ACNP II Exam 1
Does acidemia promote movement of potassium IN or OUT of cells?
Acidemia promotes potassium movement OUT of the cells.
What's the most common cause of intra-renal AKI?
Acute tubular necrosis § Occurs most often after surgery or severe sepsis. § Ischemia and reduced levels of ATP generate toxic oxygen free radicals with a loss of antioxidant protection that causes cell swelling, injury and necrosis. § Activation of inflammatory cells (neutrophils, macrophages and lymphocytes) and complement and release of inflammatory cytokines contribute to tubular injury § Transport of sodium and other molecules is disrupted with damage primarily to proximal tubular epithelium and shedding of the brush boarder with the appearance of tubular granular casts in the urine.
What infusion would you order for salicylate poisoning?
Alkalinize urine with isotonic NaHCO3 infusion to maintain urine pH at 8 or above *Dialysis indicated for severe intoxications, levels greater than 100 mg/dl acute or greater than 40mg/dl chronic
What is the RIFLE criteria?
Allows grading of AKI based on creatinine, GFR, and urine output. Risk, Injury, Failure, Loss, ESRD
In the early stages of hypoperfusion in pre-renal AKI, a hormone will kick in to help keep the GFR at a constant level. What hormone is this?
Angiotensin II maintains GFR at a relatively constant level through afferent arteriolar dilation and efferent arteriolar vasoconstriction
You review the arterial blood gas results of a patient and note the following results pH 7.45, PCO2 30, and HCO3- 22. What is the condition? a. Metabolic Acidosis, compensated b. Respiratory Alkalosis, compensated c. Metabolic Alkalosis, compensated d. Respiratory Acidosis, compensated
Answer: b Rationale: The patient's ABG was: pH 7.45, PCO2 30, and HCO3- 22. This ABG is considered abnormal because the PCO2 is NOT normal. Notice the pH - it may be at the upper end of normal, but it is still in the normal range (7.35 - 7.45) -so NORMAL Notice the PCO2 is LOW (30). The normal range is 35 - 35. This implicates the Respiratory system is involved. When the PCO2 is LOW, a state of Respiratory Alkalosis is occurring (CO2 goes down à pH goes UP) Now look at the bicarb (HCO3-) - it is normal at 22 (normal range is 22-26). This should tell you there is not a Metabolic component to the imbalance. So, we have a NORMAL pH, a LOW PCO2, and a NORMAL bicarb.
You are caring for a patient on a mechanical ventilator. This morning's blood gas results reveal the following: pH 7.50, PCO2 30. You determine he has respiratory alkalosis. Which laboratory value would most likely be noted in this condition? a. Sodium level of 145 b. Potassium level of 3 c. Magnesium level of 2 d. Phosphorus level of 4
Answer: b Rationale: Respiratory alkalosis is defined as a deficit of carbonic acid or a decrease in hydrogen ion concentrations that results from the accumulations of base or a loss of acid without a comparable loss of base in the body fluids. This occurs in conditions that cause overstimulation of the respiratory system. Clinical manifestations of respiratory alkalosis include headache, tachypnea, paresthesia, tetany, vertigo, convulsions, hypokalemia, and hypocalcemia.
You order a nasogastric tube that is attached to low suction on your new admission. Which disorder is this patient at risk of developing? a. Metabolic Acidosis b. Metabolic Alkalosis c. Respiratory Acidosis d. Respiratory Alkalosis
Answer: b Metabolic Alkalosis Rationale: Metabolic Alkalosis is defined as a deficit/loss of hydrogen ions or acids OR due to an excess of base (bicarbonate) resulting from the accumulation of base or from a loss of acid without a comparable loss of base in the body fluids. This occurs in conditions such as hypovolemia, the loss of gastric fluid, excessive bicarbonate intake, the massive transfusion of whole blood, and hyperaldosteronism. Loss of gastric fluid via nasogastric suction or vomiting causes Metabolic Alkalosis as a result of the loss of hydrochloric acid.
Joe B. has been admitted with DKA. The nurse documents the patient is experiencing Kussmaul respirations. Based on this documentation, which of the following did the nurse observe? a. Respirations that cease for several seconds b. Respirations that are regular but abnormally slow c. Respirations that are labored and increased in depth and rate d. Respirations that are abnormally deep, regular, and increased in rate
Answer: d Rationale: Kussmaul respirations are characterized by deep, rapid, and labored breathing. This distinct, abnormal breathing pattern can result from certain medical conditions, such as diabetic ketoacidosis. Apnea is described as respirations which cease for several seconds. In bradypnea, respirations are regular but abnormally slow. In hyperpnea, respirations are labored and increased in depth and rate
An unresponsive patient is brought into the ED. ABG results are the following: pH 7.12, PCO2 90, and HCO3- 22. What is this condition? a. Metabolic Acidosis with compensation b. Respiratory Acidosis with compensation c. Metabolic Acidosis without compensation d. Respiratory Acidosis without compensation
Answer: d Respiratory Acidosis without compensation Rationale: The acid-base disturbance is Uncompensated Respiratory Acidosis (ABG: pH 7.12, PCO2 90, and HCO3- 22) Recall, normal pH is 7.35-7.45. Normal PCO2 is 35 - 45. Normal Bicarb (HCO3-) is 22 - 26 In respiratory acidosis the pH is decreased because the PCO2 is elevated. Notice the bicarb level is still within normal limits; the *kidneys have not had time to adjust for this acid-base disturbance (*which takes approx. 3-5 days). Additionally, the pH is NOT normal, and the bicarb has not increased to induce metabolic alkalosis to counteract the acidosis, so this condition is uncompensated.
What should you assess in hyponatremic pt?
Assess their volume status: -Skin, mucus membranes, heart and lung sounds, presence of JVD and/or peripheral edema. Assess neuro status.
An 81 year old female nursing home patient has had nausea, diarrhea, and decreased oral intake for two days. She has Alzheimer's dementia and hypertension and her medications include Donepezil, enalapril, and amlodipine. On exam, her temperature is 100.1 F, BP is 100 / 70, and respiratory rate is 20/minute. She appears confused and lethargic. Her EKG is shown below. Which of the following is the first line of treatment? A. kayexalate B. Calcium chloride C. Magnesium D. Furosemide
B. Calcium chloride
A 71 year old male patient with a history of COPD presents with respiratory distress. Which of the following acid-base disorders is characterized by a pH of 7.3, PCO2 of 75, and HCO3 of 36? A. Respiratory alkalosis B. Respiratory acidosis C. Metabolic acidosis D. Metabolic alkalosis
B. Respiratory acidosis
What is a fever of unknown origin (FUO)?
Body temperature of 101 F (38.3 C) or above rectally for > 3 weeks without an apparent cause, despite workup for at least 1 week in patients without neutropenia or immunosuppression
Causes of hypervolemic hyponatremia
CHF, nephrotic syndrome with massive edema, cirrhosis causing peripheral vasodilation
What should you consider in your geriatric patient with hyponatremia?
Carefully assess their fluid intake. If they have chronic hyponatremia, they need to be aware of potential bone loss and tendency to fracture. Mild hyponatremia is associated with increased mortality.
What age gender and ethnicity are renal calculi most prevalent in?
Caucasian males
What is the treatment of hypocalcemia for symptomatic patient with tetany or seizures?
Check the phosphorous first. In severe hyperphosphatemia (> 6.5 mg/dL) administration of calcium may exacerbate the formation of calcifications. In these cases, dialysis may be indicated. The serum magnesium must also be checked and corrected for calcium treatment to be effective. Then proceed with one of the first two calcium treatments below: 1. Calcium chloride: 1gram 10% solution IV over 3-5 minutes 2. Calcium gluconate: 1 gram 10% solution IV over 3-5 minutes for 2 doses (NOTE: Calcium gluconate is generally preferred due to decreased risk of tissue toxicity with possible extravasation) 3. Follow with 1 gram/hr calcium gluconate in 500 ml D5W or NS over 3 hours as the effect of the initial infusion is transient.
When should you consult urology for kidney stones?
Consult Urology for stone removal or stones > 5 mm, also for UTI with obstruction (URGENT indication for Urologic consultation)
What is the oliguric phase of AKI?
Decreased urine output <400-500 ml/day
Elderly patients are at an elevated risk of developing AKI, but which meds further increases their risk?
Diuretics, ACE, ARBs, NSAIDS
How often is serum Na monitored in symptomatic hyponatremia?
Every 2-4 hours
What are causes of hyperthermia?
Exogenous heat exposure Endogenous heat production: Atropine or Ecstacy Other causes: -malignant hyperthermia from some anasthetics -neuroleptic malignant syndrome -serotonin syndrome
What is the single most important measure to protect a patient from developing contrast-induced AKI (CI-AKI)?
Fluid volume loading prior to study. The common approach for adequate IV volume expansion is 0.9NS at a rate of 1.0-1.5 mL/kg/hr for 3-12 hours prior to the procedure and continued for 6-24 hours after the procedure aiming to maintain the urine output at >150mL/hour.
What medications can you give when treating kidney stones?
For pain control: • NSAIDs (Ketorolac) are proven in randomized control trials to be as effective as narcotics for treatment of renal colic. Avoid use in patients with renal dysfunction • Opioids or combination analgesics (hydrocodone/acetaminophen) may be necessary when pain is unrelieved by NSAIDs • Combination of NSAIDs and opioids is superior to each agent alone (EX: Morphine 5mg +ketorolac 15mg) • Antiemetics (Ondansetron) Other meds: • Antispasmodic - relaxes smooth muscle of the ureters and has been shown to promote stone passage in 5-7 days; these include alpha-blockers (doxazosin, tamsulosin) or calcium channel blockers (nifedipine) •Type I absorptive hypercalciuria thiazide therapy: ---Decreases renal excretion of calcium ---Increases bone density by 1% per year ---Has limited long term use
Your pt has a serum Na greater than 146 and a urine osmolality (UOsm) greater than 400, what does this suggest?
