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Renal

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Answer
Estimated Renal Plasma Flow   = [urine PAH] x Flow rate = PAH clearance (Underestimates RPF by 10%)  
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Renal Blood Flow   = Renal Plasma Flow / (1-Hct)  
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Filtration Fraction   = GFR / RPF  
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Filtered Load   = GFR x plasma concentration  
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Angiotensin II   Vasoconstriction (but not the afferent arteriole), Pressure Natriuresis (PCT Na absorption), Aldosterone & ADH release, thirst. Antagonized by ANP. Synthesized in liver.  
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Glucosuria   Begins at 200mg/mL. Transport saturated @ 350mg/dL  
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Proximal Convoluted Tubule   All Glucose, Protein, MOST Bicarb, Na, H20. Iso-osmotic  
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Thin Descending Loop of Henle   Passive H20 absorption & urea excretion -> urine hypertonic  
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Thick ascending Loop of Henle   NKCC pump (Where furosemide acts) actively reabsorbs salts, indirectly absorbs Mg & Ca. Impermeable to urea, H20 -> urine hypotonic  
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Distal Convoluted Tubule   Na/Cl co-transporter (where Thiazides act). ENaC sodium reabsorption. PTH-mediated Ca reabsorption. Impermeable to urea (maintains at least some osmolarity to the hypotonic urine).  
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Collecting Tubules   Aldosterone-mediated Na reabsorption for K. ADH mediated H20 & little urea reabsorption  
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PTH in the Kidney   Increases PTC calcium absorption, decreases DCT PO4 absorption. Alpha1 hydroxylase expression to produce 1,25 (OH)2 Vitamin D.  
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Anion Gap Metabolic Acidosis Etiology   PCO2<40. MUDPILES: Methanol, Uremia, DKA, Paraldehyde, Phenformin, Iron, INH, Lactic acidosis, Ethylene glycol, Salicylates  
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Non Anion Gap Metabolic Acidosis Etiology (8-12)   PCO2<40. Diarrhea, Glue Sniffing, hyperchloremia, Renal tubular acidosis (Type 1: H pump defect, Type 2: renal bicarb loss, Type 4: Hyperaldo-> HyperK -> No ammonia excretion)  
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Respiratory Acidosis Etiology   Hypoventilation (primary lung problem). PCO2 > 40  
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Respiratory Alkalosis Etiology   PCO2<40. Early aspirin ingestion, Hyperventilation.  
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Metabolic Alkalosis Etiology   PCO2>40. Diuretics, Vomiting, antacids, Hyperaldosteronism.  
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Metabolic Acidosis Formula   1.5(HCO3) + (6 to 10) = PCO2 (WINTER’S FORMULA)  
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Metabolic Alkalosis Formula   .7(HCO3 increase above 40) = PCO2 increase  
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Respiratory Alkalosis Formula   Acute: .2(PCO2 decrease) = HCO3 drop CHRONIC: .5(PCO2 decrease)= HCO3 drop  
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Respiratory Acidosis Formula   Acute: .1(PCO2 elevation) = HCO3 increase Chronic: .35(PCO2 Elevation) = HCO3 increase  
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Nephritic Syndromes   Type III Hypersensitivities (-Godpastures). Sx: Hematuria, HTN, Oliguria, Azotemia. Acute Post-Strep Glomerulonephritis, Membranoproliferative G., Rapidly Progressive/Crescentic G., Goodpasture’s, Berger’s/IgA Nephropathy, Alport’s.  
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Enlarged/hypercellular glomeruli, neutrophilic infiltrate. EM: Supepithelial humps. IF: Granular   Acute Post-streptococcal Glomerulonephritis. Pediatric. Peripheral/periorbital edema. Self-resolves  
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Subendothelial Humps, Tram tracking (Mesangial cell consume Dense deposits & lay down new BM   Membranoproliferative Glomerulonephritis. Slowly progressive to renal failure.  
