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120 Cards in this Set
- Front
- Back
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What is the more significant problem with hyponatremia - excess water or decreased sodium?
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Excess water
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What are the three general processes that aid in excreting a water load?
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Water filtration
ADH inhibition Urine dilution |
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What are some disorders in which ADH levels may be suppressed?
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Advanced renal failure
Primary polydipsia (MDMA also) Beer drinker's potomania |
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What are some causes of hyponatremia with normal/elevated plasma osmolality?
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High plasma osmolality: Hyperglycemia, mannitol
Normal plasma osmolality: Pseudohyponatremia (Hyperlipidemia, Hyperproteinemia), Glycine solutions |
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What are some causes of renal sodium loss?
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Diuretic agents
Osmotic diuresis (glucose, urea, mannitol) Adrenal insufficiency Salt-wasting nephropathy Bicarbonaturia (renal tubular acidosis, disequilibrium stage of vomiting) Ketonuria |
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What are some causes for extrarenal sodium loss?
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Diarrhea
Vomiting Blood loss Excessive sweating Fluid sequestration (bowel obstruction, peritonitis, pancreatitis, muscle trauma, burns) |
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In what disorders is ADH elevated?
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Depletion of circulating volume - true volume depletion, heart failure, cirrhosis, thiazide diuretics
SIADH Hormonal changes - adrenal insufficiency, hypothyroidism, pregnancy |
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What causes increased volume of extracellular fluid, low sodium, and low serum osmolarity?
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CHF
Cirrhosis Nephrotic syndrome Renal failure (acute, chronic) Pregnancy |
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What are some causes of hyponatremia, low serum osmolarity, and normal fluid volume?
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Thiazide diuretics
Hypothyroidism Adrenal insufficiency SIADH Cancer - pulmonary, mediastinal, extrathoracic CNS - acute psychosis, mass lesions, inflammation, stroke, hemorrhage, trauma Drugs (SSRI, TCA, Opiates) Pulmonary conditions - infections, acute respiratory failure, positive-pressure ventilation Postoperative state Pain Severe nausea HIV infection Beer potomania, tea-and-toast diet |
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How does the brain respond to hyponatremia?
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The rapid response is the brain swells, so it excretes sodium, chloride, and potassium.
The slow response involves the brain excreting its organic electrolytes As the hypotonic state is slowly corrected, the brain regains its original balance of electrolytes and fluid. |
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How would you treat recent hyponatremia different from chronic (1+ week) hyponatremia, with regard to the brain?
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In recent hyponatremia, the brain has adapted by excreting its ionic electrolytes, which easily diffuse back into the brain when the correct electrolyte balance is infused.
In chronic hyponatremia, the organic electrolytes have also been excreted, which take a lot longer to diffuse back in, so if you administer the correct solution too quickly, the brain may lose fluid - leading to osmotic demyelination. |
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What are the symptoms of hyponatremia?
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Decreased appetite
Weakness, fatigue Impaired Gait Disorientation Nausea and vomiting Headache Seizures Lethargy |
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What laboratory tests are usually ordered for a patient with hyponatremia?
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Serum and Urine osmolarity
Chem 10 panel Urine electrolytes FENa Cortisol TSH |
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What kinds of imaging studies may be useful in a patient with hyponatremia?
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CT brain, MRI brain
CXR, Chest CT |
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How would one treat hyponatremia with contracted extracellular fluid volume?
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0.9% saline solution - results in clinical and biochemical improvement
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In hyponatremia with contracted ECF volume, what is the...
...serum osmolarity (relative)? ...urine osmolarity? ...urine volume (relative)? ...urine sodium concentration? |
Serum osmolarity is low
Urine osmolarity is > 500 Urine volume is usually decreased Urine sodium concentration < 20 |
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In hyponatremia with (near-)normal ECF volume, what is the...
...serum osmolarity (relative)? ...urine osmolarity? ...urine volume (relative)? ...urine sodium concentration? |
Serum osmolarity is low
Urine osmolarity is > 100 Urine volume varies with intake Urine sodium concentration > 40 |
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If the ECF is (near-)normal and there is hyponatremia, would a 0.9% saline solution be beneficial?
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Either no change or there would be worsening hyponatremia
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In hyponatremia with expanded ECF volume, what is the...
