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### 168 Cards in this Set

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 Provide the normal gas values (including pH). pH: 7.35-7.45 Drop the 7 pCO2: 35-45 Multiply 45 x 2 pO2>90 Divide 45 by 2 HCO3 = 22 (up to 28) What is the Henderson-Hasselbalch equation? pH=HCO3/pCO2 Acid-Base Disorder: pH 7.40 HCO3 23 pCO2 40 pH nl HCO3 nl pCO2 nl Normal ABG Acid-Base Disorder: pH 7.50 HCO3 35 pCO2 42 pH Basic (Alkalosis) HCO3 Elevated (Must be metabolic) pCO2 Normal (No compensation) Thus, it's a metabolic alkalosis without compensation. Acid-Base Disorder: pH 7.33 HCO3 13 pCO2 28 pH: Acidic HCO3: Low pCO2: Low--must be compensatory mechanism because don't have an alkalosis Metabolic acidosis with respiratory compensation. Acid-Base Disorder: pH 7.42 HCO3 32 pCO2 64 pH Normal HCO3 High--metabolic alkalosis pCO2 High--respiratory acidosis Mixed disorder; combined metabolic alkalosis and respiratory acidosis Acid-Base Disorder: pH 7.20 HCO3 18 pCO2 40 pH Low--Acidosis HCO3 Low pCO2 Low Metabolic acidosis without compensation. (normal pCO2 is 35-45) Acid-Base Disorder: pH 7.20 HCO3 24 pCO2 54 pH: Acidosis HCO3: Normal pCO2: Elevated Respiratory acidosis without compensation. Acid-Base Disorder: pH 7.52 HCO3 22 pCO2 22 pH: Alkalosis HCO3: Normal pCO2: Low Respiratory alkalosis without compensation. Acid-Base Disorder: pH 7.66 HCO3 36 pCO2 30 pH: Alkalosis HCO3: Elevated pCO2: Normal/Low Combined metabolic and respiratory alkalosis. Acid-Base Disorder: pH 7.47 HCO3 14 pCO2 22 pH Alkalosis HCO3 Low pCO2 Low Respiratory alkalosis with compensation. Acid-Base Disorder: pH 7.46 HCO3 35 pCO2 53 pH Alkalosis HCO3 Elevated pCO2 Elevated Metabolic alkalosis with compensation Acid-Base Disorder: pH 7.39 HCO3 12 pCO2 22 pH Normal HCO3 Low--Met acidosis pCO2 Low--Resp alkalosis Mixed: Metabolic acidosis and respiratory alkalosis Acid-Base Disorder: pH 7.34 HCO3 31 pCO2 62 pH Acidosis HCO3 Elevated pCO2 Elevated--acidosis Respiratory acidosis with compensation Acid-Base Disorder: pH 7.10 HCO3 15 pCO2 50 pH Acidosis HCO3 Low--acidosis pCO2 High--acidosis Combined metabolic and respiratory acidosis. Respiratory acidosis vs alkalosis: Causes Resp acidosis: Hypoventilation: -Airway obstruction -Lung dz -Opioids, narcotics, sedatives -Weakening of respiratory mm Resp alkalosis: -Hyperventilation (early high altitude exposure) -ASA ingestion (early) Metabolic acidosis vs alkalosis: Causes Met acidosis: CHECK ANION GAP (Na+ - (Cl + HCO3); nl range is 8-12 If normal gap****: Diarrhea Glue sniffing Renal tubular acidosis Hyperchloremia If anion gap: MUDPILES***** Methanol Uremia DKA Paraldehyde/Phenformin Iron tablets or INH Lactic acidosis Ethylene glycol Salicylates Met alkalosis: Diuretic use Vomiting Antacid use Hyperaldosteronism Rental tubular acidosis: Type I vs Type II vs Type IV Type I (distal)-Defect in CD's ability to excrete H+. Assocd w/hypokalemia and risk for Ca2+ kidney stones Type II: Proximal; defect in proximal tubule HCO3- reabsorption. Assocd w/hypokalemia and hypophophatemic rickets. Type IV: Hyperkalemia; hypoaldosteronism or lack of CD response to aldosterone; assocd w/hyperkalemia, inhibition of ammonium excretion in proximal tubule. Leads to acidic urine due to dec'd buffering capacity. How does acidosis/alkalosis affect extracellular K concentrations? Because of H+/K+ pump: Acidosis: increases extracell K+ Alkalosis: decreases extracell K+ A patient with recent kidney transplant on cyclosporin for immunosuppression requires an antifungal agent for candidiasis What drug would result in cyclosporin toxicity? Ketoconazole (interferes with cyp450) A patient presents with renal insufficiency What alterations need to be made in his doses of