GI, cutaneous or insensible fluid losses
What is the treatment for hypomagnesemia in the patient with severe symptoms (seizures and/or ventricular arrhythmias)?
Give 2 grams IV in 50 ml of D5W over 5-10 minutes. May be given IVP if patients have fatal arrhythmias. Torsade de Pointes is a possibility. Then start an infusion as mentioned for mild to moderate sx. Pt should remain on continuous cardiac monitoring if arrhythmias have been documented or it is indicated for patient safety.
What is the most common cause of hypercalcemia?
Hyperparathyroidism
Hyponatremia with edematous state of excess total body sodium content with or without hemodynamic compromise. ADH secretion is stimulated.
Hypervolemic hyponatremia
What do the brain cells do in hyponatremia vs hypernatremia?
Hyponatremia = swollen Hypernatremia = shrinkage
Hyponatremia that occurs when there is a low serum osmolality (SOsm). There is an excess of body water with both intra- and extracellular fluid (ECF) dilution. The patient's clinical signs occur due to the excess water causing cell swelling.
Hypotonic hyponatremia
Hyponatremia that may result from any cause of sodium loss, is a state of deficient total body sodium content. ADH secretion is stimulated.
Hypovolemic hyponatremia
What is the treatment of severe hypercalcemia (typically seen with malignancy)?
IV NS to restore volume and induce diuresis of more than 200 ml/hr. The usual rate of administration is 200- 300 mls/hr initially, then titrate down to maintain desired urine output 1) Calcitonin (Calcimar, Miacalcin) 4-8 IU/kg every 12 hr SQ or IM - antiresorptive properties, increases renal calcium excretion 2) IV Bisphosphonates - use cautiously in patients with impaired renal function. They inhibit calcium release by interfering with osteoclast mediated bone resorption. Examples include: o Pamidronate (aredia) 60-90 mg IV over 24 hours, repeat in 7 days o Etidronate (Didronel) 7.5 mg/kg in 250 cc NS over 2-3 hrs for 3 days o Zoledronic acid (Zometa) 4 mg IV over 15 minutes, repeated in 7 days 3) Furosemide (Lasix) 40-80 mg IV every 8-12 hours to maintain a urine output of 150-200 cc/hr. A continuous infusion of NS or ½ NS should be maintained. o Loop diuretics reduce paracellular reabsorption of calcium in the loop of Henle enhancing calcium excretion. They must be used cautiously if the patient is already hypovolemic despite IV hydration. Occasionally (rarely) they will be given with IV hydration of NS plus 6 - 8-gram sodium diet 4) HD with a low calcium dialysis bath
What infusion would you order for alcoholic ketoacidosis?
IV glucose (D5W or 5% dextrose in 0.9% NS at 100-150 ml/hr.) plus thiamine (100mg)
When would you want to order a Urine Na and Fractional excretion of Na (FENa)?
If oliguria is present
What is saponification?
In acute pancreatitis fatty acids are released due to fat necrosis. These fatty acids combine with calcium to form insoluble salts (saponification). This can cause hypocalcemia.
There are 4 phases of AKI, what are they?
Initiation Phase Extension Phase Maintenance Phase Recovery Phase
What's the dose of KCL you can give to correct potassium?
It is difficult to correlate body deficits with serum K; you can estimate 100 mEq/L loss for each 0.3 mEq/L decrease you see in the serum K when less than 4 mEq/L If acute loss, you can give 40-60 mEq PO and recheck in 4 hrs. If chronic, give 10-40 mEq in 1-2 divided doses. PO is best route
What is KDIGO?
Kidney Disease Improving Global Outcomes. The gold standard of AKI definition.
How does metabolic acidosis occur in AKI?
Low Bicarbonate level; results from the inability of the kidneys to excrete hydrogen; renal reabsorption of the filtered bicarbonate is impaired.
When treating a patient with kidney stones, what is your main priority?
Management of acute pain
Your pt is hypokalemic and you take a look at their ABG. They have an elevated HCO3, what may this indicate?
May suggest a mineral corticoid excess
What is the treatment for hypomagnesemia in the patient with mild to moderate symptoms?
Mild - moderate symptoms are non-emergent: 4Gms mag sulfate IV in 1 liter of D5W over 3-6 hours then 2-4 grams in D5W over the next 12-24 hours. The initial goal is to reach a mag level higher than low-normal (> 1.5), unless the patient is having or prone to arrhythmias. Then your goal is a level of 2.0 mg/dL. Magnesium levels in all degree of depletion should be monitored post infusion. The frequency should be 6-12 hours depending on the patient's clinical status.
What is the treatment for mildly decreased magnesium level or for those with chronic hypomagnesemia?
Oral replacement. Magnesium chloride (Mag-L-100), 2 tablets TID OR Magnesium Oxide (Mag-Ox 400) 400 mg PO BID OR Magnesium lactate (Magtab SR) 84 mg PO BID. Even if the magnesium is only mildly decreased in hospitalized patients, they may not be able to tolerate PO replacement thus, IV supplementation may be needed.
What is the formula for plasma osmolality (Posm)?
Posm = 2(Na)+BUN/2.8+Glucose/18
Describe EKG changes in hyperkalemia
Progression of peaked T waves and a shortened QT interval initially. As hyperkalemia worsens, you will see a widened QRS complex, the disappearance of a P wave, and the fusion of QRS and T wave to form a sine wave. Patients react differently to potassium levels. Most but not all patients will show EKG changes with potassium > 6.5 mEq/L. There are rare instances when patients maintain a normal EKG with potassium of 9. mEq/L.
What meds would you give for... renal hypercalciuria? hyperuricemia? hypercitraturia?
Renal hypercalciuria: hydrochlorothiazide effective as long-term therapy Hyperuricemia: decrease purine in diet or allopurinol, or both Hypercitraturia: potassium citrate supplements 20mEq TID
What condition is seen in hypertonic hyponatremia? What infusions are associated with it?
Seen in hyperglycemia ***each time BS increases by 100, the Na decreases by 1.6 mEq/L*** Seen in mannitol or glycerol infusions.
Which sodium level do these symptoms correlate with? o Acute: headache, confusion, lethargy, nausea o Chronic: Occasionally none to mild confusion or lethargy
Serum Na 110-120 mEq/L
Which sodium level do these symptoms correlate with? o Acute: Nausea, malaise, gait instability o Chronic: none to gait instability (fall risk in elderly)
Serum Na 120-125 mEq/L
Which sodium level do these symptoms correlate with? o Acute: nausea, seizures, coma o Chronic: Rarely none, greater confusion, or lethargy
Serum Na less than 110 mEq/L
Key EKG changes in hypokalemia
Sinus brady, ST depression, decreased amplitude of T wave, prolonged QT. When both hypokalemia and hypomagnesemia exist, the potential for arrhythmias is higher
Describe subjective and PE findings of hypophosphatemia
Subjective: Severe hypophosphatemia can lead to a metabolic encephalopathy resulting from ATP depletion. Patients may complain of irritability, confusion, weakness, and paresthesia. The variety of symptoms depend on the severity and chronicity of the phosphate depletion Objective (physical findings): Physical exam should focus on the following systems: Respiratory, Musculoskeletal, Neurological, and Gastrointestinal. Abnormalities may include - muscle weakness, proximal myopathy, dysphagia and ileus (all effects on the smooth muscle). Pulmonary function can also be impacted with impaired diaphragmatic contractility. In critically ill patients this can lead to prolonged mechanical ventilation
What is hyperpyrexia? What can cause it?
Temperature over 41.5C (106F) Seen in severe infections or CNS hemorrhage Antipyretics help some but you need to cool them down with cooling blankets, etc
What neurological signs may be seen in hypomagnesemia and hypocalcemia?
Trousseau's and Chvostek's signs
Your pt has a Na less that 115 mEq/L and are having moderate symptoms. How should you treat them?
Two options: 1. Give 3% hypertonic as in severe symptoms 2. OR treat on basis of volume status as discussed in mild or asymptomatic patients.
What's the most important test to order in the initial workup of AKI?
Urinalysis
How long does AKI take to resolve?
Usually resolves within a 3-month time frame
Causes of hyponatremia include
Water excretion is less than water consumption. Causes may include: • Decreased kidney function, impaired GFR • Diuretic effect that impairs formation of dilute • Non-osmotic antidiuretic hormone (ADH) release concentrating urine
What is nephrogenic systemic fibrosis?
a newly recognized skin disorder in patients with renal failure that has been associated with exposure to gadolinium-based MRI contrast. NSF is characterized by skin induration preferentially affecting the extremities and can involve internal organs also.
What is hyperphosphatemia?
a serum phosphorus level that exceeds 5 mg/dL (normal is 2.5-4.5)
8. What is the BEST first choice of treatment for a patient with a serum potassium of 6.4 mEq/L with QRS widening and frequent PVCs on EKG? a. 1 G calcium gluconate (10% solution) IV over 2 minutes b. 80 mg furosemide IVP c. Placement of a subclavian line for hemodialysis d. NPO, 0.9% NS at 100 cc/hr, stat cardiology consult
a. 1 G calcium gluconate (10% solution) IV over 2 minutes
17. When calculating your patient's fluid requirements, how much do you allow for insensible losses? a. 400-500 mL/24 hours. b. 600-800 mL/24 hours. c. 1,000 mL/24 hours. d. depends on age and gender.
a. 400-500 mL/24 hours.
