2022 Flashcards
Outline 5 reported risk factors for canine pancreatitis
- overweight body condition
- diabetes mellitus
- hyperadrenocorticism
- hypothyroidism
- prior history of GI tract disease
- high-fat diets
- hypertriglyceridaemia
- malnutrition
- exposure to toxins (zinc, organophosphates)
- hypercalcaemia
- pancreatic duct obstruction
- reflux of duodenal contents into the pancreatic duct
- pancreatic trauma (sx/blunt)
- parasites (ie. flukes)
- hepatobiliary diseases
- small intestinal disorders
- pancreatic ischaemia/reperfusion injury
- infection with Babesia rossi
- various drugs; thiazide diuretics, furosemide, azathioprine, L-asparaginase, sulfonamides, tetracycline
Discuss the pathogenesis of canine pancreatitis
- if inhibiting substances are blocked or if enzymes are activated whilst still in the pancreas, the pancreas inappropriately beings to digest itself
- ie. the conversion of trypsinogen (inactive) to trypsin (active form) can be triggered by enterokinase, bile, lysosomal enzymes, or other stimuli
- the result is disruption of pancreatic membranes, arteriolar dilation, increased vascular permeability, oedema and haemorrhage –> subsequent pain, leukocytic infiltration and peripancreatic fat necrosis
- reduced pancreatic blood flow and leukocyte infiltration can lead to pancreatic necrosis
- secondary infections can occur dt bacterial translocation from the intestines
- arterial hypotension, portal venous pooling, hypovol may lead to shock
- peripheral venoconstriction and leakage of pancreatic enzymes into the abdominal cavity and vascular compartment compound the damage
- regional tissue invasion and destruction caused by release of pancreatic enzymes can be extensive –> end results include damage to liver, kidneys, lungs, heart, abdominal lymphatics, extrahepatic biliary tract obstruction
- *note the feline pancreas is also prone to ascending biliary infections and bile reflux because the pancreatic and bile ducts merge before reaching the duodenal papilla
How does the normal pancreas protect itself from autodigestion?
- packaging inactive enzymes into zymogens helps prevent premature activation of major digestive enzymes before they are released into the duodenum
- enzymes inhibitors also exist within the pancreas (alpha-antitrypsin) and circulate in plasma (eg. alpha-macroglobulins, antichymotrypsin, alpha-antitrypsin)
- once zymogens are released into the intestinal lumen, they undergo peptide cleavage by enterokinase secreted by duodenal mucosal cells —> this breakdown activates pancreatic enzymes and allows them to begin digesting nutrients
How do acute and chronic pancreatitis differ?
- acute pancreatitis is characterised by an infiltration of neutrophils, moderate to severe pancreatic necrosis, oedema, and/or haemorrhage . Acinar tissue and ducts remain intact. More likely to have severe signs.
- chronic pancreatitis is long-standing inflammation associated with low-grade, mononuclear inflammation and fibrosis. Chronic pancreatitis may be a sequela to recurrent, acute pancreatitis. More likely to have mild signs.
What are 3 physiological features that make the kidneys particularly vulnerable to ischaemic and nephrotoxic insult?
- kidneys receive 20-25% of circulating cardiac output
- ischaemia can result in renal hypoperfusion, decreased nephrotoxin distribution volume, decreased tubular flow and increased vasoconstriction - to maintain cardiac and cerebral perfusion in the face of haemodynamic abnormalities renal vasoconstriction occurs with a resultant decrease in GFR –> subsequent hypotension (MAP <80mmHg) causes loss of autoregulation that ordinarily helps to maintain renal perfusion
- Toxins (esp. blood bourne) toxins; the glomerular capillary surface provides a large area for toxin-endothelial interaction. Tubular mechanisms increase toxin concentration in the distal nephron. High oxygen consumption and metabolic activity, and transcellular transport apparatuses also contribute to the kidneys’ sensitivity to toxins.
