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104 Cards in this Set
- Front
- Back
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where does nitrogenous waste come from |
protein breakdown |
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what does ARF result in |
lack of acid-base maintenance. abnormal fluid and electrolyte management. loss of ability to excrete nitrogenous waste. Can also result in epo reduction leading to anemia. |
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ARF with BUN:cr ratio >20:1 come from what? |
prerenal source |
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BUN:Cr high without ARF could be ? |
GI bleed |
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prerenal causes of ARF? |
CHF, hemorrhage, dehydration. Cirrhosis, nephrosis and gastrosis. renal artery stenosis. (old man with atherosclerotic ds or young woman with fibromuscular dysplasia) |
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what to expect when you find these findings when the patient has ARF? anuria or frequent but small volume voids. suprpubic pain. palpably ir percussed distended bladder or enlarged prostate. High BUN:Cr US often localized the problem |
post renal causes |
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what common allergy medication can exacerbate BPH? |
diphenhydramine. |
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ARF post renal cause tx? |
bladder cath. saluresis and diuresis. (give tons of fluids then diuretics). Prompt tx often leads to complete reversal of injury. |
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50% of ARF comes from prerenal, renal or post renal? |
Renal |
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where do I send my patient when the patients has signs of ARF present for 1 to 2 weeks, but no acute uremia? |
nephrologist
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where do I send my patient when the patients has signs that have been present for 1 to 2 weeks and they have acute uremia? |
internal medicine |
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ARF with obstruction present. Where do I send the patient? |
urologist for surgery consult. |
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•Sudden loss of function with abnormalities that cannot be managed as an out patient safely. THere may or may not be a friction rub present. Where do I send the patient |
Admit to hospital |
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how can cirrhosis cause prerenal ARF |
The liver is not making albumin to create an oncotic pressure to keep the fluid in the plasma. |
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how can nephrosis cause prerenal ARF |
losing protein because you are peeing it out like in nephrotic syndrome. |
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how can gastritis cause prerenal ARF |
protein losing enteropathy or low protein diet that leads to poor oncotic pressure leading to water loss. |
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I want to raise my Creatinine from 1 to 2, how? |
shut down GFR by 50% |
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what 3 things can go wrong intrarenally in ARF |
glomerulonephritis. acute interstitial nephritis, acute tubular necrosis. |
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what will you see in the urine with glomerulonephritis? |
RBC's |
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what will you see in the urine with acute interstitial nephritis? |
eosinophils. WBC casts or WBC's. |
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what will you see in the urine with acute tubular necrosis? |
muddy brown casts |
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what causes ATN? |
IV contrast and rhabdomyolysis causing myoglobin to touch the tubules. Both myoglobin and IV contrast cause necrolysis to renal tubules. tx with fluid and diuresis to dilute and eliminate the offending agents. |
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what is the least common cause of ARF |
post-renal cause |
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what causes post-renal ARF? |
BU BU Bladder dysfunction/obstruction. Urethral obstruction. BPH in men. ureteral obstruction bilateral or unilateral if single kidney. |
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most common cause of ARF? |
pre-renal with 40 to 80% of cases |
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what are 3 things that cause pre-renal ARF? |
volume depletion. vascular resistance. Low cardiac output. |
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examples of vascular resistance that can cause pre-renal ARF? |
sepsis. anaphylaxis. afterload reducing meds like ACE I's and NSAID's. Renal artery stenosis. |
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causes of low cardiac output that leads to ARF? |
heart failure. PE. pericardial tamponade. ventilator effect from positive end pressure ventilation. |
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ARF immediate dx is critical. If you suspect decreased renal perfusion you should? |
test for volume status and urine output. |
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ARF immediate dx is critical. If you suspect glomerulonephritis you should? |
test urine sediment and serologic tests. |
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ARF immediate dx is critical. If you suspect urinary tract obstruction you should? |
get renal ultrasound. Remember the that before the obstruction everything will be dilated. |
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dx that. Etiology is poor renal perfusion. serum BUN:Cr is >20:1. Urinary sodium is <20. FE sodium (or FEna) is <1% Urine osmolality >500 Urinary sediment yields benign or hyaline casts. |
pre-renal azotemia |
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FENA |
fractional excretion of sodium |
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dx that. serum BUN:Cr is >20:1. Urinary sodium is variable. FE sodium (or FEna) is variable. Urine osmolality <400. Urinary sediment yields normal or red cells, white cells or crystals. |
post renal azotemia |
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dx that. Etiology is ischemia or nephrotoxins. Serum BUN:Cr is <20:1. Urinary sodium is >20. FE sodium (or FEna) is >1% (when oliguric) Urine osmolality is 250to 300. Urinary sediment yields granular muddy brown casts or renal tubular casts |
acute tubular necrosis |