2. Which of the following is NOT euvolemic hyponatremia? a. Blood loss b. Renal failure c. SIADH d. Diuretics
a. Blood loss
4. Symptoms of hypomagnesemia include all of the following EXCEPT a. Complete heart block b. Muscle cramps c. Chvostek's sign d. Ventricular tachycardia
a. Complete heart block
5. A 66 yo female with AKI (serum creatinine 4.6mg/dL presents with mild pain. Her physician initiates therapy with naproxen. You recommend the following? a. Discontinue naproxen, initiate therapy with acetaminophen b. Discontinue naproxen, initiate therapy with ibuprofen c. Discontinue naproxen, initiate therapy with meloxicam d. Continue naproxen, but at a reduced dose. e. Continue naproxen, but monitor kidney function closely.
a. Discontinue naproxen, initiate therapy with acetaminophen
What are the subjective and objective findings of hyperphosphatemia?
a. Ectopic tissue calcification (serum phosphorous [P] x serum Ca) greater than 55 Sites: cornea or acute conjunctivitis, grainy feeling of skin itching, vascular calcification seen on Xray or CT. Other sites can include cardiac tissue with valvular and arterial calcification, conduction defects on ECG. These can increase cardiac mortality. Calciphylaxis is tissue ischemia that can result from the calcification of smaller blood vessels with thrombosis. b. Chronic hyperphosphatemia contributes to the development of renal osteodystrophy
9. Which of the following is NOT a recognized risk factor for kidney stone formation? a. High calcium diet b. High animal protein intake c. Low fluid intake d. Residence in certain parts of the U.S., including Carolinas, Georgia and Alabama
a. High calcium diet
How do you treat hyperphosphatemia?
a. Peritoneal or hemodialysis for patients with renal failure or acute hyperphosphatemia. Recovery of renal function will correct the condition within 12 hours. Saline and/or acetazolamide (15 mg/kg every 48 hours) can be given to induce phosphaturia if needed for more aggressive treatment b. Dietary restriction on phosphorous (800-1000 mg/daily) c. Patients with chronic condition will benefit from oral phosphate binders: i. Calcium acetate 667-1334 mg PO TID with meals ii. Sevelamer 800-3200 mg PO TID with meals iii. Lanthanum 500-1000 mg PO TID with meals
What is the most common cause of AKI? a. Pre-renal b. Intrinsic or intra-renal c. Post-renal or obstructive
a. Pre-renal
What type of AKI is this? kidney hypo-perfusion leading to lower GFR from hypotension or hypovolemia a. Pre-renal b. Intrinsic or intra-renal c. Post-renal or obstructive
a. Pre-renal
What type of AKI is this? • Hypovolemia • Hemorrhagic blood loss • Loss of plasma volume (burns, peritonitis) • Water and electrolyte losses (severe vomiting/diarrhea, intestinal obstruction, uncontrolled DM, inappropriate use of diuretics) • Systemic hypotension or hypo-perfusion • Septic shock • Cardiac failure or shock • Massive pulmonary embolism • Stenosis or clamping of renal artery • Increased intra-abdominal pressure (compartment syndrome) • Medications: NSAIDs a. Pre-renal b. Intrinsic or intra-renal c. Post-renal or obstructive
a. Pre-renal
4. A 66 yo female is admitted to hospital with a GI bleed. She has a pmhx of DM and a baseline serum creatinine of 1.4 mg/dL. Laboratory work today reveals a BUN 65mg/dL and a serum creatinine of 2.8 mg/dL. Meds include: metoprolol, atorvastatin and glyburide. Based on the patient's BUN and serum creatinine concentration, which of the following is a likely cause of AKI? a. Pre-renal AKI due to GI bleed b. Intrinsic AKI due to diabetes c. Post-renal AKI due to obstruction d. Intrinsic AKI due to history of CKD e. Pre-renal AKI due to chronic medication
a. Pre-renal AKI due to GI bleed
What are the differential diagnoses for hyponatremia?
a. Pseudohyponatremia - can be seen in patients with hypertriglyceridemia greater than 1,000 mg/dL, familial hypercholesterolemia and proteinemia greater than 10 gm/dL as in multiple myeloma b. Dilutional hyponatremia resulting in increased total body water +/- solutes c. Solute depletion hyponatremia resulting in decreased solutes and increased total body water
Which of the primary acid/base disorders do these conditions fall under: • Depression of respiratory center • Neuromuscular failure • Lung Disease a. Respiratory acidosis b. Metabolic acidosis -non-gap c. Metabolic alkalosis d. Metabolic acidosis -with gap e. Respiratory alkalosis
a. Respiratory acidosis
What other labs should you order for pt with hyperphosphatemia?
a. Serum phosphorous greater than 5 mg/dl in adults (> 6 in children) b. An elevated serum phosphorous can be accompanied by low calcium as a result of intravascular chelation of calcium by phosphorous c. BUN, serum creatinine or creatinine clearance for renal insufficiency. In patients with GFR 30-59 mL/min, measure serum phosphate and calcium every 6 months; increase frequency as GFR decreasesd. PTH and vitamin D levels. PTH increases phosphate excretion. Vitamin D deficiency or resistance can cause hypophosphatemia both by decreasing GI phosphate absorption and by causing hypocalcemia and secondary hyperparathyroidism that results in more urinary phosphate excretion. e. Serum calcium to calculate PHOS X CA product: Danger above 55 f. If patient is hypoventilating, check ABG.
What labs should be ordered for hypophosphatemia?
a. Serum phosphorous is less than 2.5 mg/dl b. Hemolysis due to severe hypophosphatemia; CBC, increased serum free hemoglobin and decreased haptoglobin. Defective clots retraction and thrombocytopenia can occur which can aggravate mucosal hemorrhage c. Rhabdomyolysis due to severe hypophosphatemia, especially in alcoholics. Increased creatinine kinase (CK) level and positive urinary myoglobin d. Look for a metabolic acidosis with a decreased serum bicarbonate and arterial pH e. ECG - there is an increased incidence of ventricular arrhythmias in the setting of an acute MI. If these patients require emergent heart surgery, there is an increased need for vasoactive drug support f. If the cause is not apparent from the clinical situation, a measurement of urine phosphorous excretion helps define the mechanism. - Renal excretion of > 100 mg by 24-hour urine collection indicates excessive renal losses - Low serum 25(OH)D3 suggests dietary Vitamin D deficiency - An elevated intact PTH may be seen in primary or secondary hyperparathyroidism
19. Which of the following is the most common composition of kidney stones? a. calcium oxalate b. uric acid c. struvite d. sodium phosphate
a. calcium oxalate
Your patient has a serum Na less than 135 and an SOsm less than 270 (norm 280-295), what type of hyponatremia do they have? a. hypotonic hyponatremia b. isotonic hyponatremia c. hypertonic hyponatremia
a. hypotonic hyponatremia
What is the only type of hyponatremia that requires the treatment to be directed at the serum Na? a. hypotonic hyponatremia b. isotonic hyponatremia c. hypertonic hyponatremia
a. hypotonic hyponatremia Otherwise, treatment includes: • Therapy is guided by symptoms, level of serum sodium and rapidity of development • Rate of correction is critical to avoid CNS insult
18. The most effective preventive strategy to prevent recurrence of renal lithiasis is which of the following? a. increase in hydration b. early treatment of urinary tract infection c. limitation of calcium intake d. use of probenecid
a. increase in hydration
9. The MOST concerning symptom of acute, severe hypocalcemia is: a. laryngospasm. b. dry, brittle nails. c. Trousseau's sign. d. rebound hypercalcemia.
a. laryngospasm.
15. A 50-year-old woman with heart failure with tachycardia, S3 heart sound, and basilar crackles bilaterally. Blood pressure is 90/64 mm Hg. Labs: BUN 58mg/dL and creatinine 2.4 mg/dL. This clinical presentation is most consistent with: a. prerenal azotemia b. acute glomerulonephritis c. tubular necrosis d. postrenal azotemia
a. prerenal azotemia
20. The MOST common cause of persistent hyperphosphatemia is: a. renal failure. b. ingestion of a high phosphate diet. c. hypercalcemia. d. none of the above.
a. renal failure.
4. Which of the following is recommended for patients with hyponatremia according to expert panel recommendations? a. urgent correction by 4-6 mmOl/L is recommended in symptomatic patients with acute hyponatremia, to avoid brain herniation and neurologic damage from cerebral ischemia. b. to avoid osmotic demyelination syndrome (ODS) in patients with chronic hyponatremia, the minimum correction of serum sodium is 9 mmol/L in a 24 hours period. c. pharmacologic treatment of SIADH is recommended as first-line therapy above fluid restriction alone. d. vasopressor receptor antagonists (vaptans) are recommended as part of combined therapy for patients with hypovolemic hyponatremia.
a. urgent correction by 4-6 mmOl/L is recommended in symptomatic patients with acute hyponatremia, to avoid brain herniation and neurologic damage from cerebral ischemia. -A panel of US experts on hyponatremia issued guidelines on the diagnosis, eval, and treatment of hyponatremia. For tx of symptomatic patients with acute hyponatremia (<24-48 hours), the panel recommended urgent correction by 4-6 mmol/L to prevent brain herniation and neuro damage:Severe symptoms: 100 mL of 3% over 10 minutes x3 as needed.Mild to moderate symptoms, in patients at low risk for herniation: 3% NaCl infused at 0.5-2 mL/kg/hr.