...serum osmolarity (relative)? ...urine osmolarity? ...urine volume (relative)? ...urine sodium concentration? |
Serum osmolarity is low
Urine osmolarity > 100 Urine volume is usually decreased Urine sodium concentration < 20 |
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If the ECF is expanded and there is hyponatremia, would a 0.9% saline solution be beneficial?
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There would be little change in hyponatremia, and worsening of edema
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What are some of the general principles behind treating hyponatremia?
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Recognize mild hyponatremia may be symptomatic
Ensure the right diagnosis - etiology may be multifactorial Therapy may be diagnostic and therapeutic (volume challenge) Proportionality 3% saline and aquaretics require hypotonicity Volume restriction alone is substandard treatment |
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What are the treatment principles for hyponatremia when a patient presents in a very ill condition?
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It is usually acute hyponatremia <24-48h
There are substantial symptoms and brain hasn't yet adapted Increase Na quickly with 3% saline - 1-2mEq/L until no more symptoms. If seizing administer 1 amp NaHCO3 Some water restriction Address underlying etiology |
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What are some treatment principles when a patient presents with hyponatremia and is not very symptomatic?
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Usually chronic hyponatremia > 24-48h
Mild-no symptoms, brain volume adaptation has occurred Treat based on diagnosis: Volume depletion, hypervolemia, isovolemia |
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How do you treat a patient with hyponatremia from tea-and-toast diet?
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Increase solute intake
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How do you treat a patient with psychogenic polydipsia?
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Restrict fluids, then administer fluids once ADH has reset itself
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How do you treat a patient with SIADH?
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Treat underlying cause
Demeclocycline and Aquaretics can be useful |
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A 25 yo f presents with fatigue, mild nausea, 1 week of prolonged diarrhea
VS: 95/50, 110, 99.9, 20, 98% Neck veins flat, fast HR, regular rhythm, soft abdomen Patient lethargic, falls asleep easily Na 120, BUN/Cr 32/1.4 What is a possible etiology and treatment? |
Volume depletion
Administer saline until sodium recovers |
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How does hyperglycemia affect sodium levels?
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Hyperglycemia causes a reduction in sodium levels
For every 100 increase in glucose > 100-400, sodium decreases by 1.6 For every 100 increase in glucose > 400, sodium decrease by 2.4 |
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How does excess protein cause isotonic hyponatremia?
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When total protein is higher, the serum has less water, causing the perceived hyponatremia
Treat the underlying condition to correct hyponatremia |
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With hyponatremia and hypernatremia, is the problem with varying levels of salt or varying volumes of water?
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Varying volumes of water
Hyponatremia - too much water Hypernatremia - too little water |
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What happens to the brain if it has adapted to chronic hypernatremia and you try to correct by rapidly administering hypotonic fluid?
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The brain will swell - causing cerebral edema
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What are some causes for hypertonic sodium gain?
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Hypertonic sodium bicarbonate infusion
Hypertonic feeding preparation Ingestion of NaCl or sea water Sodium-chloride rich emetics Hypertonic saline enemas Intrauterine injection of hypertonic saline Hypertonic NaCl infusion Hypertonic dialysis Primary aldosteronism Cushing's syndrome |
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What are some symptoms of hypernatremia?
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Decreased appetite
Fatigue, weakness, impaired gait Disorientation, N/V, headache Lethargy Seizures Polydipsia, Polyuria |
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How is hypernatremia diagnosed?
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Usually evident by history
Usually an inpatient issue, or outpatient with no access to water Typically only occurs when the patient has a free water loss AND inability to replenish supply. |
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What are the hypernatremia treatment principles?
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No more than 10 mEq/L change in 24h
Correct the water deficit Decrease free water loss |
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How do you calculate the free water deficit?
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Water deficit
Man: 0.6[(Actual Na - Desired Na)/Desired Na] Woman: 0.5[(Actual Na - Desired Na)/Desired Na] |
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When administering water to correct a water deficit, is it better IV or PO (through GI system)?
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Through GI system
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What are some ways to prevent further water loss in a patient with hypernatremia and water deficit?
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Administer water
Ddavp Thiazide type diuretic Non-steroidal |
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How do you identify solute diuresis as the cause for polyuria?
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Solute excretion is > 1200 mosm/day
NaCl, NaHCO3, Urea, Glucose |
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How do you identify water diuresis as the cause for polyuria?
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Solute excretion < 600 mosm/day
Nephrogenic DI, Central DI (Urine osmolarity <300 mosm/day) Psychogenic polydipsia (Urine osmolarity <100 mosm/day) |
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With Central DI, what will be the results of a water deprivation test?
