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Nephrology
Internal Medicine
| Question | Answer |
|---|---|
| What is the definition of acute renal failure? | rapid rise in BUN or creatinine over hours or days |
| What is BUN derived from? | protein waste products |
| How does liver disease effect BUN levels? | falsely low |
| Why does creatinine clearance slightly overestimate GFR? | there is some tubular secretion of creatinine; it is not all freely filtered |
| What is the cause of renal failure in patients with cirrhosis (hepatorenal syndrome)? | 1. portal hypertension leads to splanchnic vasodilation 2. decreased volume is sensed by JG apparatus → activation of RAAS 3. renal vasoconstriction → decreased renal perfusion |
| Patient with drop in oxygen saturation when they sit up | orthodeoxia, characteristic of hepatopulmonary syndrome |
| How would creatinine be effected in a patient with a large renal stone obstructing a ureter? | creatinine does not rise if there is a loss of only one kidney |
| How is postrenal azotemia diagnosed? | finding bladder distention or examination, bilateral hydronephrosis, or large volumes or urine after passing Foley |
| What is the most common cause of intrinsic acute renal failure in hospitalized patients? | acute tubular necrosis |
| 1. Patient with fever, rash and oliguria after starting a new drug? 2. What is the best initial test? | 1. Allergic interstitial nephritis 2. ↑ WBC on U/A (best is Hansel's stain for eosinophils in urine) |
| 1. Most important initial test to perform in a person who presents with painful muscles and dark urine. 2. Treatment | 1. EKG for possible cardiac complications of hyperkalemia 2. Ca2+, hydration, bicarbonate to alkalinize urine |
| 1. What is the metabolic complication of ethylene glycol overdose? 2. Treatment | 1. formation of toxic metabolic oxalic acid 2. fomepizole followed by dialysis to remove the ethylene glycole |
| 1. Most common cause of acute hyperoxaluria with metabolic acidosis? 2. Most common cause of chronic hyperoxaluria? 2. | 1. ingestion of antifreeze 2. Crohn's disease from fat and calcium malabsorption |
| Mechanism of action of allopurinol | prevents conversion of xanthine to hypoxanthine to uric acid |
| Most common cause of hypercalcemia | hyperparathyroidism |
| What is the difference in presentation between acute interstitial nephritis (AIN) and direct toxins to the kidney? | 1. AIN occurs with the first dose and presents with fever, rash, and eosinophils 2. direct toxins take several days/weeks |
| What is the least nephrotoxic aminoglycoside | tobramycin |
| What is renal insufficiency? | renal failure that is not severe enough to require dialysis; aka azotemia |
| Patient with recent vascular catheter develops signs of renal failure. | atheroembolic disease |
| Which HIV drug is most associated with neprholithiasis? | indinavir (protease inhibitor) |
| Acute flank pain, hematuria, pyuria and fever: 1. patient with + urine cultures 2. patient with history of diabetes, sickle cell or NSAID use 3. What is the most accurate diagnostic test? | 1. acute pyelonephritis 2. papillary necrosis 3. Ct scan |
| Most likely prevention of contrast-induced renal failure. | hydration |
| 1. Patient with edema, hematuria and hypertension 2. What test confirms the diagnosis? | 1. glomerulonephritis 2. renal biopsy |
| 1. Patient with sinusitus and renal disease 2. best initial test 3. most accurate test 4. Treatment | 1. Wegener's granulomatosis 2. C-ANCA 3. biopsy of kidney or nasal septum/lung 4. cyclophosphamide and steroids |
| 1. Patient with chronic asthma, elevated WBC skin lesions. 2. Treatment | 1. Churg-Strauss 2. glucocorticoids and cyclophosphamide |
| What areas of the body are effected by polyarteritis nodosa? | virtually every organ except the lung |
