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Nephrology
| Question | Answer |
|---|---|
| in acidosis is serum K increased or decreased | increased |
| how to determine if compensation is appropriate in the setting of metabolic acidosis | 1.5HCO3 +8 +/- 2 should = pCO2 |
| GI etiologies of normal anion gap metabolic acidosis | diarrhea, ileostomy |
| does giving bicarb IV in metabolic acidosis when pH<7 help mortality? | NO |
| when is metabolic alkalosis usually seen | cases of volume contraction |
| what are the chloride responsive types of metabolic alkalosis | They have urine chloride <15 mEq/L. Caused by vomiting or prolonged NG tube drainage, pyloric stenosis, laxative abuse, diuretics, and post-hypercapneic states |
| what are the chloride resistant types of metabolic alkalosis | they have urine chloride >15. Severe Mg or K deficiency, diuretics, increased mineralocorticoids (inc Cushings, primary aldosteronism, and renal artery stenosis), licorice, chewing tobacco, and inherited disorders like Bartter's syndrome |
| symptoms of metabolic alkalosis | irritability, neuromuscular hyperexcitability, concomitant signs of hypokalemia (weakness, cramping, ileus) |
| tx of metabolic alkalosis | no tx necessary if mild; hydrate if cause is volume contraction. In severe hypokalemia and hypermineralocorticoid states, the problem is chloride resistant and cannot be corrected until potassium is replaced. |
| 2 important rule for ABGs | 1) there can only be 3 acid base disorders at the same time. 2) the body can never overcompensate for the primary acid base disorder |
| acute compensation for respiratory acidosis | HCO3 goes up by 1 and pH drops by .08 for every 10 rise in CO2 |
| chronic compensation for respiratory acidosis | HCO3 goes up by 3 and pH drops by 0.04 for every 10 rise in CO2 |
| acute compensation for respiratory alkalosis | HCO3 goes down by 2 for every 10 drop in CO2 |
| chronic compensation for respiratory alkalosis | HCO3 goes down by 4 for every 10 drop in CO2 |
| what's a quick way to determine what the CO2 should be in metabolic acidosis | look at last 2 digits of pH (if pH is 7.28, the CO2 should be 28, etc) |
| compensation for metabolic alkalosis | CO2 goes up by 0.06 for every 1 increase in HCO3 |
| major ICF cations | K and MG |
| major ICF anions | proteins, organic phosphates (ATP, ADP, AMP) |
| major ECF cation | Na |
| major ECF anions | Cl and HCO3 |
| do diarrhea and normal saline hydration change serum osmolarity | no |
| how to use urine Na to distinguish between renal and extrarenal causes of hypovolemic hyponatremia | If urine Na>20, then it's a renal cause. If urine Na <20, it's an extrarenal cause |
| causes of euvolemic hypotonic hyponatremia | water intoxication (primary polydipsia), SIADH |
| causes of hypovolemic hypotonic hyponatremia | loss of both Na and H20 due to renal losses (diuretics, partial urinary tract obstruction, salt wasting nephropathies) or extrarenal losses (vomiting, diarrhea, burns, third spacing due to pancreatitis or peritonitis) |
| causes of hypervolemic hyponatremia | CHF, nephrotic syndrome, cirrhosis |
| symtoms of moderate or gradual onset hyponatremia | confusion, muscle cramps, lethargy, anorexia, nausea |
| symptoms of severe or rapid onset hyponatremia | seizures or coma |
| when to suspect pseudohyponatremia | when measured and calculated serum osmolarities are different. Often seen in multiple myeloma of hyperlipidemia |
| treatment of hyponatremia | serum sodium should be corrected 1/2way to lower range of normal within 24 h. NEVER correct faster than 1 mEq/h. If hypovolemic, usually just need NS not hypertonic saline. For hypervolemia, water and Na restriction. In CHF, captopril + furosemide. |
