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Flashcards in Metabolism 5 Deck (100)
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What functional reserve do the kidneys have and what occurs with damage of nephron

- large functional reserve but their regenerative capacity is limited
- surviving nephrons undergo hypertrophy
- damaged glomeruli are not replaced surviving undergo hyperplasia
- irreversible damage to one component - impaired function of the other components


at what GFR is each occurring at
1) diminished renal reserve
2) renal insufficiency
3) renal failure
4) end-stage renal disease (renal failure)

1) 50-99% normal
2) 25-50% normal
3) 20-25% normal
4) 5% normal


what is meant by renal disease and renal failure

renal disease = any deviation from normal renal structure or function
renal failure = decompensated renal disease with inability of the kidneys to maintain essential homeostatic functions required by the body


what are the most common factors responsible for death of animals in renal failure

most commonly attributable to severe retention of waste products, metabolic acidosis, hyperkalaemia or iatrogenic overhydration


Why are animals in clinical renal failure (uraemia) typically depressed, lethargic, inappetent or anorexic and (at least in small animals) frequently vomiting

- failure to excrete nitrogenous waste like urea
- urea itself not toxic but toxic waste products such as potassium, sulphate and phosphate are
- trigger chemoreceptor trigger zone for vomiting
- direct injury to vascular endothelial
- impairment of leukocyte and cardial skeletal muscle function


why do uraemic patients become dehydrated what does it result in

reduced renal function therefore reduced concentration ability - polyuria
- increased by vomiting or diarrhoea
result in compensatory polydipsia


what is anasarca and what factors contribute

- anasarca (generalised oedema formation) may reflect hypoalbuminaemia in protein-losing nephropathies (glomerulopathies)
- vascular injury by circulating waste products also promotes oedema formation by increasing vascular permeability


What is the most common acid-base imbalance seen in uraemic patients and what clinical sign might suggest that an animal has this imbalance?

- metabolic acidosis due to generate ammonium (NH4+) ions, increased retention of H+ ions, and impaired resorption of bicarbonate (HCO3-) ions
- compensatory hyperventilation


7 consequences of renal failure

1) retention of metabolic waste
2) impaired regulation of fluid volume
3) electrolyte imbalance
4) acid-base imbalance
5) disturbed endocrine function
6) immune dysfunction
7) systemic hypertension


List 4 consequences of systemic hypertension caused by decreased liver function

1) arteriolar smooth muscle hypertrophy +/- fibrinoid change leading to increased blood pressure (cycle)
2) thrombosis and/or tissue infarction - stoke
3) capillary rupture - haemorrhage - retinal haemorrhage (sudden onset blindness)
4) cerebrovascular accidents (strokes) with acute onset of neurological signs


why are animal cachexia in renal failure

- anorexia, vomiting +/- diarrhoea and subsequent catabolism of body tissues


vascular lesions why occur and what are the consequences

due to circulating uraemic toxins
leads to - hyaline degeneration (tunica intimal/medial deposits of collagen, amyloid) or fibrinoid change
- can lead to tissue haemorrhage, oedema, thrombosis and/or infarction


what lesions occur in oral cavity and what is the cause

ulcerative stomatitis on ventral aspect of the tongue, floor of the oral cavity, the gums and inner lips and cheeks
1) secretion of excess urea in saliva and conversion to ammonia (NH3) by urease-positive bacteria in the oral cavity - direct chemical mucosal injury
2) ndamage to submucosal arterioles by circulating toxins - thrombosis and ischaemic necrosis of the overlying mucosa (hypoxia)


what is uraemic gastritis, in what species most common, clinical symptoms and cause

- gastric mucosal ulceration and haemorrhage - vomiting, haematemesis and melaena in uraemic dogs
- similar pathogenesis to ulcerative stomatitis


4 other consequences that occur in the stomach due to renal failure

1) secondary bacterial infection
2) swollen and intensely congested
3) dystrophic mineralisation of gastric mucosa
4) dehydrated may develop constipation


