Path 1- Urinary 1

kelseyfmeyer's version from 2015-04-16 18:52

Lecture 2 (1 is only review)

Question Answer
what are the things that actually kill you if you have renal failure? (3)(1) metabolic acidosis (2) pulmonary edema (3) HYPERkalemia (cardiotoxicity)
how much leeway do you have with kidney damage?the kidneys have a 75% functional reserve to maintain endocrine and metabolic function (so. 75% damage before any problems start to show)
list some clinical indicators of renal failure?Altered urine quantity (polyruia, anuria, oliguria), Altered urine quality (USG-->isosthenuria), Proteinuria, Azotemia, Uremia
why is there polyuria in renal failure?due to failure of sodium and water resorption in the tubules (might also lead to polydipsia)
when might you see oliguria or anuria?acute renal failure
why does isosthenuria occur in renal failure?loss of renal function → failure to concentrate urine (ISO= 1.008 - 1.012) (normal 1.015 to 1.045 for dogs, and 1.035 to 1.060 for cats)
when do you see azotemia?when there is inc levels of UREA AND CREATININE in the blood. Occurs when there is > 75% loss of nephrons
What should you know about uremia?it is a SYNDROME! (uremic syndrome) (characterized by numerous lesions and clinical signs caused by toxic levels of urea in the blood associated with renal failure. Patients are severely ill and/or have systemic lesions.)
**Uremia can cause systemic lesions by what two mechanisms? (1) Endothelial injury resulting in vasculitis, thrombosis, infarction (uremic vasculopathy). (2) Caustic injury to epithelium of mucosal surfaces due to production of large amounts of ammonia by urea-splitting bacteria (uremic toxicity)
uremia (uremic syndrome) can affect the mouth how?Ulcerative glossitis and stomatitis
uremia (uremic syndrome) can affect the stomach how?Ulcerative gastritis with mineralization
Additional systemic (non-renal) lesions from uremic syndrome include? (7)Ulcerative colitis (horses and cattle), Vascular thrombosis, Fibrinous pericarditis, Pulmonary edema, Endocardial mineralization, Intercostal mineralization, other soft tissue mineralizations
causes of renal failure/ azotemia are categorized how?prerenal, intrarenal, and postrenal
what are the two kinds of renal failure?acute and chronic
explain prerenal renal failurereduced glomerular filtration and/or hypoxic injury due to impaired renal perfusion
What are the two main conditions which would cause prerenal renal failure?(1) circulatory collapse (shock, hypovolemia, severe dehydration) (2) renal ischemia, which could be caused by vasculitis (viral, bacterial, autoimmune, type III hypersensitivity, drug reactions) or embolic disease leading to renal infarction (thrombosis, DIC, bacterial sepsis, tumor emboli)
explain Intrarenal failuredamage to the renal tissue such as: acute tubular necrosis, glomerulonephritis, tubulointerstitial nephritis, or pyelonephritis
what are the two clinical presentations of acute tubular necrosis?oliguria, anuria
Tubular necrosis results in further renal injury by what two mechanisms?(1) leakage of tubular ultrafiltrate into the renal interstitium (causes interstitial necrosis and inflammation) (2) intratubular obstruction resulting from sloughed necrotic epithelium (tubular casts)
what are some bacteria which might cause tubular necrosis?Leptospira, E. coli, Streptococcus, Staphylococcus, Proteus spp.
what are some viral infections which might cause tubular necrosis?canine hepatitis virus, canine distemper virus, canine herpesvirus
what is a nephrotoxin?substances that accumulate to a toxic concentration within the tubules
what are some examples of nephrotoxins?pigments(Hb, myoglobin, bile/bilirubin), Heavy metals(lead, mercury, arsenic, cadmium, thallium), Oxalates (ethylene glycol (anti-freeze), oxalate-rich plants (Rhubarb, Greasewood, Sorrel, Halogeton) ), plants (Pigweed, Oaks, grapes and raisins, lilies), vit D, nephrotoxic drugs
what does excessive amounts of vit D do? when does this happen?Leads to nephrotoxicity. USUALLY from oversupplementation. Can also lead to (or be caused by? He doesnt specify) hypercalcemia, and calcinogenic plants (Cestrum, Solanum, etc.)
List some nephrotoxic drugs(didnt seem to emphasize) antimicrobial drugs (Aminoglycosides: streptomycin, neomycin, gentamycin; tetracyclines; Amphotericin B), NSAIDs (aspirin, phenylbutazone, carprofen, flunixin, ibuprofen, naproxen), immunemodulatory drugs (cyclosporin), antineoplastic chemotherapeutics (cisplatin, carboplatin, cyclophosphamide, ifosfamide, mitomycin C, methotrexate, gemcitabine)
list three major causes for (acute) intrarenal failureacute tubular necrosis, Acute glomerulonephritis, Acute pyelonephritis
(Acute glomerulonephritis can be caused by?)immune complex glomerulonephritis, bacterial, viral, toxic
(Acute pyelonephritis is caused by?)ascending bacterial infection from the urethra, ureters, and renal pelvis
describe Postrenal renal failure. aka?urinary obstruction with pressure atrophy and necrosis. aka obstructive nephropathy
what are the three main causes of postrenal renal failure?(1) urolithiasis (2) tumors (transitional cell carcinoma) (3) iatrogenic (accidental ligation of ureter)
obstructions can lead to what two conditions?hydroureter and hydronephrosis (and possibly organ rupture with resulting uroabdomen)
When prolonged and progressive, CRF may lead to..?end stage kidney
*The term end-stage kidney is used to describe renal disease which is...?chronic, advanced, generalized, progressive, and irreversible.