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Crescent-Moon Shape LM & IF   Rapidly progressive glomerulonephritis. Rapidly progresses to renal failure.  
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Linear IF. IgA mesangial deposits   Berger’s Disease/ IgA Nephropathy. Mild, Post-infx. Recurrent hematuria.  
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Linear Immunofluorescence, Anti-GBM antibodies   Goodpasture’s Syndrome (Type II hypersensitivity). Hemoptysis, hematuria.  
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Split basement membrane   Alport’s Syndrome. Collagen Type IV mutation. Deafness, ocular disorders.  
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Nephrotic Syndromes   Proteinuria. Frothy urine, hypoalbuminemia, peripheral & Periorbital edema, hyperlipidemia. Membranous Glomerulonephritis, Minimal Change Disease, Focal Segmental Glomerular Sclerosis (FSGS), Diabetic Nephropathy, SLE, Amyloidosis.  
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Diffuse capillary & BM thickening, granular immunofluorescence, spike & dome EM   Membranous Glomerulonephritis. #1 in adults  
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Normal glomeruli & foot process effacement   Minimal Change Disease #1 Pediatric. Tx: steroids  
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Segmental sclerosis & hyalinosis   Focal Segmental Glomerular Sclerosis. HIV  
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K-W Nodules, BM thickening   Diabetic Nephropathy  
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Diffuse capillary & BM thickening. Wire-loop leisions w/ subepithelial deposits   SLE Nephropathy. 5 patterns.  
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Amyloid Deposits (Congo red +, Apple green)   Amyloidosis: MM, TB, RA, chronic conditions.  
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Renal Cell Carcinoma   Polycythemia, palpable mass, hematuria, flank pain. Associated w/ VHL (ch3), Smoking, obesity, 50-70yos. Paraneoplastic: EPO, ACTH, PTHrP, Prolactin  
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Wilm’s Tumor   #1 Pediatric. Embryonic structures. WT1 deletion (Ch11). May be part of WAGR: Wilms, Anirida (no iris), GU malformation, MR  
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Transitional Cell Carcinoma   #1 of Urinary tract. Painless hematuria. Associated w/Phenacetin, Smoking, Aniline dyes, Cyclophosphamide.  
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Pyelonephritis   WBC casts pathognomonic. Affects cortex. Fever, CVA tenderness. Corticomedullary scaring, blunted calyx.  
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Diffuse Cortical Necrosis   Abruptio Placentae, Septic shock -> DIC & Vasospasm -> Bilateral renal cortex infarction  
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Drug-Induced interstitial Nephritis   Penicillins, NSAIDs, Diuretic-Hypersensitivity -> Interstitial Inflammation -> Systemic signs + Hematuria 2wks post-administration  
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Acute Tubular Necrosis   #1 ARF. Ischemia/shock, Trauma, Toxins -> epithelial detachment, necrosis -> muddy brown casts. Death in early oliguric phase, recovery in 2-3 wks.  
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Renal Papillary Necrosis   DM, Acute Pyelonephritis, Chronic Phenacetin use(ie-tylenol), Sickle Cell Anemia -> Hypoxic injury to medulla-> necrosis.  
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PRERENAL Acute Renal Failure   High Osmolarity (>500), BUN/Cr Ratio (>20), low Na (10)& FeNa (1%) (Hypotension -> low RBF)  
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INTRINSIC Acute Renal Failure   Low Osmolarity (<350), Moderate Na (20)& FeNa (2%), Low BUN/Cr (ATN, Ischemia, Toxins) Epithelial & Muddy Brown Casts.  
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POSTRENAL Acute Renal Failure   Low Osmolarity (<350), high Na(40), FeNa (4%), Moderate BUN/Cr (>15). BPH, Stones, Neoplasia.  