- Cortical structures (eg. proximal tubule, LOH) are prone to ischaemic and toxic injury because of their high metabolic rate and reception of 90% of the renal blood circulation
Outline the 3 primary classifications of azotaemia in dogs and cats
- Pre-renal: secondary to deficiencies in renal blood flow, abnormal perfusion pressure or imbalances in renal vascular resistance (ie. hypovolaemia, hypotension, sepsis, hemorrhage, CHF, renal vessel thrombosis)
- Renal/Intrinsic: occurs with morphologic changes in renal vasculature, glomeruli, tubules or interstitium. (ie. pyelonephritis, FIP, sepsis, leptospirosis, immune-mediated glomerulonephritis, lyme disease, hypercalcaemia, amyloidosis, neoplasia (lymphoma), toxins; lilies, NSAIDS, amphotericin B, doxorubicin)
- Post-renal: urethral obstruction, ureteral obstruction (calculi, strictures, mucous plugs, trauma, neoplasia)
Describe the pathophysiologic mechanisms by which acute kidney injury causes;
Bradycardia
Hyperkalaemia; secondary to decline in excretory function. The increase in extracellular potassium concentration makes excitable cells refractory to repolarization, thus resulting in decreased conduction of cardiac and neuromuscular tissue.
- sine waves, ventricular fibrillation, standstill
Describe the pathophysiologic mechanisms by which acute kidney injury causes;
Vomiting
- uremia triggering the CTZ
- uremic ulcers
Describe the pathophysiologic mechanisms by which acute kidney injury causes;
Diarrhoea
- uremic gastritis and enteritis
Define anuria
anuria is defined as urine output <0.08ml/kg/hr
Define oliguria
urine output <1ml/kg/hr in a hydrated, well-perfused patient
Outline the aetiopathogenesis for the most common causes of left ventricular hypertrophy in older cats
- HCM is a primary myocardial disease
- left ventricular concentric hypertrophy occurs in the absence of an identifiable increase in afterload (eg. aortic stenosis, systemic hypertension) or presence of an endocrine disorder (hyperthyroidism, or acromegaly)
*mutations in sarcomeric genes alter the ability of cardiomyocytes to contract and relax normally resulting in concentric hypertrophy –> additionally myofibers frequently become disoriented –> with severe HCM ongoing myocardial necrosis and replacement fibrosis occur that results in a stiffer, less compliant LV. Slowed relaxation and decreased compliance (diastolic dysfunction) of the LV result in increased diastolic pressure. Since the mitral valve in open in diastole, increased pressure also occurs in the left atrium, pulmonary veins and pulmonary capillaries, producing LA enlargement, pulmonary oedema and/or pleural effusion (ie. CHF) when the disease is severe
Discuss the pathogenesis of the clinical disease caused by feline (primary) hypertrophic cardiomyopathy
- LA enlargement –> blood flow stasis predisposes thrombus formation (left auricle) –> terminal aorta, coronary artery, brachiocephalic trunk, right subclavian artery (thromboembolic disease)
- systolic anterior motion of the mitral valve (hypertrophied papillary muscles)
- SAM results in dynamic subaortic stenosis and mitral regurgitation –> turbulent blood flow jets that produce a systolic heart murmur
- sudden death; poss. ventricular tachyarrhythmia degenerating into ventricular fibrillation *the disease left ventricular myocardium is a logical place for an ectopic focus of depolarisation to develop
- pulmonary oedema and/or pleural effusion, so are tachypnoeic and frequently dyspnoeic
Discuss the application(s) and limitation(s) of the SNAP NT-proBNP test cats presenting with suspected congestive heart failure
N-terminal-pro- brain natriuretic peptide
is the best perfoming biomarker for HCM, but false-positives are possible and cannot be used as the sole basis for making a diagnosis of HCM.
Discuss the neurological control of the STORAGE phase of micturition
- controlled by the sympathetic nervous system
- the hypogastric nerve stimulates detrusor beta receptors, causing relaxation of the detrusor muscle and filling of the urinary bladder
- the sympathetic nervous system also stimulates alpha-1 receptors of the bladder neck and internal urethral sphincter, which causes smooth muscle contraction and closure of the urethra to urine outflow
- as bladder filling continues, stretch receptors in the detrusor muscle mediate sensory information to the brain via the hypogastric and pelvic nerves
