2011 Flashcards

1
Q

CS with a C6-T2 spinal cord lesion

A
  • normal mentation and CNs
  • UMN hind legs; increase muscle tone, increased reflexes
  • UMN or LMN forelimbs (+/- flaccid, reduced reflexes)
  • altered CPs all limbs
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2
Q

CS of left cerebral hemisphere lesions

A
  • altered mentation and behaviour
  • contralateral proprioceptive and CNs deficits
  • leaning to right
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3
Q

CS bilateral trigeminal nerve lesions

A
  • altered jaw tone (lock jaw vs. slack jaw)
  • reduced facial sensation bilaterally
  • reduced palpebrals bilaterally
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4
Q

Cs of Ixodes holocyclus toxin

A
  • LMN flaccid paralysis affecting all muscles to varied extent
  • GI stasis, dyspnoea, ataxia/paresis, lack of gag, palpebral
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5
Q

pathogenesis of canine pancreatitis

A
  1. co-localisation of zymogen granules and lysosomes leading to activation of trypsinogen to trypsin (active form) witihin the co-localised organellels
  2. trypsin activates more trypsinogen and other zymogens
  3. premature activation of digestive enzymes leads to local damage of exocrine pancreas with oedema, bleeding, inflammation, necrosis and peripancreatic fat necrosis
    4.inflammatory process recruits WBCs and cytokine production —> cytokines circulate and lead to distant complications; DIC, hypotension, MOD, disseminated lipodystrophy, pancreatic encephalopathy
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6
Q

discuss known risk factors for canine pancreatitis

A
  1. Genetic/hereditary predisposition; Mini Schnauzers, yorkshire terriers, poodles, dachshunds, cocker spaniels
  2. Dietary Indiscretion + Hypertriglyceridaemia (>500mg/dL)
  3. Severe blunt trauma; ie. HBC
  4. Pancreatitis hypoperfusion; ie. GA, shock
  5. Infectious diseases; Babesia canis, Leishmania
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7
Q

discuss the use of PLI

A

pancreatic lipase immunoreactivity is specific for the measurement of pancreatic lipase concentrations in serum and is thus the most specific diagnostic test for pancreatitis, and highly sensitive
1. in clinic tests; (semiquantitative evaluation of seurm pancreatic lipase immunoreactivity) SNAP cPL –> positive suggestive of pancreatitis, negative suggests that pancreatitis is very unlikely
2. Spec cPL(seurm sample); confirms diagnosis and determines a baseline concentration

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8
Q

total T4 for canine hypothyroidism

A

1.Define test: total t4 is a measurement of circulating thyroxine; it should be low in dogs not producing adequate thyroid hormones
2. Indications: Clinical suspicion is present; lethargy, mental dullness, decreased appetite, cold intolerance, weight gain, alopecia (rat tail), GI signs
3. Limitations: multiple factors can cause low T4 in euthyroid patients, ~50-60% of dogs have low TT4 at some point in the day, breeds (sighthounds), drugs (TMS, pheno, clomipramine, glucocorticoids), obesity, estrus, pregnancy, + euthyroid sick syndrome (HyperA, hypoA, infection, DM)
4. Interpretation; sensitivity of TT4 alone for diagnosing hypoT is ~75%, specificity ~95%. If TT4 conc >2mg/dL can rule out hypoT, but need to assess TSH + fT4 to diagnose

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9
Q

UPCR

A
  1. Define: urine protein: creatinine ratio allows quantitative measurement of suspected renal proteinuria. It is a unitless number obtained by dividing urine protein (mg/dL) by urinary creatinine (mg/dL). Important ; a form of CKD, substage in IRIS staging, progressive damage to nephrons, can lead to hypoalbuminiaemia + more, prognostic)
  2. Indications: suspicious of renal proteinuria (glomerular/tubular) + inactive sediment
  3. Limitations: can be elevated with contamination of urine; haematuria, pyuria, semen. day to day variability (low UPCs ~1.0 can vary daily up to 80%, higher UPCs 12.0 ~ 35% variability).
  4. Interpretation: Determine type of proteinuria (post-renal, pre-renal (Bence Jones proteins, myo/haemoglobin), renal (functional ie. heat, stress, fever, seizures - should resolve in 1 week, pathological)
    - pathological renal proteinuria; glomerular (filtration barrier disruption) vs. tubular (impaired ability to resorb protein).
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10
Q

fructosamine assay in feline DM

A
  1. Define: fructosamine is formed from irreversible binding of glucose to amino groups in plasma proteins. Fructosamine conc. reflects mean BG concentration over the last 1-2weeks. Most newly diagnosed diabetic cats have fructosamine levels 7.21mg/dL (>400umol/L). Fructosamine levels are unaffected by stress.
  2. Indications: to differentiate between stress induce hyperglycaemia and DM
  3. Limitations: diabetic cats with concurrent hyperT or hypoproteinaemia may have normal fructosamine levels due to lower plasma protein levels and rapid protein turnover rates, thus unreliable in cats with concurrent hyperT. Cats with mild DM or recent onset (<1-2wks) may have normal fructosamine levels.
  4. Interpretation: used to confirm DM diagnosis
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11
Q