| 1. Palpable purpura with arthralgies 2. What is the pathophysiologic cause 3. Treatment | 1. Henoch-Schonlein purpura 2. systemic deposition of IgA 3. supportive because disease is self-limiting |
| Characteristics of Glomerulonephritis | 1. Edema (low oncotic pressure; Salt and water retention) 2. Hematuria with dysmorphic RB cell (red cell squeeze through the glomeruli) 3. Proteinuria < 2g/24hr 4. Fractional excretion of Na <1% (you are retaining it, you can't be excreting it)" |
| Churg-strauss Syndrome: best lab test? | eosinophilia and positive C-ANCA |
| Churg-Strauss Syndrome: most accurate test | Biopsy |
| Goodpasture Syndrome: best initial test | Antibasement membrane antibodies to type IV collagen |
| Goodpasture Syndrome: most accurate test | lung or kidney biopsy; IF shows linear deposit |
| Goodpasture Syndrome: treatments | plasmapheresis and steroid, +/- cyclophosphamide |
| Polyarteritis Nodosa: best initial test | P-ANCA |
| Polyarteritis Nodosa: most accurate test | biopsy (need angiogram done before bx) |
| Polyarteritis Nodosa: Treatments | cyclophosphamine and steroid |
| Henoch-Schonlein Purpura: Treatments | Steroids if disease is severe or porgressive |
| IgA nephropathy (Berger Disease): best initial test | increase IgA |
| IgA nephropathy (Berger Disease): most accurate test | renal biopsy |
| IgA nephropathy (Berger Disease): Treatments | no effective treatment; steroid won't reverse IgA problem; use ACEI or ARBS for proteinuria |
| Postinfectious Glomerulonephritis: characteristics | Smoky, cola or tea colored urine; due to strep pyogenes, Hep B and C, CMV, chronic staph infections) |
| Postinfectious Glomerulonephritis: best initial test | ASO (antistreptolysin) test or AHT(antihyaluronic acid) test |
| Postinfectious Glomerulonephritis: most accurate test | renal biopsy; EM shows humps of IgG and C3 |
| Postinfectious Glomerulonephritis: Treatments | 1. supportive 2. manage fluid overload and HTN with diuretics |
| Thrombotic thrombocytopenic Purpura: characteristics | Pentad presentation: 1. hemolytic anemia; 2. uremia; 3. thrombocytopenia; 4. fever; 5. neurologic problems |
| Hemolytic uremic syndrome: characteristics | Triad presentation: 1. hemolytic anemia; 2. uremia; 3. thrombocytopenia |
| In Hemolytic uremic syndrome 1. What antibiotics do you give? 2. How do you treat thrombocytopenia? | 1. none; if antibiotics are given, organism may release more toxins as it dies 2. do not transfuse platelets bc they precipitate and worsen the CNS and renal abnormalities |
| 1. crescent formation of glomerulus on biopsy 2. treatment | 1. rapidly progressive glomerulonephritis 2. steroids and cyclophosphamide |
| What are the two common types of amyloidosis? | 1. AL from light chains 2. AA from chronic infection or inflammation |
| What defines nephrotic syndrome? | renal disease sufficient to produce a level of proteinuria greater than 3.5 gram per 24 hours, hyperlipidemia, edema and low serum albumin |
| What is the cause of hyperlipidemia in nephrotic syndrome? | loss of lipoproteins on the surface of chylomicrons and LDL so these lipids are not cleared from the bloodstream |
| Most common form of idiopathic nephrotic syndrome in adults | membranous |
| Cause of casts on urinalysis: 1. hyaline 2. red cell 3. white cell | 1. dehydration 2. glomerulonephritis 3. pyelonephritis |
| Cause of the following casts on urinalysis: 1. broad, waxy 2. granular | 1. chronic renal failure 2. acute tubular necrosis |
| What are the indications for dialysis? | A E I O U 1. Acid/base disorders 2. Electrolytes (↑K) 3. Intoxication 4. Overload of volume 5. Uremia (pericarditis, encephalopathy) |
| Cause of hypocalcemia in renal failure (2)? | 1. low vitamin D 2. high phosphate which precipitates calcium |
| What is used to treat hyperphosphatemia from end-stage renal disease? | phosphate binders: 1. calcium carbonate 2. calcium acetate |
| What is used to treat hyperphosphatemia from end-stage renal disease when calcium mis abnormally high (from vitamin D replacement? | 1. sevelamer 2. lanthanum |
