Nephrology and Urology Flashcards
What does RIFLE mean in classification of acute renal failure (ARF) or acute kidney injury (AKI)?
- Risk of renal dysfunction
- Injury to kidney
- Failure of kidney function
- Loss of kidney function (persistent ARF)
- End-stage kidney disease (ESKD) or end-stage renal disease (ESRD)
Risk of renal dysfunction
a. GFR criteria: increased serum creatinine 1.5-fold or GFR decrease more than 25%
b. Urine output (UO) criteria: UO less than 0.5 mL/kg/hr for 6 hours
Injury to kidney
a. GFR criteria: increased serum creatinine 2-fold or GFR decrease more than 50%
b. UO criteria: UO less than 0.5 mL/kg/hr for 12 hours
Failure of kidney function
a. GFR criteria: increased serum creatinine 3-fold or GFR decrease more than 75% or serum creatinine more than 4mg/dL (350 μmol/L) in setting of acute increase of at least 0.5 mg/dL (44 μmol/L)
b. UO criteria: UO less than 0.3 mL/kg/hr for 24 hours (oliguria) or anuria for 12 hours
Loss of kidney function (persistent ARF)
Complete loss of kidney function for more than 4 weeks
End-stage kidney disease (ESKD) or end-stage renal disease (ESRD)
Complete loss of kidney function for more than 3 months
Prerenal causes of ARF (60-70%)
- Hypovolemia
- Hypotension
- Ineffective circulating volume (CHF, cirrhosis, nephrotic syndrome, early sepsis)
- Aortic aneurysm
- Renal artery stenosis or embolic disease
Intrinsic renal causes (25-40%)
- Acute tubular necrosis
- Nephrotoxins (NSAIDs, aminoglycosides, radiologic contrast)
- Interstitial diseases (acute interstitial nephritis, SLE, infection)
- Glomerulonephritis
- Vascular diseases (polyarteritis nodosa, vasculitis)
Postrenal causes (5-10%)
- Tubular obstruction
- Obstructive uropathy (urolithiasis, BPH, bladder outlet obstruction)
Diagnostic Studies to order in ARF
- GFR
- Serum creatinine and BUN
- Urinalysis
- Serum cystatin C
- Urine biomarkers (IL-8 and kidney injury molecule-1 [KIM-1])
- Renal U/S
BUN in diagnosing ARF
- Provides an estimate of renal function, but is much more sensitive to dehydration, catabolism, diet, renal perfusion and liver disease
- Urea is reabsorbed in the nephron during stasis, which causes false elevations of BUN; therefore, this is not a reliable indicator of renal function
Urinalysis in diagnosing ARF
- It is essentially normal in prerenal and postrenal causes of ARF with only a few hyaline casts
- Granular casts, WBCs and casts, RBCs and casts, proteinuria, and tubular epithelial cells indicate intrinsic renal causes of ARF
Serum cystatin C and urine biomarkers in diagnosing ARF
-These are new biomarkers that shows promise for detecting AKI
Prerenal causes blood and urine studies
- Urine sodium <20 mEq/L
- Fractional excretion of sodium (FENa) less than 1%
- Urine osmolality greater than 500 mOsm/kg
- Elevated BUN-to-plasma Cr ratio (20:1)
- Urine specific gravity greater than 1.020
Intrinsic renal causes blood and urine studies
- Increased urine sodium greater than 40 mEq/L
- FENa greater than 1-2%
- Urine osmolality of 300-500 mOsm/kg
- Decreased BUN-to-plasma Cr ratio (<15:1)
- Urine specific gravity of 1.010 to 1.020
Postrenal causes blood and urine studies
Urine sodium, FENa osmolality, and BUN-to-Cr ratio can vary depending on how long the obstruction has been present
What on the renal U/S would indicate a chronic problem in ARF?
A kidney smaller than 10 cm
What are other laboratory findings associated with a loss of renal function?
