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