2010 Flashcards

1
Q

Pathogenesis of URT infection in cats

A
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2
Q

explain the ‘chronic carrier state’ in 2 common URT feline viruses

A
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3
Q

explain the terminology used to characterise a heart murmur

A
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4
Q

describe the murmur typically associated with; mitral valve insufficiency;

A

characteristically causes a plateau or regurgitant murmur (holosystolic timing) and is best heard at the left apex in the area of the MV.

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5
Q

describe the murmur typically associated with; aortic regurgitation

A

low left base and at the right base because the murmur radiates up the aortic arch, which curves towards the right. - systolic ejection murmur becomes louder as CO or contractile strength increases.

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6
Q

describe the murmur typically associated with; patent ductus arteriosus

A

continuous (machinery) murmur occurs throughout the cardiac cycle, indicating that a significant pressure gradient continuously exists between two connecting vessels. There is no interruption of the murmur at the time of S2; instead, the intensity is often great at that time. The murmur becomes softer toward the end of diastole, and at slow heart rates it may even become inaudible. The PDA murmur is loudest high at the left base above the pulmonic valve area; this murmur tends to radiate cranially, ventrally and to the right. The systolic component is usually louder and heard well all over the chest, whereas the diastolic component is more localised to the left base in many cases.

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7
Q

describe the murmur typically associated with; left ventricular outflow tract turbulence in a cat

A
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8
Q

outline the origin of BUN

A

Urea synthesis occurs in hepatocytes via the urea cycle, which is one method of incorporating NH4+ into molecules for excretion of excess NH4+ that is formed in tissues or intestine. After urea passively enters plasma from hepatocytes, it has two possible fates.
Urea passes freely across the glomerular filtration barrier and is excreted in urine or resorbed by renal tubules: 50-65% of urea present in glomerular filtrate is resorbed in proximal and collecting tubules. Urea resorption in proximal is enhanced by H20 resoprtion in proximal tubules and by increased ADH activity in the medullary collecting ducts.
Urea enters the intestinal tract of monogastric animals (via the biliary system or blood) where it is degraded by enteric bacteria (with urease), passively absorbed into portal blood, or excreted in faeces. In cattle, urea enters the rumen (via saliva and blood), where it is degraded to NH4+.

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9
Q

outline the origin of creatinine

A

Crt is the product or creatine degradation. Creatine phosphate serves as a high-energy molecule for muscle contractions (creatine + ATP <-> creatine PO + ADP). Creatinine enters the plasma after the degradation of creatine or creatine PO4 in muscle fibres (the animal’s muscle or dietary meat). Creatinine is excreted from the bodye via the kidneys and intestine.
Creatinine passes freely across the glom.filtration barrier; it is not resorbed by tubules. Small quantities may be secreted by proximal tubules when there is increased plasma [creatinine]
Crt is also excreted or degraded in faeces of people and in saliva of cattle. Alimentary tract excretion is suspected to occur in dogs, cats and horses, as Crt is diffusible across most cell membranes.

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10
Q

outline causes of decreased creatinine

A

A decrease in serum or plasma is not clinically recognized or clinically significant. Animals with a decreased muscle mass would tend to have lower creatinine, and the presence of a hypoproteinaemia could yield a slightly lower creatinine.

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11
Q

outline causes of increased creatinine

A

Pathological process cause decreased GFR; the initiating process may be prerenal, renal or postrenal
Increased creatine production and release from damaged myocytes could contribute to increased serum creatinine when renal function is impaired (ie. myoglobinuric nephrosis secondary to rhabdomyolysis in horses) but Crt is quickly cleared from plasma if renal function is adequate. Baseline serum creatinine may vary among individuals because of variations in total body muscle mass or meat intake, but these factors are not expected to cause more than a mild azotaemia. Greyhounds have a greater mean serum creatinine than the mean value for dogs in the general population, and some greyhounds have values mildly above the creatinine upper reference limit.
Neonatal foals can have an increased serum creatinine if born to dams with dysfunctional placentas that prevented normal clearance of fetal creatinine by placental blood. In contrast to congenital renal failure, this azotaemia should diminish quickly after birth and resolve over several days because creatinine will be excreted via the urine

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12
Q

outline causes of a decreased BUN

A

Decreased urea synthesis; hepatic insufficiency (hepatocellular disease, portosystemic shunts), urea cycle enzyme deficiencies
Increased renal excretion of urea: disorders that cause impaired proximal tubular resorption of urea (glucosuria), central or nephrogenic diabetes insipidus

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13
Q

describe the different functions of the cerebellum

A
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14
Q

explain the pathophysiological basis of the clinical signs that may be seen with cerebellar disease

A
  • intention tremors (oscillations)
  • inability to fine tune motor skills; ataxia/dysmetria
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15
Q

describe the indications, clinical significance and limitation of;
parathyroid hormone assay

A

To diagnose hyperparathyroidism;
PTH may be elevated or in the normal reference range. Serum PTH concentration must be interpreted relative to calcium concentration. If ionized calcium is elevated, serum PTH in the upper half of the reference range or greater is consistent with hyperparathryoidism.Values below reference range are expected if parathyroid gland function is normal and rule out hyperparathyroidism. Serum PTH in the lower half of the reference range is inconclusive.

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16
Q

describe the indications, clinical significance and limitation of;
faecal occult blood

A

While helpful for detecting occult GI hemorrhage, diets containing red meat or having high peroxidase activity, such as fish, fruits, or vegetables, can cause false-positive results. Animals should be fed a meat-free diet for at least 72 hours before a fecal occult blood test. The presence of peroxidase-producing bacteria within the GI tract also may cause false-positive results. Despite false-positive results, a negative fecal occult blood test result does rule out significant GI hemorrhage.

17
Q

describe the indications, clinical significance and limitation of;
specific canine pancreatic lipase

A
18
Q

describe the indications, clinical significance and limitation of;
bronchoalveolar lavage

A