Day 1 Nephrology Flashcards
What are the 3 functions of the kidney?
What is the excretion formula and is normal?
What do kidneys make in their endocrine function?
Excretion(Early kidney disease/ acute)(Filtration, secretion, absoprtion), Endocrine(late chronic kidney disease), metabolic(late chronic kidney disease).
Filtration+secretion-absorption=excretion. 0.5-1 mL/ kg/ hr or 1-2 L/day
Renin to result in formation of angiotensin 2. Produces erythropoeitin which promotes formation of red blood cells in bone marrow.
What are kidneys metabolic function?
What happens during passive diffusion?
What happens in the proximal tubule?
Gluconeogensis, production of prostaglandins, activation of vitamin D.
Afferent arteriole to proximal tubule, small non protein plasma constituents are filtered, macromolecules can not be filtered, 100% of inulin is filtered, inulin can be used to calculate GFR.
Absorbs 60% of NaCl and H2O via Na and K ATP ase. NA out of the cells and k into the cells. Reabsorbs 90% of filtered HCO3, saturable, carbonic anhydrase inhibitors block tubular reabsorption of HCO3 which helps with alkalosis. Reabsorbs 100% of glucose and amino acids and K, Ca, Mg, and Urea.
What happens in the loop of henle? Difference between descending and ascending loop of henle?
What happens at distal convoluted tubule?
What happens at collecting duct?
reabsorbs Ca, Mg, 15-25% of filtered NaCl. Descending is highly H2O permeable and solute impermeable, Ascending is H2O impermeable and solute permeable.
Reabsorbs calcium, NaCl(5% of filtered), and magnesium, site of action for diuretics via Na/Cl co-transporter.
Reabsorbs 5% of Na, aldosterone mediated, site of action for amiloride and triamterene. Secretion of potassium. Reabsorbs H20. Acid base secretion(Acidemia- type A cells secrete hydrogen and reabsorb HCO3. Alkalemia- type B cells secrete HCO3 and reabsorb H).
Where do carbonic anhydrase inhibitors work? MOA? What is one?
What are some loop diuretics? Do they help with blood pressure? Where do Loop diuretics work and MOA?
What are some thiazide diuretics? Where and how do they work?
Work in proximal tubule, inhibit secretion of H+, resulting in less reabsoprtion of HCO3 and Na. Acetazolamide.
Furosemide, bumetanide, torsemide, ethacrynic acid(for sulfa allergy. NO, they affect water balance, concentrates sodium in ascending loop and then water shoots in in distal convoluted, Work in ascending loop of henle.
HCTZ, Chlorthalidone. MOA: Inhibit Na/Cl co-transporter in the luminal membrane, works in distal convoluted tubule. Helps with blood pressure.
What are some potassium sparing diuretics? Where and how do they work?
Who identifies guidelines for kidney disease?
What is normal GFR?
Spironolactone, eplerenone. Inhibit action of aldosterone or blocks Na channels. Works in Distal DISTAL convoluted tubule/collecting duct.
NKF KDOQI is CKD.
127 for males, 118 for females, plus or minus 20 for both.
What to know about accuracy and clinical utility of kidney function tests?
What is the cockcroft gault equation?
What can increase creatinine clearance? Decrease?
Serum creatinine most used(endogenous), inulin should be used but too expensive.
((140-age) x IBW)/ (72-sCr)) if female times by .85.
High stress patients, cystic fibrosis, younger age. Renal dysfunction, hepatic dysfuntion, decrease cardiac output/perfusion, older age.
When is CrCl unreliable?
Symptoms of renal dysfunction?
What markers change in AKI?
Advanced renal disease the worse it gets the more unreliable it is.
Fatigue, Malaise, pruitis, nausea.
SCr, BUN, Urine output
3 Etiology categories of AKI?
What causes prerenal AKI?
Hints someone is volume depleted? Treatment?
Prerenal(blood flow to glomerulus), Intrinsic(formation and processing of the filtrate by the golmerulus and tubular cells), Postrenal(urine excretion through the ureters, bladder, and uretha).
