Path 1 - Urinary 1

drraythe's version from 2015-05-04 01:02

Lecture 2 (1 was review only, not on exam)

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 w/ kidney dmg?The kidneys have a 75% fxnal reserve to maintain endocrine & metabolic fxn (75% dmg must occur before any problems start to show)
List some clinical indicators of renal failure?Altered urine quantity (Polyuria, Anuria, Oliguria)
Altered urine quality (USG → Isosthenuria)
Why is there Polyuria in renal failure?Due to failure of Na & H20 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 fxn → failure to concentrate urine (ISO = 1.008 - 1.012) (normal 1.015 to 1.045 for dogs & 1.035 to 1.060 for cats)
When do you see Azotemia?When there is ↑ levels of UREA & CREATININE in the blood. Occurs when there is >75% loss of nephrons (this will be evident in your BW)
What should you know about Uremia?It is also a SYNDROME! (Uremic Syndrome) characterized by numerous lesions & CS caused by toxic levels of urea in the blood associated w/ renal failure. Patients are severely ill &/or have systemic lesions
**Uremia can cause systemic lesions by what 2 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 NH3 by urea-splitting bacteria (uremic toxicity)
Uremia (Uremic Syndrome) can affect the mouth how?Ulcerative Glossitis & Stomatitis
Uremia (Uremic Syndrome) can affect the stomach how?Ulcerative gastritis w/ mineralization
Additional systemic (non-renal) lesions from Uremic Syndrome include?(7)(1) Ulcerative colitis (horses & cattle)
(2) Vascular thrombosis
(3) Fibrinous pericarditis
(4) Pulmonary edema
(5) Endocardial mineralization
(6) Intercostal mineralization
(7) Other soft tissue mineralization
Causes of renal failure/ Azotemia are categorized how?Prerenal, Intrarenal or Postrenal
What are the 2 kinds of renal failure?Acute & Chronic
Explain Prerenal renal failureReduced glomerular filtration &/or hypoxic injury due to impaired renal perfusion
What are the 2 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 rxns) or embolic dz leading to renal infarction (thrombosis, DIC, bacterial sepsis, tumor emboli)
Explain Intrarenal failureDmg to the renal tissue such as: Acute Tubular Necrosis, Glomerulonephritis, TubuloInterstitial Nephritis, or Pyelonephritis
What are the 2 clinical presentations of Acute Tubular Necrosis?Oliguria (Less pee), Anuria (No pee)
Tubular necrosis results in further renal injury by what 2 mechanisms?(1) Leakage of tubular ultrafiltrate into the renal interstitium (causes interstitial necrosis & inflammation)
(2) Intratubular obstruction resulting from sloughed necrotic epithelium (tubular casts)
What are some bacteria which might cause tubular necrosis?Lepto
E. coli

What are some viral infxns which might cause tubular necrosis?Canine Hepatitis Virus
Canine Distemper Virus
Canine Herpesvirus
What is a nephrotoxin?Substances that accumulate to a toxic concentration w/in 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 & raisins, lilies)
Vit D
Nephrotoxic drugs
What do excessive amounts of Vit D do? When does this happen?Leads to nephrotoxicity. USUALLY from oversupplementation. Can also lead to hypercalcemia (can become very severe very quickly) & calcinogenic plants (Cestrum, Solanum, etc.)
List some nephrotoxic drugs(Didnt seem to emphasize these but)
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 3 major causes for (acute) Intrarenal failureAcute Tubular Necrosis
Acute Glomerulonephritis
Acute Pyelonephritis
Acute Glomerulonephritis can be caused by?Immune Complex Glomerulonephritis
Bacterial or Viral infxn
Acute Pyelonephritis is caused by?Ascending bacterial infxn from the urethra, ureters & renal pelvis


Question Answer
Describe Postrenal renal failure. Aka?Urinary obstruction w/ pressure atrophy & necrosis. Aka obstructive nephropathy
What are the 3 main causes of postrenal renal failure?(1) Urolithiasis
(2) Tumors
(Transitional Cell Carcinoma)
(3) Iatrogenic (accidental ligation of ureter)
Obstructions can lead to what 2 conditions?Hydroureter & Hydronephrosis (& possibly organ rupture w/ resulting Uroabdomen)
When prolonged & progressive, CRF may lead to..?End stage kidney
*The term end-stage kidney is used to describe renal dz which is...?Chronic, advanced, generalized, progressive & irreversible
What is the parenchyma of an End stage kidney like?Fibrotic, atrophic, shrunken renal parenchyma w/ massive loss of fxnal nephrons & replacement w/ 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 & 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 Ca-P metabolism!!! ↓ GFR → HypERphosphatemia → Ca precipitation → Hypocalcemiastim of Parathyroid Hormone secretionCa mobilization by osteoclastic bone resorption → reduced bone mineral density (Osteopenia) known as Renal 2° Hyperparathyroidism & Chronic Hyperparathyroidism → Fibrous Osteodystrophy
How is Chronic Renal Failure related to bone abnormalities?Altered Ca-P metabolism!!! ↓ GFR → HypERphosphatemia → which leads to Ca precipitation → Hypocalcemiastimulation of Parathyroid Hormone secretionCa mobilization by osteoclastic bone resorption → ↓ bone mineral density (Osteopenia)Renal 2° Hyperparathyroidism
Chronic Hyperparathyroidism → Fibrous Osteodystrophy
*Renal 2° Hyperparathyroidism → Which ions does this affect & how? How does it affect the gland itself? What is the hormone & how is that affected? What condition can this lead to?~Leads to Hyperphosphatemia / Hypocalcemia & causes bilateral parathyroid gland hyperplasia & the PTH which is secreted causes osteoclastic bone resorption (need more Ca to balance out the P) & bc all the Ca is resorbed, the bone is replaced w/ fibrous tissue → Fibrous Osteodystrophy
What is the PCV like in Acute Renal Failure? Chronic?Acute = normal or ↑ (dehydration)
Chronic = ↓ (due to ↓ EPO induced non-regenerative anemia)
What is BUN / Creatinine like in Acute Renal Failure? Chronic?Acute = previously normal w/ progressive ↑
Chronic = previously ↑ w/ sustained elevation
What is Serum Potassium like in Acute Renal Failure? Chronic?Acute = +/- Hyperkalemia
Chronic = usually normal w/ 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 enlarged
Chronic = Often reduced
What is bone density like in Acute Renal Failure? Chronic?Acute = normal
Chronic = may be ↓ (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?Infxns (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 & Nephritis (bacteria may localize in the glomerulus or w/in 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 2 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 & 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 & 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 & causes permanent scarring w/ loss of tubules (since TBM provides a scaffold for re-epithelialization after tubular injury, if it is injured, major probs)
What are the 2 defense mechanisms of the renal intersitium?(1) Humoral antibodies may protect mucosal surfaces at the renal pelvis to defend against ascending infxn
(2) Macrophages, lymphocytes & plasma cells w/in the interstitium provide cell-mediated immune surveillance & modulation against invasive pathogens (i.e. Leptospira)
What are the 2 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 & *reduces thrombus formation*

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