digoxin and digitoxin respectively? Digoxin is renally excreted, so decrease dose. Digitoxin not renally excreted, so don't have to change dose. What effect will a renal stone that obstructs the ureter have on GFR and FF? Dec GFR Dec FF What is the maximal serum glucose concentration at which glucose can be absorbed in the tubules? Will start to spill glucose around 200 mg/dL, but will saturate at 350 mg/dL What change in a basic metabolic panel might you expect in a young pt being treated for status asthmaticus? beta-agonists will shift K+ into cells-->hypokalemia MUD PILES Methanol Uremia DKA Paraldehyde or phenformin Iron tablets or INH Lactic acidosis Ethylene glycol Salicylates A patient taking lisinopril complains of new onset, constant coughing What medication class should this patient be switched to? Angiotensin receptor blocker (sartan) A patient with heart failure exacerbation needs medical diuresis but has a sulfa allergy What diuretic can be used? Loop & thiazide are both sulfa drugs, so use Ethacrynic acid A patient presents with hypertension, hypokalemia, metabolic alkalosis, and low plasma renin. What is the diagnosis, and how do you treat it? Primary hyperaldosteronism Treat w/spironolactone Type of diuretic: Triamterene K+ sparing Type of diuretic: Acetazolamide Carbonic anyhydrase inhibitor Type of diuretic: Hydrochlorothiazide Thiazide Type of diuretic: Bumetanide Loop Type of diuretic: Spironolactone K+ Sparine--aldost antag Type of diuretic: Chlorothiazide Thiazide Type of diuretic: Ethacrynic acid Loop, not a sulfa drug Type of diuretic: Mannitol Osmotic Type of diuretic: Metolazone Thiazide Type of diuretic: Chlorthalidone Thiazide Type of diuretic: Furosemide Loop Type of diuretic: Amiloride K+ sparing Type of diuretic: Torsemide Loop Appropriate diuretic: Acute pulmonary edema Heart failure-->LMNOP Loop Appropriate diuretic: Idiopathic hypercalciuria Thiazide to retain Ca2+ Appropriate diuretic: Glaucoma Acetazolamide, Mannitol Appropriate diuretic: Mild to moderate CHF with expanded ECV Mild: Thiazide Classically for HF: Loop Appropriate diuretic: In conjunction with loop or thiazide diuretics to retain K+ Any K+ sparing diuretic Appropriate diuretic: Edema a/w nephrotic syndrome Loop Appropriate diuretic: Increased intracranial pressure Mannitol Appropriate diuretic: Mild to moderate hypertension Thiazide--HCTZ Appropriate diuretic: Hypercalcemia Loop to lose Ca2+ Appropriate diuretic: Altitude sickness Acetazolamide Appropriate diuretic: Hyperaldosteronism Spironolactone or eplerenone What is the equation for the renal clearance of any substance? Renal clearance = UxV/Px A 40 year-old pt of yours weighs 100 kg. What is her estimated plasma volume? 20% x 100 kg x 1/4 L/kg = 5L What factors/substances cause hyperkalemia? What factors/substances cause hypokalemia? Hyperkalemia: K+ sparing diuretics ACE inhibitors Acidosis Insulin-deficiency Beta-agonists Hyperosmolarity Digitalis Cellular lysis Hypokalemia: Loop diuretics Thiazides Insulin Beta-agonists Alkalosis Hyposmolarity DKA Heart/Renal failure What are the actions of angiotensin II? Direct vasoconstricting effect Raises aldosterone levels-->Inc Na and H2O reabsorption in proximal tubule Dec'd renal blood flow, but inc'd GFR and FF What is the site of action of mannitol? What is the site of action of the thiazides? Mannitol: Woks at proximal convoluted tubule Thiazides: Early distal tubule What substances can be used to estimate GFR? What substances can be used to estimate renal plasma flow? GFR: Cr, Inulin RPF: PAH What do the presence of casts indicate? Hematuria/pyuria is of renal origin Proliferative vs Membranous Glomerular Disorders Proliferative: hypercercellular glomeruli Membranous: thickening of