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Patient may become hypernatremic
Urine osmolarity > 300 (generally) Urine osmolarity increases > 50%after ddavp (incomplete) |
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With Nephrogenic DI, what will be the results of a water deprivation test?
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May become hypernatremic
Urine osmolarity < 300 (generally) Urine osmolarity increase < 50% with ddavp (incomplete) |
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How do changes in potassium affect sodium?
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Loss of potassium in ECF causes movement of potassium out of the ICF
Must be balanced by movement of cations (H+, Na+) into the ICF Entry of sodium in the ICF decreases ECF concentration, and thus plasma concentration |
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What is a cause of "spurious" hyperkalemia?
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Spurious hyperkalemia is artifactual or pseudo-hyperkalemia caused by improper handling of the blood
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What are the most common causes for true hyperkalemia?
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Renal impairment causing decreased potassium excretion
Drugs that interfere with potassium excretion Shift of potassium from ICF - hyperinsulinemia, hyperglycemia, metabolic acidosis |
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What is the most common form of impaired aldosterone function?
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Hyporeninemic hypoaldosteronism
Most common in advanced forms of diabetic nephropathy |
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How does diabetes cause hypoaldosteronism?
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The kidneys become damaged with diabetes, causing decreased renin production, and thus decreased secretion of K and less aldosterone.
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What are some ECG signs of hyperkalemia?
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Prolonged PR interval
Wide QRS Tall tented T waves |
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How does diabetic ketoacidosis affect potassium levels?
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Hyperkalemia may occur because there is hyperglycemia and lack of insulin.
Total body potassium is depleted due to prior urinary loss of K. Serum potassium levels can fall precipitously when insulin and IV fluids are commenced. |
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What are the most common causes of hypokalemia?
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Use of diuretics followed by increased GI loss
Loop diuretics GI loss - diarrhea, laxative abuse Decreased dietary intake may play a slight role |
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What are some special situations which may cause hypokalemia?
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Primary hyperaldosteronism
Renal tubular acidosis, types 1 and 2 |
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What can cause a shift toward more acidic in a patient with hypokalemia?
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Insulin
Catecholamines Periodic paralysis Thyrotoxic periodic paralysis |
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What are some causes for acidosis in hypokalemia?
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Renal tubular acidosis
Diarrhea Laxative abuse Villous adenoma Ureterosigmoidosctomy Carbonic anhydrase inhibitors |
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What would cause hypokalemia, alkalosis, unchanged or increased ECV, and increased aldosterone and renin?
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Renal artery stenosis
Renin tumor Malignant hypertension |
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What would cause hypokalemia, alkalosis, decreasd ECV, and low urine chloride output?
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Vomiting
Remote diuretic use Cystic fibrosis |
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What would cause hypokalemia, alkalosis, decreased ECV, and high urine chloride output?
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Diuretics
Bartter's Gitelman's Gentamicin HypoMg |
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What would cause hypokalemia, alkalosis, unchanged or increased ECV, increased aldosterone and decreased renin?
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Primary hyperaldosteronism - BAH, adenoma
Glucocorticoid remediable hyperaldosteronism |
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What would cause hypokalemia, alkalosis, unchanged or increased ECV, and decreased aldosterone and renin?
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Liddle's (amphotericin)
Apparent mineralocorticoid excess Hypomagnesemia Cushing's Hydroxylase deficiency |
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What are two of the primary symptoms/signs of hypokalemia?
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Muscle weakness
Paresthesias |
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What are the primary risks associated with hypokalemia?
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ECG changes once K+ < 3.0 MeQ/L
Changes in ST depression, prolongation of the QT interval, U waves |
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How is hypokalemia treated?
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IV fluids if K+ < 2.4mEq/L - there is reduced rate when patient is stable. Monitor serum potassium closely.
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Why is FENa < 1% in prerenal ARF but >1% in acute tubular necrosis?
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In prerenal ARF, sodium is being rapidly reabsorbed to try to restore intravascular fluid volume. Consequently, patients with prerenal ARF have FENa < 1%
In ATN, it is a similar situation but the damage to the tubules makes it more difficult to reabsorb sodium, so it's typically > 1-2% |
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What is the benefit of FENa in differentiating intrinsic and prerenal ARF?
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It is the most sensitive renal failure index - it relates sodium clearance to creatinine clearance.