List the 8) lesions caused by renal failure

1) gastrointestinal
2) exocrine pancreatic
3) cardiac and pericardial
4) lung
5) soft tissue
6) skeletal
7) brain


What are the cardiac/pericardial lesions that you might find in an animal in renal failure, what causes these lesions and how heal

1) hydropericardium (distension of the pericardial sac with noninflammatory oedema fluid)
○ may be due to vascular injury and increased vascular permeability
2) ulcerative uraemic mural endocarditis of the left atrium
lesions heal by scarring with dystrophic mineralisation


what is uraemic pneumonopathy

dogs in CRF may develop severe pulmonary dystrophic mineralisation and oedema with fibrin exudation into the alveolar lumina


what is a lung lesion caused by liver failure and what caused by

terminal pneumonia (e.g. due to vomiting and aspiration of feed or gastric secretions, or because of immunosuppression)


where find mineral deposits in renal failure

mineral deposition in damaged arterioles, the stomach wall, lungs, kidneys and subcutis (especially footpads)


what is secondary renal hyperparathryoidism

hyperphosphataemia (due to decreased GFR) - decreased serum ionised calcium concentration - hyperplasia of the four parathyroid glands with increased parathormone (PTH) synthesis and secretion - bone resorption by osteoclasts to boost the blood calcium concentration to normal - osteoporosis (decreased bone mass) - +/- pathological bone fractures and loosening or loss of teeth


what is rubber jaw what species common in

facial enlargement and malleability of the maxilla and mandible without fracture (“rubber jaw”)
dogs - puppies


what is renal ectopia and does it cause problems and list 2 other congenital malformations

malpositioning of one or, rarely, both kidneys generally caudally to pelvic canal
kidney normal may be hypoplastic
1) persistent foetal renal lobations
2) horseshoe kidney


define renal dysplasia, how occurs and 2 main features

disorganised renal development due to anomalous differentiation
- usually a congenital malformation but may be acquired in the early neonatal period in piglets, kittens or puppies in which nephrogensis continues
1) persistence of structures inappropriate to the stage of development
2) presence of anomalous structures


What species does polycystic kidney disease (PKD) occur, what breed and where found

cats - persian cats
in PKD, multiple renal cysts may be accompanied by cystic intra-hepatic bile ducts and sometimes cystic pancreatic ducts


what are Acquired Perinephric Pseudocysts
and where commonly seen, is it congenital or acquired

- uni- or bilateral - pockets of fluid (urine, blood, lymph or transudate) in the space between the renal capsule and the reflection of the peritoneum onto the kidney
- common in old cats
- caused by trauma, neoplasia, systemic hypertension


juvenile nephropathy,
familial nephropathy
hereditary nephropathy
list two breeds common in

• juvenile nephropathy = a non-inflammatory, degenerative or developmental renal disease of obscure pathogenesis that affects young animals
• familial nephropathy = a more restrictive term used for the same disease when it affects families of animals
• hereditary nephropathy = the definitive term used for the same disease once the inheritance of the nephropathy has been established
- english cocker spaniel and german shepherd


features of renal vasculature that predispose kidney to hypoxic injury

- renal artery and branch are end arteries so infarction of all dependent parenchyma is obstruction
- renal medulla is sensitive to hypoxia because of its relatively poor vascularity (most of its blood supply comes from the descending vasa recta) and because the packed cell volume (PCV) in the medullary capillary plexus is low because of water resorption


What is the mechanism that ensures that adequate perfusion of juxtamedullary nephrons is maintained following a significant and sustained drop in systemic blood pressure, where released from, what increase release and function

prostaglandins (especially PGE2 and PGF2α) released by specialised cells of the renal medullary interstitium
○ angiotensin II and angiotensin III - increased prostaglandin synthesis
○ the prostaglandins oppose the vasoconstrictive action of the angiotensins and induce vasodilation of the afferent arterioles of the juxtamedullary nephrons


define ischaemia, infarction and infact

ischaemia = hypoxic tissue injury resulting from a local reduction in blood flow
infarction = ischaemic coagulative necrosis of a localised area of tissue
infarct = the area of tissue which has undergone infarction