glomerular BM Nephritic Syndrome: Pathophys Presentation NephrItic = Inflammatory process. When involves glomeruli-->hematuria and RBC casts in urine a/w azotemia--elevated BUN/Cr, oliguria, HTN, proteinuria (<3.5 g/day) Azotemia vs Uremia Azotemia: elevated BUN/Cr Uremia: azotemia + systemic effect (pleuritis, pericarditis, EKG changes, etc.) Acute Poststreptococcal Glomerulonephritis: Pathophys LM/EM presentation Glomeruli enlarged, hypercellular, nphils, lumpy-bumpy appearance Subepithelial immune complex humps Frequently seen in children. Resolves spontaneously Rapidly progressive glomerulonephritis: Pathophys LM/EM presentation IF presentation LM--crescent-moon shape; crescents consist of fibrin and plasma proteins (e.g., C3b) w/glomerular fn parietal cells, monocytes, macs Severe causes: -Goodpasture Syndrome (type II hypersens); Abs to GBM and alveolar BM-->linear immunofluorescence -Wegener's granulomatosis (c-ANCA) -Microscopic polyangitis (p-ANCA) Diffuse proliferative glomerulonephritis: LM/EM presentation Pathophys Most common cause of death in SLE, Membranoproliferative GN EM: subendothelial DNA-anti-DNA IC's Berger's Disease: Pathophys Inc'd synthesis of IgA with IC's deposit in mesangium Often presents/flares with URI or acute gastroenteritis Alport's syndrome; Pathophys Presentation Mutation in type IV collagen-->split BM Can't see, can't pee, ca'n't hear (Nerve disorders, ocular disorders, deafness) What is nephrotic syndrome? NephrOtic syndrome presents with massive prOteinuria (>3.5g/day, frothy urine), edema, hyperlipidemia, fatty casts Membranous glomerulonephritis: Pathophys LM/EM presentation Diffuse capillary and GBM thickening Spike and dome appearance with subepithelial deposits (nephrotic syndrome) Caused by drugs, infections, SLE; most common adult cause of nephrotic syndrome Minimal change disease: Pathophys LM/EM presentation LM--normal glomeruli EM--foot process effacement May be triggered by recent infection or immune stimulus. Most common in children. Responds to steroids. Minimal change dz; normal glomeruli on LM but effacement of foot processes on EM (arrowhead). The full arrow points to a normal foot process. Treatment consists of steroids. Amyloidosis--congo red stain demonstrates amyloid deposits in artery wall that show apple-green birefringence under polarized light. Amyloidosis is associated with _______. Multiple myeloma, TB, RA Diabetic glomerulonephropaty: Pathophys Nonenzymatic glycosylation of GBM-->inc'd permeability, thickening Nonenzymatic glycosylation of efferent arterioles-->inc'd GFR-->mesangial expansion Diabetic glomerulosclerosis--nodular diabetic glomerulosclerosis (also known as Kimmelstiel-Wilson syndrome); characterized by acellular ovoid nodules in periphery of glomerulus. Membranoproliferative GN: Type I vs Type II-- EM appearance Causes Type I: tram-track appearance due to GBM splitting caused by mesangial ingrowth Most common cause; HBV, HCV, SLE (more association than cause) Type II: Dense dposits Associated with C3 nephritic factor What renal conditions are associated with hypocomplementemia? Post-strep GN Membranoproliferative GN (Type II) Lupus nephritis Which glomerular disease: Most common nephrotic syndrome in children · Minimal Change Dz Which glomerular disease: IF: granular pattern of immune complex deposition; LM: diffuse capillary thickening Membranous GN Which glomerular disease: IF: granular pattern of immune complex deposition; LM: hypercellular glomeruli Acute post-strep GN Which glomerular disease: IF: linear pattern of immune complex deposition Anti-GBM Abs with Goodpasture's Which glomerular disease: IF: deposition of lgG, lgM, lgA, and C3 in the mesangium IgA nephropathy Which glomerular disease: Kimmelstiei-Wilson lesions (nodular glomerulosclerosis) Diabetic glomerulonephropathy Which glomerular disease: Most common nephrotic syndrome in adults Membranous GN Which glomerular disease: EM: loss of epithelial foot processes Minimal Change Dz Which glomerular disease: Nephrotic syndrome associated with hepatitis B Membranoproliferative GN Which glomerular disease: Nephrotic syndrome associated with HIV Focal segmental glomerulosclerosis Which glomerular disease: Anti-GBM antibodies, hematuria, hemoptysis Goopasture's Which glomerular disease: EM: subendothelial humps and tram-tack appearance Membranoproliferative GN Which glomerular disease: Nephritis, deafness, cataracts Alport Syndrome Which glomerular disease: LM: crescent formation in the glomeruli Crescentic GN (aka Rapidly progressive GN) Which glomerular disease: LM: segmental sclerosis and hyalinosis Focal segmental GN Which glomerular disease: Purpura on back of arms and legs, abdominal pain, lgA nephropathy Henoch-Schloei Purpura Which glomerular disease: LM: wire-loop appearance SLE Which glomerular disease: Apple-green birefringence with Congo-red stain under polarized light Renal amyloidosis Which glomerular disease: EM: spiking of the GBM due to electron dense subepithelial deposits Membranous GN Under what circumstances would you see: RBC Cast Acute GN Under what circumstances would you see: WBC Cast Pyelonephritis, acute interstitial nephritis Under what circumstances would you see: Bacterial cast Acute pyelonephritis Under what circumstances would you see: Epithelial cell cast Renal tubular damage Under what circumstances would you see: Waxy cast Waxy = stasis of urine flow, so much be chronic renal failure Under what circumstances would you see: Fatty cast Nephrotic syndrome Under what circumstances would you see: Granular cast Non-specific, can be seen with acute tubular necrosis Glomerular histology reveals multiple mesangial nodules. This lesion is indicative of what disease? Diabetic glomerulonephropathy A teenager presents with nephrotic syndrome and hearing loss. What is the disease? Alport's Syndrome A 4 year-old boy presents with facial edema and proteinuria. What is the appropriate treatment? Steroids (this is Min Change Dz) What is the only radiolucent kidney stone? uric acid stones Calcium kidney stones: Frequency Causes 75-85% of all kidney stones Consists of calcium oxalate, calcium phosphate, or both. Caused by conditions that cause hyperCa2+ (cancer, hyperPTH) Oxalate crystals can result from ethylene glycol (antifreeze) or Vitamin C abuse Ammonium magnesium phosphate kidney stones: Frequency Causes 15% of kidney stones Caused by infection with urease-positive bugs (Proteus, Staph, Klebsiella) can form staghorn calculi that can be nidus for UTIs Uric acid kidney stones: Frequency Causes RADIOLUCENT 5% of stones Strong assocn w/gout; often seen in dz w/inc'd cell turnover such as leukemia Which kidney stones can be treated by alkalinization of urine? Which stone would be worsesned by alkaluria? Use alkaluria to tx Cystine stones (only 1% of renal stones) DO NOT use alkaluria to tx ammonium magnesium phosphate stones Calcium oxalate outlining a large right renal collecting duct system creating a "staghorn" calculus--can be calcium stone OR ammonoium magnesium phosphate (which present as STAGHORN) Calcium oxalate crystals in kidney, viewed with polarizers. Tubular failure in oxalate nephropathy can result from vitamin C or antifreeze abuse. Renal cell carcinoma: Histologic features Risk factors Presentation Site of Mets Associated disorders Polygonal clear cells in renal tubular cells Inc'd incidence w/smoking and obesity Manifests with hematuria, palpable mass, secondary polycythemia, flank pain, fever, weight