Pathophysiology of paraneoplastic syndrome; gastroduodenal ulceration + associated neoplasms

A
  • mast cell tumour (MCT) is the most common cause –> hyperhistaminaemia
  • histamine stimulates gastric acid secretion, and exerts direct effects on the gastric mucosa causing increased vascular permeability and mucosal blood flow, in addition to protein exudation
  • gastrinoma; a gastrin-secreting pancreatic tumour
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12
Q

Pathophysiology of paraneoplastic syndrome; hypoglycaemia + associated neoplasms

A
  • functional beta cell tumours of the endocrine pancreas (insulinomas) are the most common cause; others - hepatocellular carcinoma, smooth-muscle tumours of the GIT (leiomyoma, leiomyosarcoma, GI stromal tumour)
  • cause of hypoglycaemia in these latter tumours is uncertain but may be related to excess tumoral consumption of glucose, decreased hepatocellular function (in the case of hepatocellular carcinoma), or ectopic production of insulin-like growth factors (IGFs)
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13
Q

Pathophysiology of paraneoplastic syndrome; hypergammaglobulinaemia + associated neoplasms

A
  • globulins = all the non-albumin proteins in circulation (including clotting factors, enzymes hormone-binding proteins, lipoproteins, immunoglobulins)
  • IGs produced by plasma cells and mediate the humoral immune response to pathogens/inflammatory stimuli
  • polyclonal gammopathy = typically seen with infectious/inflammatory diseases
  • monoclonal gammopathy = neoplasms; B-lymphocytes or plasma cell cancers - they originate from a single ancestral precursor cell
  • most common cause of monoclonal gammopathies; multiple myeloma, solitary plasma cell tumours, B-cell lymphomas, leukaemias, less commonly solid tumours
  • important non-neoplastic causes; ehrlichiosis and leishmaniasis in dogs, FIP (cats)
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14
Q

Pathophysiology of paraneoplastic syndrome; thrombocytopaenia + associated neoplasms

A
  • decreased platelet production, increased destruction or consumption, sequestration and loss by haemorrhage
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15
Q

Pathophysiology of paraneoplastic syndrome; aenamia + associated neoplasms

A
  • lymphomas, leukaemias, multiple muelomas, histiocytic sarcoma, haemangiosarcoma
  • associated with haemorrhage, IMHA, oxidative injury to RBCs, tumour cell erythrophagocytosis, myelophthisis
    + myelosuppressive chemo effects, anaemia of chronic disease
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16
Q

pathophysiology of anaemia of inflammatory disease

A
  • inadequate production of erythropoietin (EPO)
  • decreased responsiveness of erythroid progenitors in the bone marrow to EPO
  • reducing circulating erythrocyte lifespan
  • dysregulated iron metabolism and storage
  • AID is drive by production of pro-inflammatory cytokines including TNF-a, interferon-y, interleukin-1B, IL-6 and IL-10
  • IL-6 induces hepatic synthesis of the protein hepcidin – hepcidin mediates reduced intestinal absorption of dietary iron and increased sequestration of iron within macrophages = hypoferremia + reduced erythropoiesis
17
Q

Pathophysiology of paraneoplastic syndrome; hypercalcaemia + associated neoplasms

A
  • dogs with lymphoma (T-cell immunophenotype) + anal sac adenocarcinoma
  • cats (less common); squamous cell carcinoma, lymphoma, lung carcinoma
    MOA;
    1. Ectopic production of parathyroid hormone related peptide (PTHrP) by the tumour cells –> PTHrP mimics PTH and stimulates osteoclastic bone resorption, liberating calcium from bone and releasing it into circulating. Enhanced renal absorption of calcium.
    2. Inflammatory cytokines; IL-1, TNF-a, TGF-a and B, stimulate osteoclastic bone resorption
    3. Osteolytic tumours; only occurs in the setting of widespread skeletal malignancy (ie. multiple myeloma, widespread skeletal metastasis of mammary/lung/bladder/prostate carcinomas) and is rarely seen with primary bone tumours such as osteosarcoma
18
Q