6. You are treating a patient with serum magnesium of 1.6 mEq/L and frequent PVCs on the cardiac monitor. You decide that IV supplementation would be appropriate. His PMH also includes HTN, DM2 and ESRD. What dose magnesium sulfate IV administration would you choose? a. 500 mg b. 1 GM c. 2 GM d. I wouldn't give him IV, I would use PO supplementation
b. 1 GM
3. Clinical manifestations of Hypermagnesemia are generally not seen until the serum magnesium is: a. 3 mEq/L b. 4 mEq/L c. 5 mEq/L d. 6 mEq/L
b. 4 mEq/L
6. Symptoms of hypokalemia usually do not present until the serum potassium is: a. <4 mEq/L b. <3 mEq/L c. <2 mEq/L d. It is dependent on the patient and their diagnosis
b. <3 mEq/L
10. Which of the following medications should NOT increase the risk of kidney stone formation? a. Acyclovir b. Hydrochlorothiazide c. Furosemide d. Acetazolamide
b. Hydrochlorothiazide
5. You're treating a patient with Cushing's syndrome. What would you expect his serum K+ levels to be due to his disease? a. Hyperkalemia due to mineral corticoid excess b. Hypokalemia due to mineral corticoid excess c. No effect on K+ d. It will vary depending on his magnesium supplementation
b. Hypokalemia due to mineral corticoid excess
What type of AKI is this? • Acute tubular necrosis (post-ischemic or nephrotoxic medication-Amphotericin, contrast agents) • Glomerulopathies • Acute interstitial necrosis (tumors or toxins) • Vascular damage • Malignant hypertension, vasculitis • Coagulation defects • Renal artery/vein occlusion • Bilateral acute pyelonephritis a. Pre-renal b. Intrinsic or intra-renal c. Post-renal or obstructive
b. Intrinsic or intra-renal
What type of AKI is this? disorders involving the renal parenchymal or interstitial tissue a. Pre-renal b. Intrinsic or intra-renal c. Post-renal or obstructive
b. Intrinsic or intra-renal
1. Magnesium deficiency is defined by a urinary magnesium excretion of: a. Less than 3 mEq/L in 12 hours b. Less than 3 mEq/L in 24 hours c. Less than 2 mEq/L in 12 hours d. Less than 2 mEq/L in 24 hours
b. Less than 3 mEq/L in 24 hours
Which of the primary acid/base disorders do these conditions fall under: • Nonrenal HCO3- loss (diarrhea) • Renal HCO32 loss (Type 2 renal tubular acidosis) • ↓ H secretion (Type 1 renal tubular acidosis) • Hypoaldosteronism (Type 4 renal tubular acidosis) a. Respiratory acidosis b. Metabolic acidosis -non-gap c. Metabolic alkalosis d. Metabolic acidosis -with gap e. Respiratory alkalosis
b. Metabolic acidosis -non-gap
12. BH has a pmhx of chronic Sjogren syndrome. He is currently experiencing his second episode of nephrolithiasis. Metabolic evaluation revealed the possibility of calcium phosphate stones. Which of the following interventions would NOT reduce the risk of future stone formation? a. Increase fluid intake to 2L per day. b. Start potassium citrate with a goal of urinary pH > 7 c. Start a thiazide diuretic d. Start a high calcium diet.
b. Start potassium citrate with a goal of urinary pH > 7
7. What is the definition of acute kidney injury? a. a drop in serum creatinine to less than or equal to 0.3 mg/dL within 48 hours b. a rise in serum creatinine to greater than or equal to 0.3 mg/dL within 48 hours c. an increase in urine output to greater than 0.5mL/kg/hr for 6 consecutive hours. d. a decrease in serum creatinine by 1.5 times or more baseline within the prior 7 days
b. a rise in serum creatinine to greater than or equal to 0.3 mg/dL within 48 hours
The use of which of the following medications can precipitate acute renal failure in a patient with bilateral renal artery stenosis? a. corticosteroids. b. angiotensin II receptor antagonists. c. beta-adrenergic antagonists. d. cephalosporins.
b. angiotensin II receptor antagonists.
3. A 63 yo man has suffered a GI bleed. His BUN and serum creatinine are elevated at 52mg/dL and 2.4mg/dL respectively. His blood pressure is 105/68 mm Hg, urinary sodium concentration is 10mEq/L and fractional excretion of sodium is 0.5%. Which of the following treatments is recommended at this time? a. loop diuretic, such as furosemide b. bolus of IV fluids, such as normal saline c. ACE inhibitor, such as enalapril d. thiazide diuretic, such as hydrochlorothiazide e. dopamine agonist, such as fenoldopam
b. bolus of IV fluids, such as normal saline
Your pt has a serum Na less than 135 and their SOsm is between 280-295. You're suspicious because they have extremely high triglycerides. What type of hyponatremia do they have? a. hypotonic hyponatremia b. isotonic hyponatremia c. hypertonic hyponatremia
b. isotonic hyponatremia
13. A patient with severe hypomagnesemia with seizures should receive: a. magnesium sulfate 4 grams in 1,000 mL NS to infuse over 24 hours. b. magnesium sulfate 2 grams in 50 mL D5W over 5-10 minutes. c. magnesium sulfate 8 grams in 1,000 mL D5W over 12 hours. d. magnesium oxide 400 mg PO QID.
b. magnesium sulfate 2 grams in 50 mL D5W over 5-10 minutes.
Medications known to increase the risk of renal stones include all of the following except: a. hydrochlorothiazide. b. moxifloxacin. c. topiramate. d. indinavir.
b. moxifloxacin.
19. Mark is brought to the ED by PD for evaluation after being picked up for drunk and disorderly conduct. He is well known for his chronic alcoholism and persistence in heavy drinking on a daily basis. He is extremely drunk and complaining of severe leg cramps this time. The LIKELY cause is: a. anemia from GI bleeding. b. rhabdomyolysis from hypophosphatemia. c. muscle necrosis from acidemia. d. DVT from thrombocytosis.
b. rhabdomyolysis from hypophosphatemia.
2. Which of the following is most accurate regarding symptoms associated with hyponatremia? a. even mild reductions in serum sodium levels frequently cause overt neurological symptoms. b. severe hyponatremia should be considered in pediatric patients who present with symptoms of bacterial meningitis. c. constipation is a more common presenting symptom than vomiting in patients with hyponatremia. d. symptoms of exercise associated with hyponatremia (EAH) occur in patients with an underlying health condition as opposed to healthy patients.
b. severe hyponatremia should be considered in pediatric patients who present with symptoms of bacterial meningitis. -A retrospective Chinese study reported hyponatremia in 116 of 175 children with bacterial meningitis. Multivariate analysis showed that convulsions and blood glucose levels >110 mg/dL were related to severe hyponatremia. Severe hyponatremia should be considered in pediatric patients with bacterial meningitis who have either of those findings.
A 63-year-old man presents with abdominal pain, pain during urination, and red urine. Imaging reveals a renal stone in the ureter. An appropriate treatment option would be: a. percutaneous nephrolithotmy. b. shock wave lithotripsy. c. insertion of a nephrostomy tube. d. insertion of a bladder catheter.
b. shock wave lithotripsy.
Risk factors for renal stones include all of the following except: a. male gender. b. vegetarian diet. c. family history of renal stones. d. obesity.
b. vegetarian diet.
3. Mr. E presents to the ED with seizures from hyponatremia. You should expect his serum sodium to be a. 140 or less b. 130 or less c. 120 or less d. No idea. I need to see his BMP
c. 120 or less
11. The MOST reliable way to distinguish renal loss of magnesium versus GI loss of magnesium is: a. patient's history. b. review of medications and allergies. c. 24 hour urinary magnesium excretion collection. d. 24 hour stool collection for electrolytes.
c. 24 hour urinary magnesium excretion collection.
14. The severity of acidosis in a patient with DKA can be determined by calculating the anion gap. What is a NORMAL anion gap? a. 2-3 mEq/L. b. 4-7 mEq/L. c. 8-10 mEq/L. d. 12-15 mEq/L.
c. 8-10 mEq/L.
The preferred method to identify the location of small renal stones is: a. x-ray. b. abdominal ultrasound. c. CT scan. d. radionuclide scan.
c. CT scan
Quiz 1-20 1. To maintain a normal serum sodium: a. The daily diet should contain 4 g of Na or more b. Fluid intake should contain at lest 8 oz/day of beverages that contain 200 mg of Na per serving c. Fluid intake should equal fluid output d. Fluids should be limited to 1500 cc/24 hr
c. Fluid intake should equal fluid output
Which of the primary acid/base disorders do these conditions fall under: • Loss of H+ rich fluids (GI loss) • Contraction alkalosis • Alkali administration • Volume contraction • Chloride depletion • Hypokalemia a. Respiratory acidosis b. Metabolic acidosis -non-gap c. Metabolic alkalosis d. Metabolic acidosis -with gap e. Respiratory alkalosis
c. Metabolic alkalosis
What type of AKI is this? disorders associated with urinary tract obstruction outflow a. Pre-renal b. Intrinsic or intra-renal c. Post-renal or obstructive
c. Post-renal or obstructive
What type of AKI is this? • Obstructive uropathies (usually bilateral, fibrosis) • Ureteral obstruction (edema, tumors, stones, clots) • Bladder neck obstruction (enlarged prostate) • Neurogenic bladder a. Pre-renal b. Intrinsic or intra-renal c. Post-renal or obstructive
c. Post-renal or obstructive
5. Your patient has a magnesium of 1.5 mEq/L. Which of these lab abnormalities would you also expect to see? a. Hemoglobin of 8.0 g/dL b. Sodium of 125 mEq/L c. Potassium of 3.0 mEq/L d. Potassium of 5.2 mEq/L
c. Potassium of 3.0 mEq/L
6. Hemorrhage, severe sepsis and fluid loss are all causes of ___________ a. intrinsic AKI b. post-renal AKI c. Pre-renal AKI d. intra-renal AKI
c. Pre-renal AKI
1. A 69 yo female has a PMH of chronic kidney disease, DM and HTN. Her serum creatinine is stable at 1.4mg/dL and she is not volume overloaded. She will be receiving IV contrast dye for a cardiac catheterization. 1. Which of her medications is most likely to contribute to worsening AKI? a. hydrochlorothiazide b. atorvastatin c. enalapril d. atenolol e. acetaminophen
c. enalapril
13. A 38-year-old female presents with right flank pain for several days, shaking chills, fever to 102°F, and general malaise. The flank pain has been intermittently severe, and she has a history of kidney stones. Urinalysis reveals 3+ red blood cells, 3+ leukocyte esterase, trace protein and negative glucose. Which of the following findings would most likely be seen on a renal ultrasound? a. small echogenic kidneys b. cysts c. hydronephrosis d. capsular hemorrhage
c. hydronephrosis
Your pt has a serum Na less than 135 and their SOsm is greater than 290. What type of hyponatremia do they have? a. hypotonic hyponatremia b. isotonic hyponatremia c. hypertonic hyponatremia
c. hypertonic hyponatremia
3. Which of the following is accurate according to a joint European clinical practice guidelines on hyponatremia? a. the threshold for profound hyponatremia is 129 mmol/L. b. hyponatremia is considered chronic once it lasts more than 24 hours. c. hyponatremia with a measure osmolality <275 mOsm/kg always reflect hypotonic hyponatremia. d. confirmation of SIADH in patients with hyponatremia requires measurement of vasopression.
c. hyponatremia with a measure osmolality <275 mOsm/kg always reflect hypotonic hyponatremia.