loss Paraneoplastic syndromes (ectopic EPO, ACTH, PTHrP, prolactin) INvades IVC and spreads hematogenously; mets to lung and bone Assocd w/von Hippel-Lindau syndrome and gene deletion in chromosome 3 Wilms' Tumor: AKA Presentation Cause AKA nephroblastoma (Most common renal malignancy of early childhood) Contains embryonic glomerular structures Presents with huge, palpable flank mass, andn/or hematuria Deletion of tumor suppressor gene WT1; may be part of WAGR complex (Wilms tumor, Aniridia, GU malformn, MR) Renal cell carcinoma. Histology shows polygonal cells with small nuclei and abundant clear cytoplasm with a rich, delicate branching vasculature. Transitional cell carcioma: Presentation Risk Factors Most common tumor of urinary tract system, can occur in renal calyces, renal pelvis, ureters, bladder Painless hematuria suggests bladder cancer Risk factors in your Pee SAC: Phenacetin Smoking Aniline Dyes Cyclophosphamide Pyelonephritis: Acute vs Chronic-- Histologic features Presentation Acute pyelonephritis: -Affects cortex w/sparing of glomeruli/vessels Presents w/fever, CVA tenderness, nausea, vomiting WHITE CELL CASTS CLASSIC for this Chronic: Coarse, asymmetric corticomedullary scarring, blunted calyx Tubules can contain eosinophilic casts (thyroidization of kidney) Acute pyelonephritis characterized by nphilic infiltration and abscess formation within renal interstitium. Abscesses may rupture, introducing collections of white cells to tubular lumen. Chronic pyelonephritis with lymphocytic invasion and fibrosis. Acute Interstitial Nephritis: Cause Presentation Treatment Urinalysis finding Most common cause of acute renal failure; mostly drug-induced Cause: Drugs--NSAIDS, PCN/cephalosporins (methicillin), sulfonamides (TMP-SMX, foresmide), cipro, cimetidine, allopurinol Tx w/2 weeks steroids Presentation: fever, rash, ephilia, azotemia Muddy brown (granular) casts = key finding Acute Tubular Necrosis: Cause Presentation Cause: aminoglycosides, cephalosporins, polymixins Contrast dye Rhabdomyolysis/myoglobinuria from seizures, cocaine, crush injuries FIndings: 4+ blood in urine, no RBC on urine cell count (because it's myoglobin in urine), renal failure Renal Papillary Necrosis: Causes Pathophys Sloughing of papillae-->gross hematria, proteinuria May be triggered by recent infection or immune stimulus A/W: DM Acute pyelonephritis Chronic acetaminophen use Sickle cell anemia Acute renal failure: Definition Prerenal vs Intrinsic vs Postrenal-- Pathophys and Examples Acute renal failure--abrupt decline in renal fn w/inc'd Cr and BUN over several days 1) Prerenal azoetmia--due to dec'd RBF (HYPOTENSION, dehydration, hypovolemia, shock, renal vasoconstricion as with NSAIDs)-->dec'd GFR, Na/H2O and Urea retained by kidney to reserve volume so, BUN/Cr ratio increases Intrinsic renal: Acute tubular necrosis or ischemia/toxins; necrosis leads to debris obstructing tubule and fluid backflow across necrotic tubule; results in dec'd GFR. Urine has epithelial/granular casts. BUN reabsorption impaired-->dec'd BUN/Cr ratio Postrenal--outflow obstruction (stones, BPH, neoplasia, congenital anomalies); develops ONLY with BILATERAL obstruction Acute vs Chronic Renal Failure: Most common causes Acute: Acute tubular necrosis Chronic: HTN, DM What is uremia? Clinical syndrome marked by inc'd BUN and inc'd Cr Presents with nausea, anorexia Pericarditis Asterixis (hand-flapping tremor) Encephalopathy PLT dysfn UTI caused by Proteus vulgaris. Associated renal stone? Ammonium Magnesium Phosphtate Stone-->Staghorn calculi A patient reports a long-term history of acetaminophen use. What is she at increased risk of? Renal papillary necrosis--but NSAIDs can do this too! What artery prevents a horseshoe