2012 Flashcards
Describe the function of the vestibular system
- equilibrium and balance
- information on body’s orientation, tilt, acceleration
- detects; static tilt, linear and rotatory acceleration of the head
- makes automatic, unconscious postural adjustments and maintains eyes on a target
Describe the neuroanatomical components making up the central and peripheral vestibular systems
- Peripheral;
- bony (perilymph) and membranous (endolymph) labyrinths of the inner ear
- saccules and Utricles = crista amupullaris
- semicircular canals = Macula and otoliths
–synapse onto sensory neurons that make up part of CN VIII - CENTRAL
- cerebellum + floculonodular node
- lateral vestibulospinal tract
- medial longitudinal fasciculus
Describe the clinical signs seen with vestibular disease
- ataxia; hypermetria
- head tilt
- compulsive circling or rolling
- nystagmus
- nausea
- intention tremors
List ‘target’ organs that are typically damaged by chronic hypertension
- CNS; persistent vasoconstriction of arteriolar beds leads to ischaemia = seizures, altered mentation, vestibular signs, head tilt, nystagmus, cervical ventroflexion, paresis, stupor, disorientation, facial nerve paralysis, focal neurologic deficits can occur.
- Ocular; retinal haemorrhage and arteriolar constriction and/or tortuosity may occur - damage to the choroidal vascular beds leads to necrosis and atrophy of retinal pigmented epithelium. Retinal detachment is the most common ocular abnormality, papilloedema, vitreal haemorrhage, hyphema, retinal aneurysms, secondary retinal degeneration, glaucoma.
- Renal; afferent arteriole damage, making arterioles less responsive to changes in systemic BP. This damage eventually leads to glomerular hypertension, with decreased renal function and proteinuria.
- Cardiovascular; increased workload for the heart, which results in compensatory left ventricular hypertrophy –> leads to increased oxygen demand by the myocardium and myocardial remodelling with excessive collagen. Fibrosis eventually occurs and results in the loss of compliance. Increased myocardial oxygen demand causes increased risk of myocardial ischaemia, infarction, arrythmias, and heart failure.
Briefly describe the autoregulatory mechanism by which target organs are protected from an increase in blood pressure
Xxx
Describe the pathophysiology of target organ damage when these autoregulatory mechanisms break down
Xx
Discuss the aetiology of rabies in dogs and cats
- Rabies lyssavirus (genus), Rhabdoviridae family
- can infect any warm blooded animal
- major reservoir hosts; Mustelidae (skunks, weasels), canidae (dog, wolf, fox, jackal), racoons, mongoose, meerkat
- transmitted via bites, contamination of open wounds or mucous membranes with saliva or neural tissue
- factors involved in susceptibility to rabies; quantity of virus inoculated, viral variant, bite site and age of animal.
Describe the epidemiology of rabies in dogs and cats
- occur throughout the world; America, Asia, Africa, Middle-east and some parts of Europe
- Rabies free areas; Japan, NZ, Australia, UK
- continued risk of reintroduction of rabies
- more than 27,000 cases reported yearly worldwide, true incidence is much higher.
- cats are the most commonly infected domestic animal in the USA, dogs are the main source of rabies infections in people internationally.
Describe the pathophysiology of rabies in dogs and cats
- inoculation –> rabies enter peripheral nerves OR can replicate locally in the muscle spindle
–> spreads passively by intra-axonal flow in peripheral nerves towards the CNS (can travel up to 100mm per day)
–> enters spinal cord/brainstem by retrograde axoplasmic flow –> once in CNS disseminates rapidly (100-400mm per day) - incubation period before development of CS is varied; can be prolonged. Factors that influence incubation period include age of individual exposed, degree of innervation at the bite site, distance from inoculation site to spinal cord or brain, variant of virus involved, previous vaccination status of the animal
- incubation periods (average); 3-8 wks dogs, 4-6wks cats, 3-6wk humans
- virus spreads to salivary glands via CNs –: virus is shed in saliva. Not every infected animal excretes virus in saliva. 50-90% of cases. Some patients may die before salivary glands infected (brain is infected before glands)
- period of viral shedding before onset of neurologic signs is typically 1-5 days in naturally-infected dogs and cats
- CS; aggressiveness, altered behaviour, nervousness, anorexia, ataxia, hyperaesthesia, photophobia, disorientation, change in vocalisation, inability to swallow, hypersalivation, mandibular paralysis, cranial nerve deficits, paraparesis, paralysis, seizures, coma and death (respiratory paralysis, prolonged seizure activity)
Explain the aetiopathogenesis of hypokalaemia in dogs and cats
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Outline the homeostasis of glucose. Include in your answer the major organs and hormones involved.
- Rising blood glucose –> pancreas releases insulin –> stimulate glucose uptake by cells and glycogen formation in the liver –> glucose returns to normal levels
- Declining blood glucose level –> pancreas releases glucagon –> stimulates glycogen breakdown to glucose in the liver –> blood glucose rises to normal range
List the types of fluid that can constitute abdominal effusion in cats and dogs (according to lab definitions)
- pure transudate: <25g/L protein, total nucleated cell count <1.5, predominant cells = rare monocytes and mesothelial cells
- modified transudate; 25-75 g/L protein, TNCC 1.5-7.0, variable predominant cells
- exudate; >30g/L protein, TNCC >7, polymorphonuclear neutrophils (PMNs), possibly degenerative
Describe the pathophysiological process that generates exudate effusions
linked with inflammation or infection, contains high levels of protein, white blood cells, cellular debris
- ie. bacterial or fungal infection, neoplasia, FIP, pancreatitis
Describe the pathophysiological process that generates transudate effusions
caused by systemic conditions that alter blood vessel pressure, leading to fluid leaving the vascular system - it has low protein content and appears clearer
- ie. hypoalbuminaemia, cirrhosis, portal hypertension
Describe the pathophysiological process that generates mod transudate effusions
Xd