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dx that. Etiology is immune complex related. Serum BUN:Cr is >20:1. Urinary sodium is <20. FE sodium (or FEna) is <1%. Urine osmolality is variable. Urinary sediment yields red cells, dysmorphic red cells and red cell casts. |
acute glomerulonephritis |
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dx that. Etiology is allergy, med rxn, infection, collagen vascular disease Serum BUN:Cr is <20:1. Urinary sodium is variable. FE sodium (or FEna) is variable. Urine osmolality is variable. Urinary sediment yields white cells, cell cell casts with or without eosinophils. |
acute interstitial nephritis |
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urinary sediment of benign or hyaline casts |
pre-renal azotemia |
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urinary sediment yields normal or red cells, white cells or crystals |
post renal azotemia |
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urinary sediment yields granular (muddy brown) casts and renal tubular casts. |
ATN |
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urinary sediment yields red cells, dysmorphic red cells and red cell casts |
acute glomerulonephritis |
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urinary sediment yields white cells, white cell casts with or without eosinophils. |
AIN |
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ARF staging |
stage1 = 1.5 x baseline creatinine with UO <0.5/mL/kg/hr for 6 to 12 hours. stage 2 = 2 to 3 x baseline creatinine with <0.5mL/kg/hour for >12 hours. Stage 3 = 3+ x baseline with <0.3mL/kg/hour for >24 hours or anuria for 12 hours. |
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RIFLE/AKIN criteria |
risk = 1.5 x increase in serum creatinine. injury = 2 to 3 times increase in serum creatinine. failure = <0.3mL/kg/hour for 24 hours or anuria for 12 hours. Any of the above with loss or ESRD risk |
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management of stage 1 ARF |
DC nephrotoxic agents. ensure volume status and perfusion pressure. consider functional hemodynamic monitoring. monitor serum creatinine and urine output. try to not use radiocontrast dyes when possible. |
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stage 2 ARF management. |
everything for stage 1 plus diagnostic workup. Change drug dosing. Consider ICU admission. |
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stage 3 ARF management? |
renal replacement like dialysis and kidney transplant. |
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how to prevent contrast induced ARF? |
prescreen patients for: hx of kidney disease, dehydration, DM (metformin needs stopped 48 hours prior), CHF/vascular disease (perfusion ability, gout hx, meds thats are nephrotoxic and recent IV contrast exposures. |
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broad waxy casts in the UA? |
chronic kidney disease. |
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how to reduce risk of contrast induced injury with non-pharmacological methods like? |
lowest contrast dose. Ensure patient hydrated. Decrease patient exposure to nephrotoxic meds pre and post contrast use. |
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how to reduce risk of contrast induced injury with pharmacological methods like? |
expand contrast volume with NS. oral n-acetylcysteine may be protective if given prior. (allergy occurs in 48% of people) Avoid diuretics. |
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ARF tx when life-threatening fluid, electrolyte or acid-base abnormalities exist? |
renal replacement |
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what are the goals with tx with dialysis |
maintain homeostasis. Prevent kidney injury. permit renal recovery. allow tx of underlying condition to proceed. |
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CKD definition? |
A gradual, progressive loss of the ability to excrete wastes, concentrate urine, and conserve electrolytes. |
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Chronic kidney failure definition |
the continuing irreversible reduction in nephron number (corresponds to CKD Stages 3-5) |
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stages of kidney failure by GFR |
0= >90 1= greater than or equal to 90 2= 60-89 3= 30-59 4= 15-29 5= <15 |
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Pre-renal causes of CKD |
hypoperfusion is the main problem. Renal artery stenosis. Extrinsic. Decreased oncotic pressure. Decreased renal perfusion pressure |
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example of decreased oncotic pressure causing pre-renal CKD |
cirrhosis and nephrotic syndrome. |
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example of extrinsic compression causing pre-renal CKD
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tumor and decreased oncotic pressure. |
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example of decreased renal perfusion pressure causing pre-renal CKD |
CHF |
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who gets fibromuscular dysplasia |
women less than 40. |
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what is the point of delineation from pre-renal to renal? |
glomerulus |
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intra-renal causes of CKD |
intrinsic renal vascular disease. Glomerular disease. Tubular and interstitial disease. |
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examples of intrinsic renal vascular disease leading to intra-renal CKD? |
glomerulosclerosis. recurrent thromboembolic disease. |
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examples of glomerular disease that leads to intra-renal CKD? |
nephritic and nephrotic syndromes. |
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tubular and interstitial diseases that lead to intr-renal CKD? |
nephrocalcinosis from hypercalcemia. SLE. PKD which is most commonly genetic. autoimmune. |
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post renal causes of CKD caused by what |
chronic obstruction likw BPH or neoplasm. |
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most common causes of CKD ? |
diabetic glomerular disease. HTN nephropathy. chronic glomerulitis. |
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what maladaptive mechanisms can occur leading to CKD? |