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Why is urine osmolarity/osmolality > 500 mOsm/kg in prerenal failure, but < 350 in intrinsic renal failure?
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In prerenal disease, volume depletion stimulates release of ADH, resulting in highly concentrated urine when the tubules are intact.
In ATN, the ability to concentrate urine is impaired because the medullary cells in the thick ascending limb are the first to be damaged by renal ischemia. So the osmolality/osmolarity is lower. |
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What criteria must be present before placing a patient on dialysis?
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Presence of uremic symptoms
Presence of hyperkalemia unresponsive to conservative measures Persistent ECV expansion despite diuretic therapy Acidosis refractory to medical therapy Bleeding diathesis Creatinine clearance or GFR below 10 mL/min per 1.73m^3 |
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What are the treatment options in end stage renal disease?
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Hemodialysis
Peritoneal dialysis (as continuous ambulatory peritoneal dialysis or continuous cyclic peritoneal dialysis) Transplantation |
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What is the most common treatment for patients in ESRD?
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Hemodialysis
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What are the three effects of parathyroid hormone on the kidney?
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Promotes reabsorption of calcium in the distal nephron
Inhibits reabsorption of phosphate in the proximal tubule Promotes hydroxylation which activates vitamin D, and then stimulates intestinal uptake of calcium |
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How does kidney failure change the way it reacts to parathyroid hormone?
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When the kidney fails, it is less reactive to PTH, so there is more uptake of phosphate, and less uptake of calcium.
PTH begins mobilizing calcium from the bones in order to maintain calcium levels in the blood |
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What is osteomalacia?
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Accumulation of demineralized bone matrix due to Vitamin D deficiency and metabolic acidosis. Vitamin D deficiency results from the kidneys’ declining ability to convert calcitriol, the active Vitamin D metabolite, from circulating Vitamin D.
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What is Adynamic Bone Disease?
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Loss of bone volume - a form of osteoporosis due to suppression of PTH in Stage 5 CKD in association with medications to lower serum phosphate and raise calcium
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How is Chronic Kidney Disease staged?
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Based on GFR - stage 0 has a GFR of 90, while stage 5 has a GFR < 15 (or patient is on dialysis)
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What are some risk factors for kidney failure?
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Long-term hyperglycemia
Uncontrolled hypertension Proteinuria Cigarette smoking Dyslipidemia Family History African American, Native American, Hispanice |
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What is the #1 cause of end-stage renal disease leading to dialysis or transplant?
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Diabetic Nephropathy
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What are factors that contribute to the development of diabetic nephropathy in Type 2 DM?
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Related to the duration of DM and degree of glucose elevation
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What percentage of diabetics develop ESRD?
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20-40%
Lower risk in Type 2 vs Type 1 (about 20% overall) but Type 2 is more common so there are more cases of nephropathy from Type 2. |
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What other condition associated with diabetes is usually present with diabetic nephropathy?
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Diabetic retinopathy
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Compare Type 1 and Type 2 DM nephropathy diagnosis.
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In Type 1 DM - microalbuminuria rarely present at diagnosis, and predictive of nephropathy and progression. BP usually normal.
In Type 2 DM, microalbuminuria may be present at diagnosis but is less predictive of progression - HTN is common comorbidity. |
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Is microalbuminuria more predictive of nephropathy progression in Type 1 or Type 2 DM?
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Type 1 DM
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How does elevated glucose affect the kidneys?
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Hyperglycemia - increased formation of diacylglycerol which activates PKC, affecting synthesis of endothelial cell collagen and matrix protein - endothelium is more susceptible to injury
Glycosuria - there is enhanced glucose reabsorption, ECFV expansion, atrial natriuretic peptide causes sodium excretion by afferent arteriolar dilation, with increased glomerular pressure, increased GFR. Chronic glomerular hypertension leads to GBM thickening, and glomerulosclerosis. |
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Describe the stages of diabetic nephropathy in...
...early DM ...first 5 years ...5-10 years ...10-15 years ...20+ years |
Early DM - glomerular hyperfiltration - elevated GFR, often above 150 mL/min - renal hypertrophy
First 5 years - thickening of GBM, glomerular hypertrophy, mesangial expansion from ECM accumulation 5-10 years - microalbuminuria (30-299 mg/d) - this is below limit for urine dipstick test, tight control of BP and glucose can delay onset 10-15 years - overt proteinuria > 300 mg/d - continued GBM thickening and mesangial matrix expansion - glomerular sclerosis HTN usually present, progressive decline in GFR 20+ years - renal failure - renal replacement therapy (dialysis, transplant) |
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What are three methods for screening for Microalbuminuria?