what is the paranchyma of a end stage kidney like?///fibrotic///, atrophic, shrunken renal parenchyma with massive loss of functional nephrons and replacement with scar tissue (fibrosis)
*what is a common pathway to chronic renal failure, despite the original cause of injury? what is a diagnostically relevant note about this?PROGRESSIVE FIBROSIS, and it often becomes impossible to determine an etiology at this stage
what is a hematological result of chronic renal failure?non-regenerative anemia due to reduced erythropoietin (EPO) production by renal interstitial fibroblasts
*what is a biochemical result of chronic renal failure? explain it.altered calcium-phosphorus metabolism!!! dec GFR-->hyperphosphatemia--> which leads to Ca++ precipitation-->hypocalcemia-->the hypocalcemia stims parathyroid hormone secretion--> PTH causes calcium to be mobilized by osteoclastic bone resorption--> causes reduced bone mineral density (osteopenia) --> this is known as renal secondary hyperparathyroidism and chronic hyperparathyroidism leads to fibrous osteodystrophy
*how is chronic renal failure related to bone abnormalities? altered calcium-phosphorus metabolism!!! dec GFR-->hyperphosphatemia--> which leads to Ca++ precipitation-->hypocalcemia-->the hypocalcemia stims parathyroid hormone secretion--> PTH causes calcium to be mobilized by osteoclastic bone resorption--> causes reduced bone mineral density (osteopenia) --> this is known as renal secondary hyperparathyroidism and chronic hyperparathyroidism leads to fibrous osteodystrophy
*Renal secondary hyperparathyroidism--> which ions does this affect, and how? how does it affect the gland itself? what is the hormone and how is that affected? what condition can this lead to?~leads to hyperphosphatemia / hypocalcemia, and causes /bilateral parathyroid gland hyperplasia/, and the PTH which is secreted causes osteoclastic bone resorption (need more Ca to balance out the P) and bc all the Ca is resorbed, the bone is replaced with fibrous tissue--> fibrous osteodystrophy
what is the PCV like in acute renal failure? chronic?acute= normal or increased (dehydration). Chronic= decreased (reduced EPO)
what is BUN / Creatinine like in acute renal failure? chronic?Acute= previously normal with progressive increase. Chronic= previously increased with sustained elevation
what is Serum Potassium like in acute renal failure? chronic?acute=+/- hyperkalemia. chronic= usually normal with hyperkalemia at end stage
what is Urine volume like in acute renal failure? chronic?Acute= often oliguric initially. Chronic= usually polyruric
what is Kidney size like in acute renal failure? chronic?Acute= normal or increased. Chornic= often decreased
what is bone density like in acute renal failure? chronic?Acute= normal. Chronic=may be decreased (renal osteopenia)
what are 4 portals of entry into the kidney?Ascending from ureter, Hematogenous(from the blood), Glomerular filtrate, Direct penetration
portal of entry--> Ascending from ureter--> what stuff usually gets into the kidney via this route?infections (usually bacterial) ascend up the ureter to the bladder. This usually results in suppurative pyelonephritis (bact can be coming from skin, GI, or genital tracts usually)
portal of entry--> Hematogenous--> what stuff usually gets into the kidney via this route?bacteremia can lead to bacterial embolization and nephritis (bacteria may localize in the glomerulus or within interstitial capillaries) there is also the possibility of neoplastic metastases (tumor emboli)
portal of entry--> Glomerular filtrate--> what stuff usually gets into the kidney via this route?substances secreted into the filtrate can be injurious to the renal tubular epithelium--> examples include toxins (heavy metals, nephrotoxic plants) toxic drug metabolites (NSAIDS, chemotherapeutics, aminoglycosides, amphotericin B), crystalline salts (oxalate crystals)
portal of entry--> direct penetration--> what are two ways this happens?penetrating trauma, neoplastic invasion
**what is the MOST IMPORTANT BARRIER in defense mechanisms of the kidney?Glomerular basement membrane
defense-->Glomerular basement membrane--> how does this protect?MOST IMPORTANT BARRIER! protects the nephron by filtering out most circulating bacteria and inflammatory cells\
defense--> Glomerular mesangium--> how does this protect?Mesangial cells are a component of the monocyte-macrophage system which are capable of removing macromolecules from the circulation by phagocytosis.
*Tubular basement membrane is protective how?prevents ascending bacteria from gaining access to the interstitium AND!! TBM provides a scaffold for re-epithelialization after tubular injury (tubular regeneration)
*what is the most harmful thing to the tubular basement membrane?ischemia (infarction) typically destroys the TBM and causes permanent scarring with loss of tubules (since TBM provides a scaffold for re-epithelialization after tubular injury, if it is injured, major probs)
what are the two defense mechanisms of the renal intersitium?(1) humoral antibodies may protect mucosal surfaces at the renal pelvis to defend against ascending infection (2) macrophages, lymphocytes, and plasma cells within the interstitium provide cell-mediated immune surveillance and modulation against invasive pathogens (i.e. Leptospira)
what are the two ways the vasculature can act as a defense mechanism for the kidney?(1) intact endothelial lining is a defensive barrier against bloodborne pathogens (2) intact endothelium prevents activation of clotting cascade and /reduces thrombus formation/

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