| What happens to the levels of the following electrolytes in ESRD: 1. calcium 2. phosphate 3. magnesium | 1. decreases 2. increases 3. increases |
| 1. What is the suggested blood pressure management for those with ESRD? 2. Why? | 1. <130/80 2. rapidly progressive coronary artery disease is the most common cuase of death |
| 1. How does ESRD lead to bleeding? 2. What is the treatment? | 1. uremia-induced platelet dysfunction 2. desmopressin causes release of subendothelial vWF stores and factor 8 |
| Why can hyponatremia lead to hypertension? | "1. as ECT osmolality decreases, water shifts into brain cells increasing the ICP 2. blood pressure increases to maintain cerebral perfusion pressure" |
| How does hyponatremia effect intracranial pressure? | water shifts into the cells leading to increased ICF volume and thus increased ICP |
| At what level does hyponatremia become symptomatic? | < 125 |
| "What is the treatment for: 1. mild hyponatremia 2. moderate hyponatremia 3. severe hyponetremia | 1. fluid restriction 2. normal saline (0.9%) + loop diuretic 3. 3% hypertonic saline or V2 receptor-antagonist" |
| What neurologic disorder is caused by correcting hyponatremia too rapidly? | central pontine myelinolysis |
| Why may hyperglycemia manifest with pseudohyponatremia? | ↑ glucose osmotically draws water into the vascular space and dilutes sodium |
| Most important diagnostic test when a patient has suspected hypokalemia | EKG |
| What acid base status is seen following dehydration? | volume contraction → ↑ aldosterone → metabolic alkalosis |
| How does replacement of B12 in deficient patients lead to hypokalemia? | potassium is found mostly intracellularly and with rapid cell production from B12, extracellular K+ moves into cells |
| How is magnesium related to potassium metabolism? | magnesium decreases urinary loss of potassium therefor hypomagnesemia leads to hypokalemia |
| Rx for hypovolemia from vomiting? | 1. GI loss of H+ and volume contraction → ↑ aldosterone → H+ loss and HCO3 retention 2. 2. treat contraction alkalosis with IV normal saline with the addition of potassium to replace K+ loss |
| Rx for severe hypercalcemia? | normal saline followed by furosemide |
| How do the following effect calcium levels: 1. acidosis 2. alkalosis | 1. results in hypercalcemia because albumin binds H+ and releases Ca2+ 2. results in hypocalcemia |
| Patient with multiple blood transfusions has a seizure and perioral numbness. | hypocalcemia from binding of free calcium to citrate |
| How can alcoholism lead to hypocalcemia | low magnesium from malnutrition prevents the release of parathyroid hormone from the thyroid gland |
| How does hyperglycemia manifest with hyponatremia? | high glucose level causes a transcellular shift of water out of the cell into the vascular space, diluting the sodium |
| Rx for: 1. mild hypovolemic hypernatremia 2. severe hypovolemic hypernatremia | 1. D5 1/2NS 2. D5W |
| Treatment for nephrogenic diabetes insipidus | HCTZ, amiloride, NSAIDs |
| What effect does insulin have on potassium levels? | insulin causes uptake of potassium by cells |
| Patient with muscle weakness and peaked T waves on EKG. What is the treatment? | 1. calcium chloride protects heart 2. insulin + glucose shift K+ into cells 3. Kayexalate removes K from body" |
| "Which fluid should be given: 1. hypovolemia with alkalosis 2. hypovolemia with acidosis | 1. normal saline 2. lactated ringer |
| 1. What is the tonicity of sweat? 2. What are the resulting sodium levels in the body? | sweat is mostly free water (hypotonic) and results in hypernatremia |
| How do you diagnose SIADH? | elevated urine osmolality (>100) in a patient with hyponatremia |
| Treatment for SIADH 1. severe disease 2. chronic disease in which underlying cause can't be corrected | 1. 3% hypertonic saline 2. V2 receptor antagonists (conivaptan and tolvaptan) |