| most common cause of hypernatremia | Hypovolemic causes due to loss of water and sodium. Renal losses (diuretics, glycosuria), GI, respiratory, or skin losses; adrenal problems |
| isovolemic hypernatremia causes | In this there is decreased TBW and decreased ECF but normal total body sodium. DI, skin losses (sweating), iatrogenic causes, and reset osmostat |
| hypervolemic hypernatremia | increased TBW, markedly increased total sodium, and increased ECF. Due to: iatrogenic (hypertonic infusion), mineralocorticoid excess (Cushing's), excess salt ingestion |
| tx of hypovolemic hypernatremia | fluid replacement with normal saline. correct plasma osmolarity no faster than 2 mOsm/kg/hr |
| how to correct isovolemic hypernatremia | fluid replacement with 1/2 normal saline. Correct only half the estimated water deficit in the first 24h. Do not correct Na faster than 1 mEq/L/hr in acute hypernatremia and 0.5 mEq/L/hr in chronic hypernatreia. in central DI can give vasopressin |
| how to correct hypervolemic hypernatremia | give 1/2 normal saline and furosemide |
| how does alkalosis change serum K | each 0.1 increase in pH decreases serum K by 0.4-0.6 |
| periodic paralysis: hypokalemic vs hyperkalemic | hypokalemic periodic paralysis first presents in teens and hyperkalemic periodic paralysis occurs in infancy |
| what causes cellular shifts which cause hypokalemia | alkalosis, insulin (drives K into cells), |
| what RTAs cause hypokalaemia | RTA 1 (distal) and RTA 2 (proximal) |
| what is Bartter's syndrome | JG cell hyperplasia causing increased renin/aldosterone, metabolic alkalosis, hypokalemia, muscle weakness, and tetany. Seen in young adults |
| symptoms of hypokalaemia | impaired GI motility, N&V, mild muscle weakness to overt paralysis, rhabdomyolysis, and atrial and ventricular dysrhythmias |
| tx of hypokalaemia | replace K PO or IV. IV replacement no faster than 20 mEq/hr. 20 mEq infusion of K raises serum K by 0.25 |
| what causes K to shift out of cells, causing hyperkalemia | acidosis, heavy exercise, insulin deficiency, and digitalis toxicity |
| symptoms of hyperkalemia | N&V, diarrhea, muscle cramps, weakness, paresthesias, paralysis, areflexia, tetany, focal neurologic deficits, confusion, respiratory insufficiency, arrhythmias, cardiac arrest |
| treatments for hyperkalemia mnemonic | Controlling K Immediately Diverts Bad Arrythmias: Calcium, Kayexalate, Insulin and glucose, Dialysis, Bicarb, Albuterol |
| ECG changes in hyperkalemia | 6.5-7.5: tall peaked T waves, short QT, long PR. 7.5-8: QRS widening, flattened P wave. 10-12: QRS may degrade into sine wave pattern. V-fib, complete heart block, or asystole may occur. |
| what treatment for hyperkalemia is contraindicated in pts on digoxin | cardiac membrane stabilization with calcium |
| what drugs/toxins cause hypocalcemia | fluoride, cimetidine, ethanol, citrate, phenytoin |
| how do rhabdomyolysis and tumor lysis syndrome cause hypocalcemia | increased serum phosphate |
| what does severe magnesium deficiency due to serum Ca | causes hypocalcemia |
| how to correct serum Ca levels for hypoalbuminemia | adjust measured Ca up by 0.8 for each 1 of albumin below normal |
| ECG findings in hypocalcemia | prolonged QT and ST intervals; peaked T waves also possible |
| causes of hypercalcemia mnemonic | CHIMPANZEES: Ca supplementation, hyperparathyroid/hyperthyroid, Immobility/Iatrogenic, Mets/milk alkali, Paget's disease, Addisons/Acromegaly, Neoplasm, ZE syndrome, Excessive vitamin A, excess vit D, sarcoid |
| drugs that may cause hypercalcemia | antacids, excess vit D, thiazides, lithium |
| why do granulomatous diseases cause hypercalcemia | vit D is produces by macrophages in granulomatous tissue |
| tx of acute hypercalcemia | IV fluids +/- Lasix, calcitonin, bisphosphonates. If hyperparathyroid is to blame, surgery |