Volume Depletion(Hemmorhage, GI losses, burns, dehydration, diuretics), decreased effective circulatory blood volume(decreased cardiac output, sepsis, liver failure), functional(NSAIDS, ARBS, ACEIS, ETC).
concentrated Hbg/Hct, Complain of GI symptoms(diarrhea, vomiting, excessive sweating without replenishment, BUN:SCr, poor skin turgor, sunken eyes, dry mucous membranes, AMS. Treatment is fluids.
Hints someone is decreased effective circulating volume? Treatment?
What causes intrinsic AKI?
What to know about Acute Tubular Necrosis(ATN)?
What to know about AIN?
History of heart failure, edema, dyspnea, crackles, diluted Hbg/Hct, ascites, JVD. Loop diuretics.
Results from direct kidney injury. Can be Renal vasculature, glomeruli, ATN(tubules), Interstitum(AIN).
Most common cause of intrinsic AKI(85%), 50% of these arise from renal ischemia secondary to a prolonged prerenal state(tubules have high oxygen demand), other causes are direct tubular toxins.
White blood cells in urine, hypersensitive reaction in which the renal interstitum becomes severely inflamed. Caused by medications, infections, and autoimmune disorders.
What causes postrenal AKI?
Staging AKI?
Staging with AKIN and KDIGO?
Accounts for <5% of AKI. Due to an obstruction anywhere within the urinary collection system. Obstructions above the bladder typically need to involve both kidney to cause an AKI because the other kidney can compensate. causes are prostate, urinary catheter, nephrolithiasis(kidney stone), physical compression.
RIFLE(Risk, injury, failure, loss of kidney function, end-stage renal disease).
Stage 1, 2, and 3.
Risk staging criteria in rifle?
Injury staging criteria in rifle?
Failure staging criteria in rifle?
increase SCr 1.5-1.99 fold or <0.5 ml/kg/h >6 hours
increase SCr 2-2.99 or <0.5 ml/kg/ h > 12 hours
increase SCR 3 fold or SCr> 4mg/dL with an acute raise of at least 0.5 mg/dL. Anuria for > 12 hours.
Loss of kidney function is defined as? End-stage renal disease?
AKIN difference from RIFLE?
Clinical presentation of AKI?
Complete loss of function for 1-3 months(dialysis). Renal replacement therapy > 3 months.
Same as RIFLE except if you EVER need renal replacement therapy it’s stage 3.
Decreased urine output, urine discoloration, weight gain, severe abdominal or flank pain.
What is the FeNa cut off for prerenal?
FeNa equation?
Lab test references for prerenal?
<1.
(Una x SCr x 100)/ (Ucr x Sna)
High specific gravity, normal urine sediment or hyaline cast, no RBC’s or WBC’s, <20 sodium, <1% FeNa, BUN:SCr >20.
Lab test references for intrinsic?
Other tests for AKI?
How to treat AKI?
Granular casts or cellular debris, 2-4 WBC’s and RBC’s, >40 urine sodium, >2% FeNa, <20 BUN:SCr, Low urine specific gravity.
KUB X-ray, CT, Ultrasonography, renal biopsy rarely done.
Identify and remove underlying cause if possible, supportive care(hydration, electrolyte management), Loop diuretics(only for volume overload and producing urine still), watch for diuretic resistance. Renal replacement therapy A(Acid base)E(electrolytes)I(intoxications)O(overload)U(uremia).
Pharmacokinetics of kidney failure?
digoxin in kidney failure?
Phenytoin in kidney failure?
Absorption(no change),Distribution(increased for most drugs except digoxin), Metabolism( accumulation of metabolites like allopurinol, meperidine, morphine), Elimination(decreased clearance, increased t 1/2).
Toxic effects are GI upset, blurred vision or yellow halos, weakness, dizziness, confusion, stays in body for longggg time.
nystagmus, ataxia, slurred speech, incordination, mental status changed are toxic effects. Decreased protein binding in renal failure.
Gold standard for kidney stone detection?
Kidney stone treatment?
helical CT scan without contrast
Aggressive oral rehydration, restriction of animal proteins and sodium, oral a1 adrenergic blockers, thiazide diuretics, alkalinizing agents, allopurinol. Shock wave lithrotrispy is preferred for large kidney stones(>5mm). Don’t use in uncontrolled hypertension, untreated bleeding disorders, pregnancy, urological anatomical anomolies, UTI.