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Chronic Renal Failure   HTN, Diabetes Induced  
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Renal Failure Consequences   Uremia & uremic encephalopathy. Anemia (no EPO), Renal Osteodystrophy (no VD), Hyperkalemia, Metabolic Acidosis (no excretion w/ typical high-acid diet), Na & H20 Excess (CHF & PE), Chronic Pyelonephritis, HTN  
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Fanconi’s Syndrome   Proximal Tubule LOF -> No resorption of AAs, Glucose, PO4, Uric Acid, electrolytes. Consequences: Rickets, Osteomalacia, Hypokalemia, metabolic acidosis.  
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Dialysis Cysts   Cortex & medulla. Due to Chronic Dialysis  
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Simple Cysts   Cortex. Benign.  
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Medullary Cystic Disease   Medullary. Small kidney. Poor prognosis  
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Medullary Sponge Disease   Collecting ducts. Good prognosis.  
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Hyper & Hyponatremia Sx   HypoNa: Disoriented, stuporous, coma. HyperNa: Irritable, Delirious, coma  
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High & Low Cl Etiologies   Low Cl: Metabolic alkalosis, HypoK, Hypovolemia, High aldo. HIGH Cl: Non-Anion Gap Acidosis  
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Hyper & HypoKalmeia Sx   HypoK: U waves, flat T waves, Arrhythmias, paralysis. HyperK; Peaked T waves, wide QRS, arrhythmias  
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Hyper & HypoCalcemia Sx   HypoCa: Tetany, Neuromuscular irritability. HyperCa: Delirium, Renal Stones, Abdominal pain, +/-Calcuria  
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Hyper & HypoMagnesmia Sx   HypoMg: Neuromuscular irritability, arrhythmias. HyperMg: Delirium, weak DTRs, cardiac arrest  
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Hyper & HypoPhosphatemia Sx   HypoPO4: Bone loss, osteomalacia HyperPO4: Metastatic calcification, renal stones  
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Mannitol   Mech: Osmotic diuresis. USE: Shock, drug OD, reduce ICP, IOccularP. SE: PE, dehydration, CI’d in anuria, CHF  
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Acetazolamide   Mech: Carbonic anhydrase inhibitor, excreting HCO3. USE: Glaucoma, alkalinize urine, metabolic alkalosis, altitude sickness. SE: HyperCl metabolic acidosis, neuropathy, NH3 toxicity, Sulfa allergy  
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Furosemide & Ethacrynic Acid   Mech: NKCC blocker, preventing urine concentration. USE: Edematous states, HTN, HyperCa. SE: Ototoxicity, HypoK, sulfa allergy, interstitial nephritis, gout.  
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HCTZ   Mech: NaCl blocker in DCT. USE: HTN, CHF, HyperCa tx, Nephrogenic DI. SE: HypoK Metabolic Alkalosis, hypoNa; HyperGLUC: Glycemia, Lipidemia, Uricemia, Calcemia. Sulfa allergy  
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Spironolactone   Spironolactone, Triamterene, Amiloride. Mech: Spiro: Aldosterone Receptor Blocker; Triam & Amil: CCT ENaC Blockers. Use: Hyperaldosteronism, HypoKalemia tx, CHF. SE: HyperK. Spironolactone: Gynecomastia, antiandrogenic.  
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ACE Inhibitors   Capto, Elana,Lisino-pril. Use: HTN, CHF, Diabetic renal disease. SE: CAPTOPRIL: Cough, Angioedema, Proteinuria, Taste change, hypotension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Low angII + HyperK. CI’d in Renal Artery Stenosis  
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Losartan   Angiotensin II Receptor Antagonist. Use: Same as ACE Inhibitors when patient has bradykinin-induced cough.  
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Henderson Hasselbach Equation   pH= pKa + log [HCO3]/.03PCO2 Describes acid-base response  
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Cause of Hyperkalemia & Hypokalemia   HyperK: Low insulin, aldosterone, sympathetic tone, acidosis, digitalis, hyperosmolarity. HypoK: High insulin, aldosterone or sympathetic tone, alkalosis, hypoosmolarity.  
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Anion gap   Na - (Cl + HCO3)= anion gap  
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