| How fast can hypo or hypernatremia be corrected? | ~ 0.5 mEq per hour |
| How does aldosterone effect K+ concentration? | causes hypokalemia mainly from K+ secretion from colon and small part from kidneys |
| What are the EKG findings of patients with suspected hypokalemia? | T-wave flattening and U-waves |
| What action does Kayexalate have? | resin that absorbs 1 mEq K per g and releases 1 mEg Na |
| 1. Asymptomatic hyperkalemia with nonanion gap metabolic acidosis 2. How do you confirm the diagnosis? 3. Treatment | 1. aldosterone deficiency 2. Presence of high urine sodium with oral salt restriction. 3. Fludrocortisone |
| What electrolyte changes are seen with volume contraction? | 1. K secretion 2. Na+ absorption 3. HCO3 absorption 4. H+ secretion |
| What is the anion gap a measure of? | 1. gauge of the unmeasured anions in the bloodstream 2. positively charged cations - negatively charged anions |
| In normal anion gap metabolic acidosis, how can one determine if the cause is due to renal or intestinal HCO3 loss? | 1. determine urine anion gap (Na + K) - Cl 2. positive gap indicates renal tubular acidosis |
| 1. What are the main cations of the blood? 2. What are the main anions? | 1. Na+, K+, Ca2+ 2. HCO3-, Cl-, albumin, lactate, ketoacids |
| What acid/base disturbance do salicylates create? | respiratory alkalosis + metabolic acidosis |
| 1. What is the composition of most renal stones? 2. What electrolyte irregularities increase stone formation? | 1. calcium oxalate 2. increased calcium, decreased oxalate |
| What causes struvite stones? | urinary infections with urease positive organisms |
| Radiolucent stones | uric acid |
| Extra-renal manifestations of adult polycystic kidney disease | 1. hepatic cysts 2. hypertension 3. berry aneurysms 4. mitral valve prolapse |
| What degree of proteinuria distinguishes nephritis from nephrotic syndrome? | >3g/day = nephrotic |
| What is the FeNa in glomerulonephritis? | FeNa < 1 because there is salt and water retention |
| What is the difference between Henoch-Schonlein purpura and IgA nephropathy? | both occur from IgA deposition but IgA nephropathy only effects the kidneys |
| Patient with recent viral illness 1. Develops hematuria 1-2 days later 2. Develops hematuria 1-2 weeks later | 1. IgA nephropathy 2. poststreptococcal glomerulonephritis |
| 1. Why must one biopsy in lupus nephritis? 2. What is the treatment? | 1. to determine if there is sclerosis or proliferative disease 2. sclerosis does not need therapy; proliferative disease is treated with steroids and mycophenolate |
| 1. How is nephrotic syndrome diagnosed? 2. How is the cause of nephrotic syndrome determined? | 1. protein:creatinine ratio of >3.5 2. renal biopsy |
| What is the diagnosis of SIADH based on? | elevated urine osmolality and urine sodium in a patient with hyponatremia |
| 1. Patient with flattened T waves and U waves present 2. What causes the U wave | 1. hypokalemia 2. purkinje fiber repolarization |
| What is the maximum oral dose of potassium? | no max dose because gut cannot absorb it fast enough to overload kills |
| What is the problem in renal tubular acidosis: 1. Type I 2. Type II 3. Type IV | 1. impaired distal secretion of H+ 2. impaired proximal absorption of bicarbonate 3. aldosterone deficiency |
| 1. What 2 things cause normal anion gap metabolic acidosis? 2. What laboratory test helps distinguish between the two? | 1. diarrhea and renal tubular acidosis 2. urine anion gap |
| 1. How do you quantify oliguria? 2. How do you quantify anuria? | 1. <400 mL per 24 hours 2. <100 mL per 24 hours |
| 1. When is Winter's formula used? 2. What is Winter's formula? | 1. to determine if the is appropriate respiratory compensation for metabolic acidosis 2. (1.5 x HCO3-) + 8 ± 2 |
Created by:
amichael@siumed.edu
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