| symptoms of primary hyperparathyroidism | more common in older women; usually asymptomatic but may have nonspecific complaints like weight loss, fatigue, depression, arthralgias, abd pain. Or, may uncommonly have a hypercalcemic crisis w severe hypercalcemia, volume depletion, AMS. Stones, osteop |
| dx of primary hyperparathyroidism | hypercalcemia, PTH in normal-high range, hypophosphatemia, and hypercalciuria |
| pathophysiology of renal osteodystrophy | nephron loss reduces phoshate excretion which causes hyperphosphatemia. this lowers serum Ca, increasing PTH secretion and impairs calcitriol formation which reduces in turn Gi Ca absorption, which elevates PTH further. |
| 3 types of bone disease associated with secondary hyperparathyroidism | Osteitis fibrosa cystica, osteomalacia, and adynamic bone dz |
| symptoms of renal osteodystrophy | bone pain, prox muscle weakness, pruritus, soft tissue ulcerations, and diffuse soft tissue calcifications |
| Tx of renal osteodystrophy | give antacids to reduce intestinal absorption of phosphate, give vit D and calcitriol. Subtotal parathyroidectomy may help if don't respond to medical therapy. Renal transplant in selected patients. |
| usual causes of hypophosphataemia | alcohol, malnutrition are usual causes; also seen in DKA |
| symptoms of hypophosphataemia | AMS, weakness, agitation. Severe hypophosphatemia can cause rhabdomyolysis, seizures |
| tx of hypophosphatemia | replace phosphate |
| most common etiologies of hyperphosphaatemia | renal failure (particularly ATN), tumor lysis syndrome, or iatrogenic. |
| tx of hyperphosphaatemia | Ca carbonate PO (binds phosphate in gut to decrease absorption) |
| what is hungry bone syndrome | rapid transfer of Ca into bones following removal of parathyroid nodule |
| etiologies of hypomagnesaemia | drugs (loop diuretics, amphotericin, gentamicin), insulin, hungry bone syndrome |
| What electrolyte abnormalities does hypomagnesaemia cause? | hypokalemia and hypocalcemia refractory to tx. Therefore when you encounter these, check Mg |
| tx of hypermagnesaemia | IV fluids, Ca if there are ECG changes, dialysis if tx is refractory |
| definition of oliguria | <400 ml/day |
| urine sodium and osmolarity in prerenal failure | urine Na<15; high urine osmolarity (>500), SG around 1.020u |
| urine Na and osmolarity of intrinsic renal failure | high urine Na (>15); osmolarity low (<400) |
| urine sediment in acute glomerulonephritis | RBC casts w hematuria and proteinuria, low SG |
| urinary sediment in ATN | many renal epithelial cells, pigmented granular casts |
| serology in Goodpastures | anti-GBM Abs |
| serology in microscopic polyarteritis and Goodpasture's syndrome | ANCA Ab |
| most common cause of intrinsic ARF | tubulointerstitial nephritis |
| course of tubulointerstitial nephritis | pts present w dramatic renal failure but most survive and recover normal renal function; severity correlates w survival |
| diagnosis of ATN | muddy brown granular casts, high urine sodium (FeNa>1%) |
| prevention of ATN | monitor Cr if pt is getting nephrotoxic substances; maintain adequate intravacular volume; maintain good cardiac output |
| tx of ATN | volume replacement with NS. IV diuretic therapy often used but not helpful. Match inputs of fluid and salt to output; d/c any precipitating cause; manage electrolyte disturbances particularly high K |
| clinical/lab findings in acute interstitial nephritis | similar to ATN; drug-induced interstitial nephritis associated w eospinophils in urine and other systemic signs of hypersensitivity |
| relationship between NSAIDS and interstitial nephritis | don't usually cause interstitial nephritis directly but since they inhibit prostaglandin synthesis and decrease GFR they may precipitate renal failure in susceptible pts |