kidney from ascending in the abdomen? IMA CT Scan of ADPKD ADPKD: Pathophys Presentation At risk of? AD mutation in APKD1/2-->multiple, large, b/l cysts that ultimately destroy kidney parenchyma Presents w/flank pain, hematuria, HTN (inc'd renin production), urinary infection, progressive renal failure Risk of polycystic liver dz, berry aneurysms, mitral valve prolapse ARPKD: Presentation Infantile presentation of ADPKD in parenchyma. ASsocd w/hepatic fibrosis. Can lead ot Potter's if develop renal failure in utero. Central pontine myelinosis: Cause Rapid correction of hyponatremia How does EKG reflex K+ levels? Low K+ - Flat T waves High K+ - Peak T waves What is the WAGR complex? Wilms' Tumor Aniridia GU malformn Retardation (mental) Which glomerular disease: IF: granular pattern of immune complex deposition; LM: diffuse capillary thickening Membranous GN Which glomerular disease: IF: granular pattern of immune complex deposition; LM: hypercellular glomeruli Acute poststrep GN Which glomerular disease: IF: linear pattern of immune complex deposition Goodpasture's Which glomerular disease: IF: deposition of lgG, lgM, lgA, and C3 in the mesangium IgA neprhopathy Which glomerular disease: EM: subendothelial humps and tram-tack appearance Membranoproliferative GN Which glomerular disease: Nephritis, deafness, cataracts Alport Syndrome Which glomerular disease: LM: crescent formation in the glomeruli Crescentic/Rapidly Progressive GN Which glomerular disease: LM: segmental sclerosis and hyalinosis Focal segmental glomerulosclerosis Which glomerular disease: Purpura on back of arms and legs, abdominal pain, lgA nephropathy Henock Schonlein Purpura Which glomerular disease: EM: spiking of the GBM due to electron dense subepithelial deposits Memranous GN Diagnose: pH 7.50 HCO3 35 pCO2 42 Metabolic alkalosis w/o compensation Diagnose: pH 7.33 HCO3 13 pCO2 28 Metabolic acidosis w/compensation Diagnose: pH 7.20 HCO3 18 pCO2 40 Metabolic acidosis w/o compensation Diagnose: pH 7.66 HCO3 36 pCO2 30 Metabolic and respiratory alkalosis Diagnose: pH 7.47 HCO3 14 pCO2 22 Resp alkalosis w/compensation Diagnose: pH 7.10 HCO3 15 pCO2 50 Combined metabolic and respiratory acidosis Risk factors for transitional cell carcinoma? PSAC Smoking--- Phenacetin (acetaminophen) Smoking Aniline dyes Cyclophosphamide What are the causes of acidosis with an elevated anion gap? MUDPILES Methanol Uremia DKA Paraldehyde/phenformin Fe tables or INH Lactic acidosis EtOH or ethylene glycol Salicylates What changes will be seen in a basic metabolic panel in a patient with renal failure? High K+ High PO4 Low Ca2+ High BUN/Cr CT scan reveals massively enlarged kidney bilaterally. Diagnosis? ADPKD Which electrolyte disturbance: Correcting too rapidly may result in central pontine myelinosis Hyponatremia Which electrolyte disturbance: Peaked T waves Hyperkalemia Which electrolyte disturbance: Tetany Hypocalcemia Which electrolyte disturbance: Arrhythmias High/low K+ Low Mg2+ Which electrolyte disturbance: Decreased deep tendon reflexes Hypermg2+ Which electrolyte disturbance: Flattened T waves, U waves on EKG Low K+ Which renal pathology: Most common tumor of the urinary tract system Transitional cell ca Which renal pathology: Most common renal malignancy of early childhood (ages 2-4) Wilms' Tumor Which renal pathology: Histologic appearance of renal cell carcinoma Clear cell carcinoma Which renal pathology: Histological appearance of chronic pyelonephritis Thyroidization of kidney Which renal pathology: Fever + rash + hematuria + eosinophilia AIN Which renal pathology: Cancer associated with Schistosoma haematobium Squamous cell carcinoma of bladder Which renal pathology: Treatment for cystine kidney stones Alkalinization of urine