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Random urine sample (recommended method) - albumin:creatinine ratio 30-299 mg/d
On a 24 hour urine protein collection - 30-299 mg/d On a timed collection - 20-199 mcg/min |
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What hematology test is useful for determining blood glucose?
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HbA1C should be < 7% - indicates how well blood glucose is controlled
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What are some preventive measures for diabetic nephropathy?
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Control blood pressure - goal is < 130/80
Estimate GFR yearly Screen microalbuminuria annually Smoking cessation Control lipids Protein restriction |
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How does glycemic control help prevent or slow diabetic nephropathy?
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Reduces risk of nephropathy by 54%
Reduced microvascular complications by 25% Reduced microalbuminuria by 33% |
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How does protein restriction prevent or slow diabetic nephropathy?
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Reduces intraglomerular pressure, hyperfiltration, and microalbuminuria at early stages
Several small studies suggest a 75% reduction in progression of moderate nephropathy in Type 1 patients Recommendation is <0.8 gm/kg (or below 10% of daily caloric intake) |
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How are comorbidities measured in diabetic nephropathy?
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Microalbuminuria is a marker for increased risk of CAD
Screening for CAD is important Hypertension is another comorbidity - so manage BP, medications |
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How is BP controlled in diabetic nephropathy?
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BP control reduces progression of proteinuria
Captopril (ACE-I), and atenolol (BB). ACE-I and ARBs are treatments of choice for hypertension in diabetes and can prevent or delay progression of diabetic nephropathy. |
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How is renal failure managed?
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Renal transplant
Dialysis - may be difficult in patients with diabetic autonomic neuropathy, since have trouble tolerating fluid shifts 20-30% annual mortality, mainly from accelerated atherosclerosis Type 1 DM requires combined renal/pancreas transplant |
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How is spironolactone used to treat diabetic nephropathy?
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MoA - antagonist of aldosterone receptor in distal tubule
Reduces 24h albumin excretion by 33% Blood pressure also reduced |
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What are some goals of OMT in treating chronic kidney disease, or diabetic nephropathy?
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Improve renal circulation
Reduce congestion Prevent facilitated segments Balance SANS and PANS (secondary improvement) Focus indirect treatments on T10-L2 |
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What are the clinical manifestations of UTI in the neonate?
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Fever
Temperature instability Poor feeding Jaundice Hypotonia, irritability Poor urinary stream - males |
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What are the clinical manifestations of UTI during infancy?
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Fever
Weight Loss FTT Vomiting Diarrhea Feeding problems Irritability |
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What are some clinical manifestations of UTI in the 2-5 year old?
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Fever
Vomiting Diarrhea Abdominal pain +/- Dysuria +/- Frequency +/- Urgency Enuresis |
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What are the symptoms of UTI in school aged children?
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Symptoms more classic, reliably related to the GU system
Dysuria Frequency Urgency Abdominal and/or flank pain Enuresis |
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What are some characteristics of UTI noted in the physical exam?
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Growth parameters
Blood pressure Abdominal exam - masses, suprapubic or flank tenderness GU exam Rectal exam (sometimes) Neurologic exam |
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What are some other conditions included in the DDx for Dysuria besides UTI?
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Urethritis
Diaper rash Vulvovaginitis Masturbation Pinworms Hypercalcuria Sexual abuse |
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How is a UTI diagnosed using laboratory tests?
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CMS urine - greater than 100,000 colonies/mL of a single organism - diagnostic 90-95%
Catheteirzed urine - greater than or equal to 10,000 colonies/mL Suprapubic aspiration - any growth Pyuria or hematuria - nondiagnostic Nitrites - highly suggestive Leukocyte esterases - less suggestive Bag urine specimen |
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What are the two most common pathogens that cause UTIs in children/infants?
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Escherischia coli
Staphylococcus saprophyticus |
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What is the incidence of bacteremia associated with UTI in neonates, 1-3 months, and 3-8 months?
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31% of Neonates with UTI
18% of 1-3 month olds with UTI 6% of 3-8 month olds with UTI |
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How are UTIs treated in patients less than 2 months old or who are obviously toxic?