| pathophys of nephrotic syndrome | loss of glomerular impermeability to proteins causes proteinuria, hypoalbuminuria, which in turn causes edema and serosal effusions. Hypercholesterolemia common. Hypercoagulability occurs 2' loss of proteins C, S, antithrombin III |
| immunofluorescence in FSGS | immunoglobulin and complement deposition |
| in whom is FSGS most commonly seen | HIV pts, drug abusers |
| sequelae of FSGS and tx | leads to HTN, CRG. Steroids usually not helpful |
| what causes membranous GN? | immune complex disease. Idiopathic or associated with SLE, hep B, or solid tumors |
| tx of membranous GN | steroids and cytotoxic agents (chlorambucil) |
| rule of 3rds for membranous GN | 1/3 progress to CRF, 1/3 have spontaneous remission, and 1/3 remain nephrotic but don't progress |
| systemic causes of nephrotic syndrome | sickle cell, diabetic glomerulopathy (most common 2' cause of nephrotic syndrome), multiple myeloma |
| immunofluorescence in post-streptococcal glomerulonephritis | immune complex deposition with complement (IgG, C3, C4) in granular pattern |
| presentation of PSGN | presents 14 days after infection with dark urine, edema. usually reversible but may occasionally progress, more so in adults. |
| labs in PSGN | Nephritic sediment (RBC casts), low complement |
| tx of PSGN | treat underlying cause; immunosuppressive drugs not effective |
| how to distinguish IgA nephropathy from PSGN in a case of glomerulonephrit | if pt presents w hematuria RIGHT after an infection, think IgA. 2 weeks out, think PSGN |
| most common glomerulonephritis | IgA nephropathy |
| presentation and pathology of IgA nephropathy | presents as hematuria during viral infection or after exercise; has immune complex deposition of IgA and C3 in mesangial matrix (mesangial hypercellularity) |
| effective tx of IgA nephropathy | none |
| do antibiotics during strep infection prevent PSGN | no |
| what is membranoproliferative GN associated with? | hep C, cryoglobulinemia |
| what may contribute to anti-GBM disease | cytotoxic T cells |
| pathology in CRF due to DM | Diffuse glomerulosclerosis, nodular glomerulosclerosis (Kimmelstein-Wilson nodules) |
| when do CRF patients become symptomatic | when GFR is <50% of baseline |
| water and sodium balance in CRF | initially, decreased ability to concentrate urine causes sodium wasting, easy dehydration. Later, there is volume overload as kidneys cannot excrete dietary sodium |
| potassium balance in CRF | once GFR becomes markedly decreased the ability to excrete dietary K is lost |
| calcium and phosphate balance in CRF | Hypocalcemia, hyperphosphatemia |
| urea/Cr in CRF | urea and Cr both increase but Cr more than urea |
| sx of CRF | uremic syndrome, nephrotic syndrome. US reveals shrunken kidneys with cortical thinning. |
| Tx of CRF | ACE inhibitors may slow progression. Treat reversible causes. Diet should have modest protein restriction with near normal caloric intake. This decreases nitrogen intake and avoids catabolism. Dialysis. |
| absolute indications for dialysis | Uremic pericarditis w/ or w/o cardiac tamponade, progressive motor neuropathy, intractable volume pverload, life-threatening and intractable hyperkalemia or acidosis, and toxins like ethylene glycol |
| Complications of haemodialysis | subacture bacterial endocarditis and other infections; viral hepatitis due to frequent necessity of transfusion |
| complications of peritoneal dialysis | bacterial peritonitis, hypoalbuminaemia, hypertriglyceridemia, and anemia |
| sx of uraemic syndrome | Pale complexion, wasting, purpura, excoriations due to pruritus, polydipsia, N&V, anorexia. In UA have isosthenuria (can't concentrate urine - SG always 1.010), proteinuria, abnormal sediment w/ tubular casts |
