial disease?
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Systolic, at the AV valves. The AV valves are the mitral and tricuspid
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A horse has a fever with signs of colitis. What cardiac disease can be associated with this?
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Myocardial disease
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A horse has respiratory signs likely due to EHV-1 infection. What cardiac disease can be associated with this?
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Myocardial disease
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A foal has an apparent myopathy and you diagnose White Muscle Disease (because you've had it four times a term for three years at SGU). What cardiac disease can be associated with this?
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Myocardial disease.
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What echocardiogram abnormality is expected with horses with myocarditis?
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Usually normal, may see reduced fractional shortening.
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Increased levels of cardiac troponin I in the serum suggest which cardiac disease?
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Myocarditis
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What pharmaceutical treatment is recommended for arrhythmias of myocarditis?
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Atrial fibrillation: Quinidine. Ventricular: Magnesium, Lidocaine
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What are the four types of pericarditis?
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Septic, nonseptic, neoplastic, or idiopathic
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What bacteria are most commonly associated with pericarditis?
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Streptococcal and/or Gram-negative bacteria (+/- anaerobes)
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What is the pathophysiology of pericarditis?
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Inflammation leads to thickening of pericardium which causes cardiac tamponade and restrictive pericarditis. The interference with diastolic filling results in cardiac insufficiency.
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What is the most specific diagnostic test for pericarditis?
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Echocardiogram will show pericardial fluid and a collapsed right atrium
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What will an ECG of pericarditis show?
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Electrical alternans
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What heart rate abnormality is most common in large animals?
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Tachycardia
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From where do supraventricular arrhythmias originate?
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SA Node, atrium, AV node or junction
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Are premature or escape arrhythmias more common in large animals?
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Premature!
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What is the most common acquired pathologic arrhythmia in horses?
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Atrial fibrillation (supraventricular tachycardia)
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What are predisposing factors to atrial fibrillation?
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Atrial enlargement, valve regurgitation, heart failure, myocarditis, slow atrial rate and high parasympathetic tone
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What percentage of horses with atrial fibrillation will show exercise intolerance?
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60%
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What percentage of horses with atrial fibrillation present with signs of heart failure?
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12%
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What is auscultated on a horse with atrial fibrillation?
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Irregularly irregular rhythm without an S4; variable intensity; slight tachycardia unless there is underlying cardiac disease.
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On an equine patient, you auscult an irregularly irregular rhythm and cannot hear an S4. HR = 60 bpm. What does this tell you?
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Atrial fibrillation with underlying cardiac disease.
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On an equine patient, you auscult an irregularly irregular rhythm and cannot hear an S4. HR = 40bpm. What does this tell you?
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Atrial fibrillation without underlying cardiac disease
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What is the most common underlying cardiac disease causing atrial fibrillation?
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Mitral regurgitation
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What is the treatment for idiopathic or benign A-Fib?
|
Quinidine sulfate 10 mg/lb PO q2 hours (up to six doses) Do not exceed 50 g/day. Discontinue quinidine once converted (or if QRS is >125% of baseline). Digoxin 0.011 mg/kg PO q12 hours for 1-2 days.
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What are clinical signs of quinidine toxicity?
|
Colic, diarrhea, nasal mucus edema leading to respiratory obstruction, ataxia, seizure, hypotension, collapse
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What is the treatment for quinidine toxicity?
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Bicarbonate, digoxin (if tachycardia), lidocaine (if ventricular tachycardia)
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How common is Atrial Premature Contractions in horses?
|
30% of horses have one APC per hour
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When is an APC considered to be abnormal?
|
Frequent, grouped, and/or multi-focal in origin
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What is atrial tachycardia?
|
More than four premature complexes in a row or sustained atrial tachycardia. Yep, verbatim from the notes.
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Upon auscultation of the equine patient, a heartbeat is heard earlier than expected followed by a normal diastolic interval. HR = 48. What does this indicate?
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Atrial Premature Contraction
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How is APC diagnosed?
|
ECG shows premature P wave of conformation different than those originating from the SA node, normal QRS.
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Why is it possible to miss the P wave on an ECG of an APC patient?
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P wave may be buried in the T wave
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An ECG shows intermittently premature P wave with a conformation different than normal P waves. All QRS complexes are normal. What does this indicate?
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APC
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What is the treatment for APC?
|
Corticosteroid therapy if suspicious of viral myocarditis (EHV-1). Atrial tachycardia Quinidine 10 mg/lb via NGT q2 hours. Digoxin if heart failure.
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What are ventricular premature contractions?
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Ectopic beats originating from a ventricular focus and occurring earlier than expected.
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What defines ventricular tachycardia?
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Four or more VPCs in a row or sustained.
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What are potential causes of VPCs?
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Myocarditis, Electrolyte abnormalities
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An ECG of an equine patient shows a VPC. How common is this?
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It's not common, it's an abnormality. Even one. It's rarely normal.
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Upon cardiac auscultation of an equine patient you hear a regular rhythm with a beat occurring earlier than normal followed by a compensatory pause. What is indicated?
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VPC
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What is one of the most common myocarditis/electrolyte disturbance associated with VPCs in horses?
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GI disease and endotoxemia
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What clinical signs will likely accompany sustained ventricular tachycardia?
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Clinical signs of heart failure
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An ECG shows early and widened QRS complexes without a subsequent P wave, the T wave is deflected opposite of the QRS. What is indicated?
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VPC
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What will an ECG show in a patient with VPC?
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Widened/early QRS obliterating the P wave, with a T wave deflected opposite the QRS
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What is the treatment protocol of a horse with a HR = 140 and mutlifocal origin of QRS complexes on ECG?
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Dangerous ventricular tachycardia should be treated with MgSO4 IV, Lidocaine, Quinidine, and treatment for underlying disease
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What are conditions that can predispose a horse to bradyarrhythmias?
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Myocardial or cerebral disease.
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What is the name for an acquired abnormality of the junctional myocardium that does not allow impulse conduction from atria to ventricles?
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Third-degree AV block
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What etiologies are most commonly associated with third-degree AV block?
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Myocarditis and degenerative changes in the AV node, or electrolyte abnormalities
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An equine patient presents for exercise intolerance and intermittent signs of heart failure. Upon auscultation you note a regular rhythm. HR = 20 bpm. What is indicated?
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Third-degree AV block
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What will be depicted on the ECG of an equine patient with third-degree AV block?
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No relationship between P waves and QRS complexes. QRS may be slightly abnormal.
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What is the treatment for third-degree AV block?
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Corticosteroids if nonseptic myocarditis. Correction of electrolyte abnormalities. Strict stall rest. Possible implantation of a pacemaker.
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What is the most likely cause of heart failure in the geriatric horse?
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Chronic valvular regurgitation
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What changes can result from severe valvular regurgitation?
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Volume overload with subsequent dilation and reduced contractility of the cardiac chamber.
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Forget it, Jake.
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It's Chinatown.
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