RAAS system activation from poor renal perfusion leading to HTN. Hyperfiltration of the remaining nephrons because they are doing the job of all the dead nephrons too. Release of vasoactive hormones, cytokines and growth factors. |
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how does potassium effect muscles |
when high it makes muscles weak |
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what are some effects of metabolic acidosis on bones, muscles and how proteins are handled? tx for metabolic acidosis? |
osteoporosis. protein catabolism. muscle wasting. hyperkalemia. daily bicarb for tx. |
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hematological effects of CKD and how to tx each? |
Anemia from low EPO. tx with recombinant EPO. Impaired platelet function from uremia. Dialysis |
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Trousseau's sign from what? |
hypocalemia. BP for several minutes on the arm and wait for it to hyperflex |
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Chvostek's sign for what? |
hypocalemia. smack em on the cheek muscle to elicit a maxillary muscular response. 29% specific. So it sucks. |
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what does phosphate retention lead to? |
hypocalcemia which leads to elevated PTH and more bone destruction but the phosphate is binding all the free calcium so it is a vicious cycle toward bone destruction. |
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browns tumor |
osteitis fibrosa cystica. |
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what causes hypocalemia |
malabsorption. vit D def. CKD. Loop diuretics. hypoparathyroidism. pancreatitis. septic shock. hyperphosphatemia. |
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causes of hypercalcemia |
pheochromocytoma. thyrotoxicosis. PTH producing tumor. lymphoma. thiazide diuretic use. lithium use. |
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chronic kidney disease management goals. |
slow and delay progression to stage 5. tx symptoms. avoid damage to other organ systems. limit disability, |
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primary prevention of CKD |
diet. exercise. avoidance of substance abuse. ID high risk patients |
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secondary prevention of CKD with DM patients? |
ACE I's. Screen everyone after initial dx 6 months with GFR and BUN. |
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CKD and DM patient with controlled type 2 with metformin comes in and has GFR of 59, now what? |
no more metformin. take DM patients off when lower than 60. |
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primary prevention is for what? Secondary prevention is for what? Tertiary prevention is for what? |
primary prevents ds with lifestyle. secondary is really focusing on DM which is stupid, because we are talking about CKD. Tertiary is focusing on sx control from CKD. |
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BP and lipid goals for delaying renal disease progression. |
<120 <80 LDL goal is 100. Aggressively tx triglycerides. |
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when should DM patients with CKD stop taking metformin??? |
when there GFR is less than 60 |
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what do adverse pathology can ACE I's cause in DM? |
renal artery stenosis. |
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what meds cause renal dysfunction |
IV contrast. NSAIDS. Aminoglycosides |
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when to start dialysis |
stage 4 and 5 |
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5 year ESRD survival rate? with renal disease and DM? |
35% DM and CKD is 25%. |
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most common cause of death in CKD patients is ? |
cardiovascular disease |
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average amount of hospitalizations by dialysis patients is? for renal transplant patients? |
2 admits/year for dialysis. 1 admit/year for transplant. |
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most common complication with hemodialysis |
hypotension. there is also muscle cramping and Anaphylactoid reactions can occur |
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what is peritoneal dialysis |
infusion of dextrose solution into peritoneum and then sits there for a little while, then suck it out. Access with peritoneal catheter. |
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complications with peritoneal dialysis |
peritonitis. metabolic complications. |
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how does hemodialysis work? |
moves solutes across a semipermeable membrane by diffusive clearance, ultrafiltration and solvent drag. |
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what is the most prefered hemodialysis access? what is least preferred? A. AV fistula. B.AV graft. C. Venous catheter D. Peritoneal access catheter. |
most preferred =AV fistula. Least preferred = venous catheter. |
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when to start planning for kidney transplant? |
when the patient start dialysis. |
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most common opportunistic infections in renal transplant? peritransplant <1 month |
peritransplant <1 month= wound infection. Herpes. Oral candidiasis. UTI
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most common opportunistic infections in renal transplant in early phase (1 to 6 months)? |
early (1 to 6 months) •Pneumocystis Carinii •Cytomegalovirus •Legionella •Listeria •Hepatitis B •Hepatitis C |
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most common opportunistic infections in renal transplant in late phase ( >6 months)? |
•Aspergillus •Nocardia •BK virus (polyoma) •Herpes zoster •Hepatitis B Hepatitis C |
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post renal transplant complication? |
cancer in 6 to 8%. Hypercalcemia. Hypertension. Hepatitis. (from immunosuppressive therapy) |
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survival rate of recipients and donors with renal transplants? 1, 5 and 10 year follow up. |
recipient 1 year = 95%. recipient 5 years = 81% recipient 10 years = 61% Donor 1year = 98% Donor 5 years = 90% Donor 10 years = 76% |
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when are you most likely to die post renal transplant? |
in the 1st year. |
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when should DM patients stop taking ACE I's in CKD? |
stage 4 and 5 |