Common causes of chronic renal failure include all of the following except: a. type 2 DM. b. recurrent pyelonephritis. c. hypotension. d. polycystic kidney disease.
c. hypotension.
Common symptoms of renal stones include all of the following except: a. pink, red, or brown urine. b. sharp pain in the back or lower abdomen. c. marked febrile response. d. pain while urinating.
c. marked febrile response.
18. What fluid is MOST often used to replace extracellular volume and maintain hemodynamics? a. fresh frozen plasma. b. lactated ringers. c. normal saline. d. PRBC
c. normal saline.
You see a 58-year-old man diagnosed with a kidney stone who reports pain primarily during urination. You consider all of the following except: a. improved hydration. b. alpha blocker use. c. prescribing a diuretic. d. analgesia use
c. prescribing a diuretic.
12. The absorption of magnesium is altered by: a. loop diuretics. b. thiazide diuretics. c. proton pump inhibitors. d. digoxin.
c. proton pump inhibitors.
The pH of the urine also influences the risk of precipitation and calculus formation. An alkaline urinary pH (>7.0) significantly increases the risk of _______ ________ stone formation, whereas acid urine (pH < 5.0) increases the risk of _______ _______ stone.
calcium phosphate uric acid
Your pt has a serum Na greater than 146 and a urine osmolality (UOsm) less than 300, what does this suggest?
central or nephrogenic DI
7. Laboratory diagnositic workup of hypokalemia should include: a. Urinary potassium excretion b. acid base status c. Neither a or b d. Both a and b
d. Both a and b
2. A patient presents with hypomagnesemia and Torsade de Pointes. Your best choice of treatment would be: a. Magnesium Oxide 800 mg PO stat x 1 and recheck his serum magnesium to decide on further treatment b. Magnesium Sulfate 4 GM in 1000mls NS to infuse over 24 hours; check serum magnesium at 12 hours then decide on further treatment c. Magnesium Sulfate 2 GM IVP over 10 minutes. Recheck magnesium after administration then decide on further treatment d. Magnesium Sulfate 2 GM IVP over 10 minutes followed by Magnesium Sulfate 4 GM in 1000ml NS to infuse over 24 hours
d. Magnesium Sulfate 2 GM IVP over 10 minutes followed by Magnesium Sulfate 4 GM in 1000ml NS to infuse over 24 hours
Which of the 4 primary acid/base disorders do these conditions fall under: • Ketoacids (starvation, alcoholic, diabetic) • Exposures (methanol, ethylene glycol, salicylates) • Lactic acid (shock, drug related) • Profound uremia a. Respiratory acidosis b. Metabolic acidosis -non-gap c. Metabolic alkalosis d. Metabolic acidosis -with gap e. Respiratory alkalosis
d. Metabolic acidosis -with gap
4. You are evaluating Mary K. for hypernatremia. Her lab results reveal a serum sodium of 154 and urine osmolality of 418. Based on these results you decide the etiology of her hypernatremia is: a. Central Diabetes Insipidus b. Osmotic diuresis from ingesting sugary drinks c. Nephrogenic diabetes insipidus d. Running 10 miles for exercise during a heat wave
d. Running 10 miles for exercise during a heat wave
11. Which of the following strategies would NOT prevent nephrolithiasis recurrence in a patient with uric acid stones? a. Potassium citrate supplementation b. Low-sodium diet c. Allopurinol use d. Targeting urinary pH < 5.5
d. Targeting urinary pH < 5.5
2. A 69 yo female has a PMH of chronic kidney disease, DM and HTN. Her serum creatinine is stable at 1.4mg/dL and she is not volume overloaded. She will be receiving IV contrast dye for a cardiac catheterization. 2. Following the catheterization, she develops acute kidney injury and is fluid overloaded. She is receiving furosemide 200mg IV every 6 hours with an increase in urine output from 600mL in the last 24 hours to 1300mL in the last 24 hours. Which of the following would you recommend next to improve urine output? a. add spironolactone, 50mg orally daily b. switch to bumetanide, 4 mg IV every 6 hours c. increase the dose of furosemide to 1 g IV every 12 hours d. add metolazone, 5mg orally daily e. add dopamine, 5mcg/kg/minute IV
d. add metolazone, 5mg orally daily
16. Which of the following fluids are isotonic to plasma? a. lactated ringers. b. normal saline. c. D5W. d. all of the above.
d. all of the above.
16. A 65 year-old patient presents with hypertension and peripheral edema. Urinalysis reveals pale urine, with a specific gravity of 1.002, 2+ protein, trace glucose, and is negative for red blood cells and leukocytes. Serum electrolytes include BUN of 58 mg/dl and creatinine of 4.5 mg/dl. These are unchanged from previous results obtained 3 months and 6 months ago. Of the following, what other laboratory abnormalities would you expect? a. hypercalcemia b. metabolic alkalosis c. hypophosphatemia d. anemia
d. anemia
10. You are called to the bedside of your patient that has developed hypocalcemia acutely. He is post ictal. What is your FIRST step in assessment of his condition? a. consult neurology. b. administer calcium chloride. c. place him on a cardiac monitor. d. check his phosphorus then decide on administering calcium chloride.
d. check his phosphorus then decide on administering calcium chloride.
15. What is the FIRST step in reviewing arterial blood gas results? a. check the HCO3 result. b. check the anion gap. c. check the paO2. d. check the pH.
d. check the pH.
Which of the following is most accurate regarding treatment of hyponatremia? a. use of a V2 receptor antagonist is contraindicated in asymptomatic patients with hypovolemic hyponatremia. b. hypertonic saline is recommended in normovolemic (euvolemic), asymptomatic patients with hyponatremia. c. in general, chronic hyponatremia can be safely corrected more quickly than acute hyponatremia. d. consider potassium repletion in patients with hypovolemia secondary to the use of diuretics.
d. consider potassium repletion in patients with hypovolemia secondary to the use of diuretics.
8. A 56 yo female presents to the ED due to increased swelling of left ankle for 2 days after falling outdoors playing with grandchildren. She has been taking ibuprofen 400mg to 800mg every 4 to 6 hours to relieve the pain. PMHX: HTN Meds: Lisinopril Labs: elevated serum creatinine and BUN AKI induced by NSAIDs is suspected. If this suspected diagnosis is correct, which of the following additional laboratory results is most likely? a. decreased serum chloride level b. decreased serum potassium level c. decreased serum sodium level d. elevated serum potassium level e. elevated serum sodium level
d. elevated serum potassium level
EXAM PRACTICE QUESTIONS 1. Which of the following is most accurate regarding the presentation of hyponatremia? a. patients with hypovolemic hypotonic hyponatremia rarely present with orthostatic symptoms. b. central nervous system (CNS) disturbances are more commonly associated with hypervolemic hypotonic hyponatremia than with normovolemic (euvolumic) hypotonic hyponatremia. c. patients whose medical history includes loop diuretics are more likely to develop hyponatremia than are patients that take thiazides. d. hyponatremia associated with cortisol deficiency, such as primary or secondary hypoaldosteronism, commonly presents subtly and may go underdiagnosed.
d. hyponatremia associated with cortisol deficiency, such as primary or secondary hypoaldosteronism, commonly presents subtly and may go underdiagnosed. -Sever hypothyroidism (unknown mechanism, possibly s/t low cardiac output and GFR) and adrenal insufficiency are also a/w non-osmotic vasopression release and impaired sodium reabsorption, leading to hypotonic hyponatremia. Hyponatremia a/w cortisol deficiency, such as primary or secondary hypoaldosteronism, commonly presents subtly and may go undiagnosed. A random cortisol level check, especially in acute illness, can be misleading if the level is normal (when it should be high). Testing for adrenal insufficiency and hypothyroidism should be part of the hyponatremic workup, because these disorders respond promptly to hormone replacement. Depending on the etiology, mineralcorticoid will also need replacement.
You see a 58-year-old woman who is being treated for renal stone. Analysis of a stone passed in the urine reveals that it is composed of calcium oxalate. In counseling the patient about preventing future stones, you consider all of the following except: a. reducing sodium in her diet. b. limiting consumption of beets, rhubarb, nuts, and chocolate. c. encoring her to get daily calcium requirements from food. d. if calcium supplements are needed, this medication should be taken on an empty stomach.
d. if calcium supplements are needed, this medication should be taken on an empty stomach.
17. A 32-year-old female patient presents with renal colic and hematuria. The patient has a long-standing history of unresponsive treatment for urinary tract infections with documented Proteus species. Urinalysis reveals crystals resembling coffin lids. KUB reveals a staghorn calculus in the right kidney. Which of the following is the best clinical intervention? a. High fluid intake with a low salt diet b. A low purine diet c. Laser lithotripsy d. percutaneous nephrolithotomy
d. percutaneous nephrolithotomy
14. An 80-year-old male presents with fatigue and difficulty emptying his bladder. Physical exam reveals a distended bladder, but otherwise unremarkable. Labs are: BUN 88mg/dL, Creatinine 2.8mg/dL. This clinical assessment is consistent with: a. prerenal azotemia b. acute glomerulonephritis c. acute tubular necrosis d. postrenal azotemia
d. postrenal azotemia
All of the following are common precipitating factors in acute renal failure except: a. anaphylaxis. b. infection. c. myocardial infarction. d. type 1 DM.
d. type 1 DM.
Struvite stones are typically found in people: a. with type 2 diabetes. b. who live in colder climates. c. who abuse alcohol. d. with a history of kidney infections.
d. with a history of kidney infections.