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Consider hospital, antibiotics
Less than 2 months - ampicillin/gentamicin or ampicillin/cefotaxime Infants and older children - 3rd generation cephalosporin Hydration |
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If a patient has a UTI and is over 2 months and is not toxic, what kind of treatment protocol is used?
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IM Ceftriaxone once or until afebrile, then complete with 10-14 days of PO antibiotics
May also do only PO ABx 10 day course with observation |
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How are older children with UTIs treated who have no systemic symptoms?
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Empiric PO ABx
TMP-SMZ Amoxicillin with or without Clavulanic acid Cephalosporins Hydration |
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How are UTIs followed up?
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Repeat UA and Urine Culture 48-72 hours after treatment has begun, if still symptomatic
48-72 hours after treatment is completed 1 month after treatment is completed. q3 months for one year |
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What is the recurrence rate for a single UTI incident within the first year?
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25-30%
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What is the recurrence rate if the patient has 2 UTIs?
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60-75%
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When should the urinary tract be imaged following a UTI?
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All males and infants with first UTI
All children with clinical evidence of pyelonephritis with first UTI FIrst UTI in females over 1 year old with...history of abnormal voiding pattern, FTT or short stature, elevated BP, abnormal abdominal or genital exam All children with recurrent UTI |
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What are the benefits to doing a renal ultrasound?
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Can identify hydronephrosis or abscesses
Examines the bladder to identify dilated distal ureters, hypertrophy of bladder wall, or presence of ureteroceles or bladder masses |
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What cannot be excluded by an ultrasound?
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Vesicoureteral Reflux (VUR)
Not sensitive for detecting acute renal inflammation |
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What is a voiding cystourethrogram (VCUG)?
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Detects reverse flow of urine from bladder into the ureters (reflux)
Rules out posterior urethral valves in boys Assess bladder function (emptying) Requires catheterization and instillation of contrast media Radiation exposure is significant |
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How does a renal isotope scan work?
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DSMA (dimercaptosuccinic acid) scan
Isotope is taken up by functioning tubules of the kidney Assess renal function and integrity - most sensitive for detecting renal scars Assesses renal function in severe reflux, particularly those that require surgery |
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What is the most sensitive means for detecting renal scars?
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Renal Isotope Scan
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Describe vesicoureteral reflux (VUR)
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A dysfunction of the ureterovesical junction
30-50% of children radiographically evaluated for UTI have VUR There is strong familial tendency Reflux nephropathy causes 15-20% of all ESRD in children and young adults May be primary or secondary to neurogenic bladder, bladder outlet obstruction, vesical calculi, or severe cystitis |
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What are the different classifications of VUR?
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Grade 1 - reflux into nondilated ureter
Grade 2 - reflux into upper collecting system without dilatation Grade 3 - Reflux into dilated ureter and/or blunting of calyceal fornices Grade 4 - reflux into a grossly dilated ureter Grade 5 - massive reflux, ureteral dilatation, tortuosity, loss of calyceal details |
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How do you treat VUR prophylactically?
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With Grade I and II VUR, treated until reflux resolves
If they need RUS and VCUG, treat until evaluation is complete 3-6 months ABx in children with normal urinary tract radiographically but recurrent UTI TMP-SMX (1/2 normal dose), Amoxacillin, nitrofurantoin (1/3 normal dose) |
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How is VUR managed?
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Antibiotic prophylaxis
Serial UA and urine cultures Yearly reassessment - nuclear cystogram Surgery - for grade IV and V reflux, or if other associated anatomic anomalies of ureter (ureteroceles), or multiple UTI despite prophylaxis in lower grade reflux Grade III - may need open surgery or medical management |
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What is Deflux?
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Approved in 2001 - delivers hyaluronic acid/dextranomer gel by endoscope injection
Less effective than open surgery, but may be better than ABx prophylaxis Minimally invasive but requires anesthesia Lack of long term follow-up data |
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What is the success rate of Deflux, with Hyaluronic Acid/Dextranomer Gel?
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Less successful over time, but there is 44-92% (huge range) success rate by 3 months
May be best for children Grades II, III, IV |
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How do you approach a newborn which may have hydronephrosis based on prenatal ultrasounds?
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Repeat RUS after neonate born, with serum creatinine
If that is negative then no worries - if positive, then check with VCUG to rule out reflux. |
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Who else should be evaluated for UT problems via imaging?
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Siblings and offspring of parents with VUR (RUS, VCUG)
33% of siblings, and 75% of offspring have VUR if the mother does. |