| CNS effects of uraemic syndrome | foot drop, carpal tunnel, clonus, asterixis, seizure |
| cardiac and pulmonary effects of uraemic syndrome | hypertension -> LVH, diastolic dysfunction; accelerated atherosclerosis -> ischaemic heart dz; pleuropericardial inflammation/pericarditis; mitral and aortic valve calcifications; pulmonary edema/pleural effusions |
| Hematologic effects of uraemic syndrome | normochromic normocytic anaemia due to low EPO, defective plt function -> prolonged bleeding time. ANC and WBC function reduced -> increased likelihood of infection |
| GI effects of uraemic syndrome | mild GI bleeding, N&V, anorexia |
| metabolic effects of uraemic syndrome | high TGs, insulin resistance w impaired glucose tolerance |
| presentation of polycystic kidney dz | AD, presents in 30s-40s with flank pain. Ass'd with berry aneurysms, hepatic cysts, and diverticulosis |
| complications of polycystic kidney dz | HTN, recurrent UTI, kidney stones |
| which RTAs occur in the distal tubules | types 1 and 4 |
| which RTA occurs in the proximal tubules | type 2 |
| what causes type 1 RTA | defect in hydrogen secretion, causing acidosis and hypokalaemia. Can be caused by SLE, sarcoid, medications (lithium, ampho B). Pts may also get hypercalcemia and renal stones |
| what causes type 2 RTA | defect in bicarb reabsorption (bicarb wasting). Can be caused by multiple myeloma, heavy metals, and meds (acetazolamide). |
| K in type 2 RTA | low-normal |
| what causes type 4 RTA | defect in aldosterone secretion and ammonium excretion. Pts have low renin and low aldosterone. Causes: diabetic nephropathy, renal transplant, obstructive uropathy |
| K levels in type 4 RTA | high |
| plasma bicarb level in type 1 RTA | low |
| urine pH in type 1 RTA | >5.3 |
| plasma bicarb in type 2 RTA | 12-20 |
| urine pH in type 2 RTA | >5.3 |
| plasma bicarb levels in type 4 RTA | typcically >17 |
| urine pH in type 4 RTA | <5.3 |
| age range for kidney stones | 20-50 (M:F 3:1) |
| recurrence of kidney stones | 36% will have another in 1 yr |
| most common type of kidney stone | calcium oxalate (75%) |
| appearance and treatment of calcium oxalate stones | strongly radiopaque; treat w thiazides |
| appearance and treatment of struvite stones | 15%. moderately radiopaque; common in proteus UTIs. treat by lowering urine pH |
| uric acid stones | <1% of stones. radiolucent. increased incidence in myeloproliferative dz and gout; treat by raising urine pH |
| cystine stones | moderately radiopaque; seen in congenital cystinuria (NOT HOMOCYSTINURIA). Hexagonal crystals, positively birefringent. treat by raising urine pH |
| UA and diagnosis of kidney stones | 85% will have RBCs in urine. urinary pH can help: if <5, suggests uric acid stones; if >6, suspect proteus (struvite stones) |
| in what disorders do you see alkaline urine | type 1 RTA, UTI with proteus or ureaplama |
| when do you see acidic urine | ASA overdose, type 2 RTA |
| where do you see hyaline casts | prerenal acute kidnet injury |
| where do you see muddy brown casts | ATN |
| gold standard for diagnosing kidney stones | IVP |
| tx of kidney stones | analgesia, hydration. If stones are unlikely to pass (>5 mm); extracorporeal shock lithotripsy is successful 85% of the time and percutaneous nephrolithotomy (establishes connection from skin to collecting system) is used when stones are too large or hard |
| uses for IVP | kidney or urethral trauma or tumors, urethral diverticulum, stones, and assessment of renal damage from pyelo |
| uses of cystometry | BPH, congenital anomalies, and incontinence |
| uses of cystoscopy | biopsy, resection of tumors, crushing of stones, and catheterization of ureters |
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