How does geographic location affect renal calculi development?
depends on rainfall, average temp., humidity, dietary patterns * more common in southeastern US due to heat, and dehydration, resulting in low urine volumes
A serum creatinine may not reflect the extent of renal impairment in elderly patients due to ___
diminished muscle mass
Which of the primary acid/base disorders do these conditions fall under: • CNS stimulation • Hypoxemia • Anxiety a. Respiratory acidosis b. Metabolic acidosis -non-gap c. Metabolic alkalosis d. Metabolic acidosis -with gap e. Respiratory alkalosis
e. Respiratory alkalosis
Hyponatremia with normal body sodium content, no edema, normal hemodynamics
euvolemic hyponatremia
How often should you monitor Na when treating hypernatremia?
every 2-4 hr in acute hypernatremia, every 4-6 hrs in chronic hypernatremia -also- • Monitor and replace other electrolyte abnormalities and/or losses • Low sodium diet • Assess the need to treat diabetes insipidus
Do these meds cause hyper/hypokalemia? -NSAIDs, ACE, ARBs, Cyclosporine, digoxin toxicity
hyperkalemia
What electrolyte imbalance would these conditions cause? -Renal failure -Decreased aldosterone synthesis as seen in adrenal insuff or heparin therapy -Decreased renal aldosterone effect seen in potassium-sparing diuretics and certain renal diseases(diabetic, obstructive or sickle cell nephropathies)
hyperkalemia
Hyponatremia that occurs when there is a high SOsm. There is dilution of extracellular fluid sodium by the water shifting from cells into high concentrations of non-sodium solute (e.g., glucose or mannitol). The patient's clinical signs occur from the primary disorder and not from the redistribution of water
hypertonic hyponatremia
What electrolyte imbalance is caused by these conditions? -Primary hyperaldosteronism of adrenal disease -Secondary aldosterone excess in hypovolemic states -Secondary aldosterone excess in renal vascular hypertension -Renin secreting tumor -Cushing's syndrome or adrenal hyperplasia -High dose prednisone, fludrocortisone, authentic licorice ingestion (exogenous mineralocorticoid effect)
hypokalemia
Low mag levels can increase potential for which electrolyte imbalance?
hypokalemia The excretion of potassium by the distal tubules is exacerbated by an abnormally low magnesium
What is azotemia?
increase in nitrogenous waste products in blood (elevated BUN/creatinine)
What do tubules do to try re-expand circulating blood volume?
increased tubular sodium and water reabsorption
What infusions do you administer for DKA?
intravenous NS (0.9% NS) and insulin infusions
What does a FENa > 1% indicate?
intrinsic cause of AKI
Hyponatremia that occurs when there is a normal SOsm. It occurs when there is a laboratory artifact, hyperlipidemia that is extreme, or hyperproteinemia that displaces water in the lab sample. The patient's body water is normal, and they are asymptomatic.
isotonic hyponatremia
Potassium level when you start seeing severe weakness or rhabdo?
less than 2.5
What is the second most common cause of hypercalcemia?
malignancy
What are the risks of renal calculi formation?
o Age o Sex o Race o Geographic location o Seasonal factors o Fluid intake- adequate water intake lowers risk o Diet: High animal protein diet o Occupation o Genetic predisposition o And co-morbidities, such as HTN, DM2, Obesity, Atherosclerosis,History of UTIs (urinarytract infections) o Hx of small bowel resection, gastric bypass, and colectomy o High urinary pH - MAIN risk factor for calcium oxalate and phosphatestones
What imaging should you order for suspicion of kidney stones?
o CT or MRI renal without contrast (renal stone protocol) *Gold standard o Plain abdominal x-ray (KUB): useful for frequent calcium stone former (DOES NOT detect noncalcium stones) o Ultrasound kidneys- inexpensive & safe, good diagnostic tool for hydronephrosis also o Intravenous pyelography (IVP)
What are two causes of primary water loss that may cause hypernatremia?
o Central (pituitary) diabetes insipidus; lack of ADH secretion o Nephrogenic (renal) diabetes insipidus; failed response to ADH
Name 6 medications associated with renal stone formation
o Colchicine o Chemotherapy agents o Vit D supplements o Steroids o Triamterene o Indinavir- protease inhibitor
What are the most common causes of fever in the geriatric population?
o Connective-tissue diseases (RA, Polymyalgia rheumatic, etc.) o Malignancies- Colon CA, lymphoma, leukemia o Intra-abdominal infections and TB o Medication effect. Medications may need to be adjusted more frequently in the elderly because of hepatic/renal function or low BMI
What is the treatment for non-emergent hyperkalemia with a normal ECG?
o Give Furosemide 40-80 mg IV to increase excretion o Sodium polystyrene resin (Kayexalate) 15-45 grams with an osmotic cathartic (sorbitol orlactulose) can be given o Loop or thiazide diuretics o Hemodialysis or peritoneal dialysis to remove K if renal failure is present
Your patient has hypokalemia and you want to see if the kidneys are wasting it so you do a 24 hr urine. What is the amount of potassium in a 24 hr period that would indicate renal potassium wasting?
o If it is greater than 25 mEq/L/24 hr, there is renal potassium wasting o If it is less than 25 mEq/L/24hr, there is non-renal potassium wasting
What labs to check for kidney stones
o Obtain UA, including urine pH - pH 6.0 or more: suggests renal tubular acidosis - pH 8.0 or more or pyuria: should lead to urine cultures and consideration of struvite stones o Strain urine to obtain sample for stone analysis o Serum Chemistries: calcium, electrolytes/BUN, creatinine, phosphate, and uric acid levels o CBC o Consider obtaining serum intact parathyroid hormone (PTH) as part of the screening evaluation if primary hyperparathyroidism is suspected. o Ancillary protocol: 24-hour urine ordered to identify volume, pH, calcium, oxalate, citrate, uric acid, sodium, potassium, and creatinine at minimum - All children with stones - Frequent stone formers - Non-calcium stone formers - Demographic group not typically prone to stone formation (African Americans, Hispanics, or Asians)
What are some other ways a patient may have hypernatremia?
o Renal osmotic diuresis is seen in glucosuria of DM, Mannitol or glycerol infusion or high urea excretion in catabolic states such as burns o GI fluid loss through persistent diarrhea or postsurgical drainage o Cutaneous fluid loss in burns or profuse sweating o Excessive administration of hypertonic sodium bicarbonate (NaHCO3) in CPR or lactic acidosis, or 3% saline infusions
The ability to develop a fever in what age population is impaired?
older adults
Your pt has a serum Na greater than 146 and a urine osmolality (UOsm) between 300-400, what does this suggest?
osmotic diuresis
What is the treatment for non-emergent hyperkalemia with abnormal ECG?
patient should remain on a monitor until the EKG normalizes. The following therapies can be utilized: - If there are peaked T waves alone: o Insulin/glucose or albuterol to increase cellular potassium uptake (details described below) o Diuretics -loop or thiazide o Dialysis to remove potassium if patient is in renal failure. Utilize less invasive therapies first o Treatment decision is based on both potassium level and patient assessment
Name 3 substances that can inhibit renal stone or crystal formation
potassium citrate uromodulin pyrophosphate magnesium
What does a FENA <1% indicate?
prerenal AKI
What do you do with the magnesium dose if your patient has a GFR <30?
proceed slowly even if the serum magnesium is greatly decreased. These patients are at a higher risk of developing Hypermagnesemia; quickly reduce the IV dose by 50% and monitor labs frequently to avoid over correcting.
In acute alkalosis, calcium binds to ____
protein, which decreases i-cal
If you have a hyponatremic pt but their plasma osmolality is greater than 280, they're not truly hyponatremic. They have...
pseudohyponatremia. High glucose makes the results look hyponatremic when it's not.
What are staghorn calculi?
renal stones that develop in the calyx gives the impression of antlers
In regards to water repletion with IV fluids, what is the minimal amount of water a person needs to maintain homeostasis?
roughly 1400 cc/day or 60 cc/hr Minimum water requirements can be approximated from the sum of the required urine output, stool water loss and insensible losses. It calculates to approximately 500 cc/day -Water loss in stools is typically 200 cc/day -Insensible water loss, roughly 400-500 cc/day -Fluids from drains must be added.
What is happening with the thermoregulatory system in hyperthermia?
the thermoregulatory center remains unchanged at normothermic levels, while the body temperature increases in an uncontrolled fashion and overrides the ability to lose heat.
A kidney stone lodged in the upper ureter will produce refered pain where?
umbilicus
What IV fluid do you use in hypernatremic pt with moderate volume depletion?
use 0.45%NS. The saline component will restore the ECF, the free water component repletes body water
What IV fluid do you use in hypernatremic pt with severe volume depletion?
use 0.9% NS initially then follow with 0.45% NS when hemodynamically stable
What IV fluid do you use in hypernatremic pt with mild volume depletion?
use D5W but watch glucose to avoid hyperglycemia/glucosuria to prevent further renal water loss
A creatinine to urea ratio greater than 12 may suggest _____ _______
volume depletion
What is the treatment for hyperkalemia with ECG changes of absence of P waves, QRS widening or sine waves, profound clinical findings ( =hyperkalemic emergency)?