pathophysiology of FIP

A
  1. Immune-mediated disease involving viral antigen, antiviral antibodies and complement
  2. Dissemination/systemic inflam =FIPV infects monocytes and macrophages = Infected monocytes can attach to endothelium, or extravasate, allowing the virus to enter various tissues
    3.Complement fixation (FIPV + antibodies + macs + neuts) results in release of vasoactive amines and increased vascular permeability
  3. Granulomatous lesions; infected macs overproduce neutrophil survival factors
  4. Immune-complexes = blood vessel damage and vasculities
  5. ADE; antibody-dependent enhancement –> facilitating uptake of coronavirus by macs
19
Q

pathophysiology of tetanus

A
  1. Clostridium tetani spores introduced into wounds/penetrating injuries
  2. Aerobic conditions = production of exotoxins tetanospasmin and tetanolysin
  3. Tetanospasmin causes classic tetanus signs - enters the motor nerve axons near the NMJ and ascends via retrograde intra-axonal transport to the neuronal body in the spinal cord –> ascends bilaterally to the brain (travels at 75-250mm/day)
  4. Tetanospasmin = inhibits release of glycine and GABA neurotransmitters = resulting in CNS hyperexcitability.
    = also within the parasympathetic cardiac inhibitory centre = increased vagal ton and catecholamine release
    - Binding of tetanospasmin to presynaptic sits of inhibitory neurons in irreversible.
  5. Tetanolysin; non-spasmogenic toxin that causes local tissue damage and hemolysis = bacterial multiplication
  6. Dogs and cats more resistant than people and horses. generalised and localised forms (more common) - occur near wound site and result in contraction of the group of muscles
  7. Cs develop in 5-10days typically, range 3-21 days.
20
Q

treatments for AFIB

A
  1. Rate control; slows conduction through the AV node
    - beta-adrenergic blockers (sotalol, atenolol)
    - calcium channel blockers (diltiazem)
    - digoxin
  2. Rhythm Control;
    - for dogs with AF in absence of significant structural disease or extra-cardiac causes. Cardioversion
    - electrical (92% success rate)
    - pharmacological; amiodarone +/- lignocaine (35% success rate)
21
Q

DDx. for 9yo dog with prostatomegaly

A
  • BPH
  • Prostatitis
  • neoplasia
22
Q

DDx. for unilateral mucopurulent nasal discharge in a 10yo DSH

A
  • Fungal; Crypto, Aspergillosis
  • Neoplasia
  • Polyp
  • FB
23
Q

DDx. for splenomegaly in a 5yo FS lab

A
  • inflammation; infectious + classed according to cell type (eosinophilic, lymphoplasmacytic, necrotizing)
  • hyperplasia; in response to immune mediated diseases or destruction of RBCs
  • congestion; venous drainage impaired (drugs, torsion, RSCHF, CdVC or hepatic vein obstruction, liver disease)
  • infiltration; neoplastic (haemangiosarcoma, fibrosarcoma, histiocytic sarcoma, leiomyosarcoma, myelolipoma), nodular hyperplasia, amyloidosis
24
Q

Explain the diagnostic steps in diagnosing HypoA

A
  1. CS: crisis vs. chronic (lethargy, weakness, vomiting, diarrhoea, anorexia) +/- PU/PD, tremors, melena
  2. CBC: absence of stress leukogram, lymphocytosis, eosinophilia, +/- mild, nonregen anaemia
  3. Chem: Sodium <135mmol/L, Potassium >5.5mmol/L (sodium:potassium <27:1 was found to have 93% sensitivity + 96% specificity). +/- inc. ALT, Ca, low albumin, cholesterol
  4. Basal cortisol: rule out HA if >2ug/dL.
  5. ACTH stim: minimal/absent response
  6. Plasma ACTH measurements: in atypical HA (elevated with primary and low with secondary hypoA)
  7. US: small, flattened adrenals (<3.2mm thickness)
25
Q

Explain the treatment and monitoring of an addisonian dog

A
  1. Crisis:
    - IVFT
    - Electrolyte/metabolic imbalances; hyponatraemia, hyperkaelamia, hypercalcaemia, hypoglycaemia, metabolic acidosis
    - Glucocorticoids; post ACTH stim test* prednisolone, hydrocortisone
  2. Maintenance
    - mineralocorticoids; fludrocortisone, desoxycortisone (DOCP 1.1mg/kg SQ q30days)
    - glucocorticoids; Pred 0.1-0.2mg/kg PO SID
  3. Monitoring;
    - glucocorticoids; CS (+/- endogenous ACTH levels)
    - mineralocorticoids; electrolyte monitoring q3-4months for 2 years, then q6mnths thereafter