Lecture 29 Flashcards
adverse effects of: necrosis, inflammation, neoplasia, or myocardial degeneration on cardiac funtion(2)
reparative fibrosis if animal survives
depression of myocardial contractility and/or arrhythmia->cardiogenic shock or CHF
most common cause of cardiac arrhythmia/dysrhythmia
occur secondary to myocardial damgae
potential causes of hydropic or fatty degeneration of cardiac myofibers
systemic diseases, severe anemias, toxemias
brown atrophy
sever intra cellular accumulation of lipofuscin pigment
aged animals, especiallly high producing dairy cattle
2 main forms of tissue mineralization
dystrophic-in necrotic tissue (eg Johnes disease)
metastatic- in live tissue, high [ ] of Ca or phosphate in circulation (eg Vit D toxicity)
when is capacity for division of cardiac myofibers lost
decreased in late fetal life and lost in early neonatal period
where are foci of myocardial necrosis most likely to be found in heart
left ventricle- subendocardial myocardium of IC septum and in the papillary muscles
how long must patient survive for lesions of necrosis of cardiac myofibers to be grossly obvious? What gross lesions are seen
4-12 hours- areas of subtle pallor
18-24 hours- necrotic zone pale, thin film of fibrin and hemorrhage
how are foci of myocardial necrosis repaired
necrotic tissue replaced by fibrosis at 7 days->gross cream white pallor
agents responsible for myocardial necrosis(5)
ischemia/hypoxia excess catecholamines nutritional deficiency (vit e) drugs/chemical toxins plants
how long can cardiac myofibers tolerate hypoxic conditions
20-30 minutes->irreversible damage
Why is myocardial infarction so common in humans
atherosclerosis (plaque build up) and systemic hypertension
examples of causes of myocardial hypoxic/ischemic injury
anemia
hypovolemic shock
thrombosis or coronary artery
5 plants that can cause myocardial necrosis
foxglove capetulip shaggy pea african succulents nerium oleander
etiopathogenesis of white muscle disease
which species
lipoperoxidation of striated myofiber membranes->cytoplasmic influx of Ca->ATP consumption to move Ca away from contractile myosin/actin and into SR->mitochondrial damage and Ca induced hypercontraction with segmental degeneration and dystrophic mineralization
in lambs and calves