§ Calcium gluconate (10 ml of 10% solution = 1 Gm): give 1 gm over 1-2 minutes to antagonize the hyperkalemic effect and decrease excitability of the cell. This should have immediate onset but can repeat in 3-5 minutes if ECG has not normalized. This therapy does not lower the potassium. Its effect can last for minutes only. Can be given peripherally - Calcium chloride may also be used but need to be careful to avoid calcium toxicity (3 x more calcium present per 10mLs). Extravasation into the tissues can cause necrosis. A central or deep vein is needed for administration. - Regular Insulin (10 units) - can be given over 2-5 minutes to increase the cellular potassium uptake. Drives potassium into the cells. Should be given without glucose if serum glucose is > 250 mg/ld. - Insulin with glucose - Glucose is given if normal glucose levels (to prevent hypoglycemia). Common therapies include: 10-20 U of regular insulin in 500 mL of 10% dextrose IV over 60 minutes OR 10 Units of regular insulin followed by 50 mL of D50W (Most common) - Albuterol (10-20 mg in 4 ml) via inhalation over 10 minutes will help increase cellular potassium uptake, effect seen in 15-20 minutes. Not commonly used. Terbutaline SC is a potential alternative. - Sodium Bicarbonate (50 mEq) IV can be given over 1-2 minutes if the patient is acidotic. Increasing pH (alkalosis) results in potassium movement INTO the cells = decreased extracellular potassium, dec K+. Effect lasts for 2-6 hours. *If used repeatedly sodium bicarb can cause dangerous hypernatremia. - Dialysis to remove potassium if there is severe renal impairment
A patient is admitted to your service and is made NPO. You are to order IVF to maintain homeostasis. You determine you must replace 2 liters of water, 154 mEq Na+ . 40 mEq K+ and 100 grams dextrose over the next 24 hours What rate would you order the replacement at? What concentration of NaCl would you order? How much KCl would you add to each liter of fluid? How much dextrose would you add to each L of fluid?
• 2 liters of water over 24 hours = 2000/24 = 85 cc/hr • 154 mEq Na+: Use ½ NS which contains 77 mEq Na+ /L • 40 mEq of K+ : Add 20 mEq/L of KCL to each liter of IVF • 100 g dextrose: Use D5 (50 g of dextrose/L)
How fast can you correct hypernatremia?
• A more rapid correction of serum Na is indicated for acute, symptomatic hypernatremia but no faster than 1-2 mEq/L/hr to avoid cerebral edema • Slower correction is indicated for a chronic hypernatremia - maximum rate of correction should not exceed 0.5 mEq/L/hr
What happens in the Maintenance Phase of AKI?
• Also called oliguric phase • Period of established renal injury and dysfunction after the initiating event has been resolved • May last from weeks to months • Urine output is lowest in this phase • Serum creatinine, BUN, and potassium levels increase • Metabolic acidosis develops and there is salt and water overload
Causes of hypovolemic hyponatremia
• Blood loss • Non-renal causes: GI fluid loss (vomiting, diarrhea, tube loss) • Renal fluid loss through diuresis or aldosterone deficiency (adrenal insufficiency), impaired renal tubular function leading to salt and water loss • Skin fluid loss (insensible loss) • Thiazide diuretics
S/S of kidney stones
• Gross blood (visible in urine) or microscopic hematuria (3 or more RBCs/hpf) may be present • Testicular pain • CVA tenderness • Pain not relieved by position • Frequency, urgency, dysuria suggest stone is in part of ureter within the bladderwall • Acute renal failure may occur when both the collecting systems are obstructed by stones
There may be underlying conditions causing hyponatremia that should be treated. How would you treat these conditions? -hypothyroidism -adrenal insufficiency -SIADH
• Hypothyroidism - replacement as indicated. Always rule out thyroid irregularities first • Adrenal insufficiency - cortisol therapy • SIADH treatment is geared at blocking the ADH effect in the kidney o Conivaptan - used in the hospitalized patient with hypervolemic or euvolemic hyponatremia only. A loading dose of 20 mg is given followed by a continuous infusion o Tolvaptan - Used in Hypervolemic or euvolemic hyponatremic patients only. Must be initiated in the hospital starting at 15 mg daily. Titrate to max dose of 60 mg daily, limit to 30- day course. o Demeclocycline - 150-300 mg PO Q6H for long-term therapy
Your patient is hyponatremic but has either mild or no symptoms at all. How do you treat them?
• If the patient is hypovolemic, give NS to correct the volume status. ADH secretion will stop, kidneys will excrete the excess water • If the patient is Hypervolemic, administer loop diuretics. Lasix 40-80 mg IV or PO is the usual treatment. ADH stops, kidneys excrete extra water E. All cases: restrict water or total fluid intake to 1000ml/24 hours or less F. DC drugs that enhance Na excretion G. Associated hypokalemia: supplement with PO or intravenous PRN
What happens in the Extension Phase of AKI?
• In progressive ischemia, there is infiltration of inflammatory cells, mostly neutrophils; release of cytokines;inflammation and cell injury contributing to tubular obstruction and back leak.
How can patients prevent kidney stones?
• Increasing urine output to 2.5 L or more daily • Avoiding colas and other soft drinks • Avoid dietary oxalate: chocolate, beets, nuts, rhubarb, spinach strawberries, tea,wheat bran, okra• Eat less animal protein • Limit sodium intake • Specific to calcium stones: maintain calcium intake of 1000-1200 mg/day
What happens in the Initiation Phase of AKI?
• Phase of reduced perfusion or toxicity in which renal injury is evolving• Usually, it lasts 24-36 hours• Prevention of injury is possible in this phase.
What are the other goals of treatment of kidney stones?
• Promote stone passage - increasing urine flow rate with high fluid intake • Reduce size of stones already formed or remove them: through percutaneous nephrolithotomy,ureteroscopy; laser lithotripsy to fragment stones for excretioninto urine • Prevent new stones from forming - adjust urine pH dependent upon stone labanalysis. • Emergencies occur when obstructing kidney stones are present AND a proximalurinary tract infectionrequires emergent decompression, stone removal and IV antibiotic
What are some differentials for kidney stone?
• Pyelonephritis • Peritonitis • In females: Ovarian torsion, ovarian cyst, ectopic pregnancy
When do you refer out for AKI?
• Refer to nephrologist if patient has signs of AKI that have not reversed over 1-2 weeks without uremia • Refer to urologist if patient has signs of urinary tract obstruction
Causes of euvolemic hyponatremia
• SIADH - most frequent cause • Use of diuretics • Renal failure both acute and chronic • Moderate to severe hypothyroidism • Water ingestion exceeding excretion
Define hypernatremia
• Serum Na greater than 146 mEq/L and represents a state of hyper osmolality • Always indicates hyper osmolality or a deficit of total body water • May also be caused by a primary Na gain in addition to a water deficit which is more common It is a "water problem" - either excess water loss or inability to acquire water. More common in debilitated elderly, infants, handicapped
When would you admit a pt for kidney stones?
• Stone > 5 mm (stones < 5 mm will likely pass spontaneously) • Uncontrollable nausea/vomiting • Requiring parenteral pain medication • Pyelonephritis/UTI Geriatric
What happens in the Recovery Phase of AKI?
• The interval when renal injury is repaired, and normal renal function is re-established • GFR returns toward normal, but the regenerating tubules cannot concentrate the filtrate • Diuresis is common (3-4 Liters/day) during this phase with decreased creatinine and urea levels and an increase increatinine clearance • Polyuria can result in excessive loss of sodium, potassium and water. • Fluid and electrolyte balance requires careful maintenance
What can cause hyperphosphatemia?
- Decreased renal excretion, acute or chronic renal failure i. GFR is usually less than 25 ml/min ii. This is the most common cause of persistent hyperphosphatemia iii. Hyperphosphatemia has been associated with increased mortality and morbidity - Redistribution of phosphorous from cell to extracellular fluids i. Tumor lysis syndrome: post chemotherapy for leukemia or lymphoma ii. Rhabdomyolysis or crush injury iii. Acute respiratory acidosis, metabolic acidosis and hypoinsulinemia reduce phosphorous flux into the cells and contribute to the hyperphosphatemia sometimes seen in DKA - Increased intestinal absorption/increased intake - mostly seen in the setting of impaired renal function i. Use of phosphate containing salts or cathartics ii. Vitamin D therapy especially in renal failure/insufficiency iii. Occasionally hypoparathyroidism and pseudo hypoparathyroidism reduce renal phosphorous clearance as well
What kind of symptoms may you see in a patient with a Na greater than 160?
- If it develops acutely may see stupor and coma. If it is chronic elevation, will see moderate to severe CNS symptoms
What kind of symptoms may you see in a patient with a Na between 151-160?
- depends on the time frame of development. If acute you may see nausea, weakness, lethargy, confusion. If there is a chronic condition, there may be no or mild CNS symptoms
What are three criteria for AKI?
-An absolute increase in serum creatinine by 0.3mg/dL or more within 48 hours -or a relative increase of at least 1.5 times baseline that is known or presumed to have occurred within a 7-day period -or a urine volume < 0.6 mL/kg/hr for > 6 hours
What other tests can be done for hypernatremia?
-Serum ADH may be helpful. -Water deprivation test: 1. Withhold all fluids 2. Monitor BP, Na and UOsm then when UOsm is nearly constant with a less than 30mOsm/L change for 2-3 hours administer AVP or DDAVP per protocol. 3. Measure urine volume and UOsm after 1 hour. Central DI will show an increase in UOsm to 600- 700 mOsm/L. Nephrogenic DI will have little or no increase in UOsm
What is the treatment for hypophosphatemia?
-Tx Vit D deficiency first - PO Neutra phos or K-Phos Neutral. 1-2 grams PO daily in divided doses -For severe deficits: IV options include a solution of sodium or potassium phosphate 2 mg phosphorous/kg in ½ NS over 6 hours. For a higher dose, give 5 mg/kg over 12 hours. -Monitor for ongoing losses and treat underlying cause
You have a patient with a Na less than 120 and they're experiencing seizures and/or coma. What fluid do you use? How fast can you bring up the Na? To what level should you bring the Na to?
-Use 3% hypertonic saline -increase serum Na by only 1-2 mEq/L/hr until Na rises by 12-15 mEq/L OR to a level of 120 mEq/L -Max correction rate is 8-12 mEq/L/24 hr or 25 mEq/L/48 hrs
How do you calculate estimated water deficit?
0.4 x Body wt. (kg) x {(serum Na/140)-1} - Replace water at rate calculated to reduce serum sodium by approximately 1mEq/L in acute hypernatremia. In chronic, reduce serum sodium by half of excess above 140 mEq/L over 24 hours -Oral rt preferred if pt conscious. DC excessive NS infusions.
What infusion would you administer for lactic acidosis?
0.9% NS. It's more effective than NaHCO3 drip. *Maintain tissue perfusion!
What is the treatment for patients with chronic hypercalcemia?
1) Prednisone 40-80 mg/day orally, this is best for hypercalcemia due to sarcoidosis, hypervitaminosis D or lymphoma 2) Furosemide (Lasix) 40-80 mg oral BID 3) Reduced calcium diet of 750-1000 mg daily 4) If patients have primary hyperparathyroidism, the decision to treat medically or surgically should be based on the fluctuations in their calcium levels. Medical therapy may be reasonable unless the patient has no obvious clinical sequelae or if they are not a surgical candidate although surgical intervention has a high success rate (95%) and a low mortality rate, if the patient does not have multiple comorbidities
The mnemonic for the management of AKI is ABCDE-IT. It's a lot of info, so what does the ABCDE part stand for?
1. Assess for acute complications (increased K, acidosis, fluid overload- correct abnormalities) 2. BP check (If SBP < 110, consider fluid challenge) 3. Catheterize (to eliminate post bladder obstructive process if present, monitor I & O) 4. Drugs: Discontinue any nephrotoxic agents, hold ACE-I. Exclude obstruction (consider renal ultrasound)
What is the treatment for a patient who is asymptomatic or has chronic hypocalcemia?
1. Calcium carbonate or other calcium salt. They must receive 2-3 grams elemental calcium a day in divided doses; start with calcium carbonate 500 mg by mouth 3-4 times a day. Total daily dose should be 1.5 grams per day. Patients will need docusate 250 mg PO BID and or Senokot 8.8 - 17.6 mg by mouth daily along with adequate fluid intake. 2. Vitamin D oral preparation. Choices include ergocalciferol (Drisdol) 50,000-200,000 U orally or IM once a day. Can also use calcitriol (Rocaltrol) 0.5-2 mcg/day 3. Watch the pt closely for the development of hypercalcemia during calcium supplementation. If it occurs, discontinue both calcium tablets and Vitamin D, monitor serum calcium until a decline is efficient. Then restart both at a lower dose. If the patient was only treated with calcitriol, then the hypercalcemia should resolve in a week.
What are the steps in diagnosing an acid/base disorder?
1. Examine pH. Is it an acid or base? 2. Look at PaCO2 and HCO3 to find abnormal value. EX: ACIDEMIA: Decreased HCO3 = met acidosis Increased pCO2 = resp acidosis ALKALEMIA: Elevated HCO3 = met alkalosis Decreased pCO2 = resp alkalosis Combined or mixed acid-base disorders - present when BOTH pCO2 and HCO3 are abnormal causing alterations in the pH. o For Combined Respiratory and Metabolic Acidosis - PaCO2 is elevated and the HCO3 is decreased. Too much acid and too little base in the blood causes an acidotic pH level,and the result is combined respiratory and metabolic acidosis. o For Combined Respiratory and Metabolic Alkalosis - PaCO2 level is decreased and the HCO3level is elevated. Too little acid and too much base cause alkalosis. STEP 3 - Determine whether compensation is appropriate. The compensatory mechanism is our body's way of trying to fix the abnormal pH. STEP 4 - Determine the anion gap. The anion gap is a way of demonstrating the accumulation of unmeasured anions. Certain forms of acidosis are characterized by these unmeasured anions. STEP 5 - Assess the delta gap - To maintain a stable total anion content, every increase in an unmeasured anion should be met with a decrease in HCO3. Comparing the change in the AG with the change in the HCO3 is a simple way of making sure that each change in the AG is accounted for. If the delta anion gap= delta HCO3, this is a simple anion gap metabolic acidosis. If the delta anion gap >delta HCO3, the HCO3 did not decrease as much as expected. This would be considered a metabolic acidosis and an anion gap metabolic acidosis.
How do you treat hypermagnesemia?
1. In all cases of Hypermagnesemia, stop all PO and IV intake 2. If the patient has ECG changes give 10% calcium gluconate 1-3 grams or Calcium chloride 500-1000 mg, Furosemide (Lasix) 40 mg IV plus ½ NS 50-100 cc/hr 3. Hemodialysis may be necessary for patients with ECG changes if the mag level is > 4.0 mEq/L 4. Symptomatic Hypermagnesemia: Prompt supportive therapy is critical including mechanical ventilation for respiratory failure and/or a temporary pacemaker for severe bradycardia. 5. In all cases, once the etiology has been determined, prevention and patient education is key
Your patient has an AG metabolic acidosis from ingesting either methanol or ethylene glycol, what infusions would you order?
1. Infuse ethanol to maintain blood level at 100-150 mg/day limits acid metabolites 2. Fomepizole 15 mg initial infusion then 10 mg q 12 hr.; limits acid metabolites *Dialysis indicated for severe intoxications; toxic levels greater than 50 mg/dl
What imaging studies might you order for AKI?
1. KUB (Kidney, ureter, bladder) x-ray of abdomen- to rule out stones and presence of two (2) kidneys 2. Renal ultrasound- should be performed on most patients with AKI to rule out obstruction and determine post-void residual; also helpful in diagnosing extra-renal causes of obstruction (pelvic tumors) 3. CT or MRI renal protocol may be required- withhold any contrast media due to renal function
The normal range of phosphorous is 2.5-4.5 mg/dL. At what level is it considered to be a severe deficit?
1.5 mg/dL The general population may have asymptomatic hypophosphatemia found on routine labs. The incidence is 1%. Incidence increases with inpatients with up to 5% of all hospitalized patients exhibiting this abnormality. The prevalence increases to 30-50% in alcoholic patients and patients with severe sepsis or trauma and patients with diabetic ketoacidosis.
How many grams of dextrose a day should be given in maintenance IV fluids?
100-150 g of dextrose a day is recommended to add to maintenance IV fluids to minimize protein catabolism and prevent starvation ketosis.
For every increase in body temperature of 1 degree above 37 degrees C, there is a _____% increase in oxygen consumption.
13%
How many mEq of Na is are in 0.9% NaCl?
154 mEq When ordering maintenance fluids, it is customary to provide 75-175 mEq Na+ /day as NaCl. This is equivalent to a 2Gm sodium diet that a patient would consume. If the renal function is compromised, this amount is decreased to 20-60 mEq/day.
What percentage of nephrons are lost by the age of 80?
20%
How many hours must you stop antivirals before contrast study?
48 hrs. Can cause nephropathy
What is the mortality rate of oliguric AKI in elderly patients?
50%
The mnemonic for the management of AKI is ABCDE-IT. It's a lot of info, so what does the IT part stand for?
6. Investigate: UA with micro, labs 7. Treat the cause. • Nephrology consult • After AKI is diagnosed management is primarily supportive in nature. • Therapy may include catheter drainage, urethral stents, or percutaneous nephrostomy if obstructive etiology is present .• Treat underlying cause • Correct fluid, electrolyte, and uremic abnormalities- IV 0.9NS should be used to maintain euvolemia as clinically indicated • Prevent complications: • Nutritional deficiencies § AKI pts are in a catabolic state; therefore, they can easily become nutritionally deficient § Total caloric intake: 30-45 kcal/kg/day - primarily from lipids and carbohydrates § Non-dialysis patients - protein restriction to < 0.6gms/kg/day § HD pts - protein intake should be < 1 grams/kg/day § Low K+ and low Na+ diet • Hyperkalemia- K > 5.5 mEq/L or EKG changes consistent with hyperkalemia (i.e., peaked T waves, loss of P-waves, QRS widening); consider kayexalate or IV administration of Calcium (10ml in 10% solution of calcium gluconate) for temporary reversal of neuromuscular effects of hyperkalemia. § K+ can be temporarily shifted into the intracellular compartment with the use of IV insulin (10units) and glucose (25gms), inhaled beta-agonist, or IV sodium bicarbonate (150mEq in 1L D5W)- if metabolic acidosis is present § HD is the definitive treatment in patients with significantly elevated K+ levels and renal failure. • Acidosis - treated IV or orally with sodium bicarbonate when serum HCO3 is less than 15mEq/L or pH is lower than 7.2 and plasma bicarbonate (8-10 mEq/L) • Adjust I&O based on fluid status. Take the use of diuretics into consideration since most patients are overloaded .• The volume depleted patient is usually resuscitated with 0.9NS • Maximize cardiac function and maintain optimal BP for renal perfusion. • DC offending medications: ACE-I, ARB, NSAIDs, etc. • INDICATIONS for HD: o Between 20-60% of patients with AKI need short term dialysis o Indications for HD included: uncontrolled hyperkalemia, severe metabolic acidosis, severe volume overload, encephalopathy, and pericarditis o A pericardial friction rub is a sign of uremic pericarditis; It is an indication for HD as it can lead to pericardial tamponade.
Where is most of dietary phosphate absorbed?
80% of dietary phosphate is absorbed in the small intestine.
How do you many a patient with metabolic alkalosis?
A. Volume depleted states: IV 0.9% NS at 100-150 ml/hr. Metabolic alkalosis states are most effectively treated with saline resuscitation until euvolemic is achieved. The increase in filtered chloride leads to improved renal handling of the bicarbonate load. These are chloride responsive. B. KCL replacement for all potassium depleted or potassium losing states C. Chloride unresponsive metabolic alkalosis does not respond to NS administration and is often associated with a normal or expanded ECF volume. a. Mineralocorticoid excess can be managed with a potassium sparing diuretic (amiloride or spironolactone)and replacing the potassium deficit b. The alkalosis caused by excessive alkali administration will respond when the medication is discontinued c. Acetazolamide (Diamox), 250-500 mg IV or PO BID; especially useful in volume expanded states. This therapy promotes bicarbonaturia although you will see an effect on lowering potassium levels also. D. Metabolic alkalosis caused/induces by excess aldosterone states may require spironolactone or eplerenone E. Severe alkalemia (pH > 7.70) with ECF volume excess and/or renal failure can be treated with isotonic (150 mEq/L) HCl through a central vein only. F. Hemodialysis against a low [HCO3 -] bath