- Azotemia
- Decreased creatinine clearance
- Metabolic acidosis
- Hyperkalemia
Treatment of ARF involves correction of the underlying problem. What are some examples of that?
- Achievement of normal hemodynamics in prerenal states (IV fluids, improving cardiac output)
- Adjustment and avoidance of medications and nephrotoxic agents in intrarenal states
- Relief of urinary tract obstruction (ureteral stents, urethral catheter) in postrenal states
- Consideration of early intervention under the supervision of a nephrologist or intensivist for management of potential renal replacement therapy
What are some indications for short-term dialysis?
- When serum creatinine exceeds 5-10 mg/dL
- Unresponsive acidosis
- Electrolyte disorders
- Fluid overload
- Uremic complications
What is chronic kidney disease (CKD)?
- Progression of ongoing loss of kidney function (GFR)
- National kidney foundation (NKF) defines CKD as GFR <60 mL/min/1.73 m2 or presence of kidney damage (proteinuria, glomerulonephritis or structural damage from polycystic kidney disease) for ≥3 months
Stages of CKD: Stage 1
Kidney damage with normal GFR greater than 90 mL/min/1.73 m2 body surface area (BSA) and persistent albuminuria
Stages of CKD: Stage 2
Kidney damage with mild decrease in GFR 60-89 mL/min/1.73 m2 BSA
Stages of CKD: Stage 3
Moderate decrease in GFR 30-59 mL/min/1.73 m2 BSA
Stages of CKD: Stage 4
Severe decrease in GFR 15-29 mL/min/1.73 m2 BSA
Stages of CKD: Stage 5
Kidney failure with GFR less than 15 mL/min/1.73 m2 BSA
What generally occurs in stages 1 and 2 of CKD?
The patient is generally asymptomatic without an increase in BUN or serum creatinine; acid-base maintenance is adaptive through an increase in remaining nephron function
What generally occurs in stage 3 of CKD?
He or she may still remain asymptomatic; however, serum creatinine and BUN increase. In addition other hormones (PTH, erythropoietin, calcitrol) become abnormal
What generally occurs in stage 4 of CKD?
The patient may become symptomatic with anemia, acidosis, hyperkalemia, hypocalcemia, and hyperphosphatemia
What generally occurs in stage 5 of CKD?
The patient is a candidate for renal replacement therapy
Common causes of chronic renal failure (4 total)
- DM
- HTN
- Glomerulonephritis
- Polycystic kidney disease
Other causes of chronic renal failure (6 total)
- Primary glomerular diseases (membranous nephropathy, minimal change disease, IgA nephropathy)
- Secondary glomerular diseases (sickle cell anemia, SLE)
- Tubulointerstitial renal diseases (nephrotoxins, infection, multiple myeloma, HIV)
- Chronic pyelonephritis (tuberculosis)
- Vascular diseases (renal artery stenosis or obstruction)
- Obstructive nephropathies (nephrolithiasis, prostate disease, neurogenic bladder)
Diagnostic studies in CKD
- Measurement of GFR (GOLD STANDARD). The Cockcroft-Gault formula or the Modification of Diet in Renal Disease (MDRD) equation will give a fairly accurate prediction of GFR
- Proteinuria and microalbuminuria
- BUN and creatinine
- Serum biomarker cystatin C
- CBC, CMP, UA
Cockcroft-Gault formula
Requires the patient age, body weight and serum creatinine
Modification of Diet in Renal Disease (MDRD) equation
- Requires serum albumin and BUN as well as patient age, body weight and serum creatinine
- MDRD is probably more accurate than Cockgroft-Gault formula
- The MDRD also takes into account gender and ethnicity
How to calculate GFR in children
Use a pediatric GFR calculator
What is proteinuria a marker of?
kidney damage
BUN and creatinine in CKD
These levels will be elevated
Serum biomarker cystatin C in CKD
It is elevated when the GFR is <88 mL/min/1.73 m2 BSA; however, its clinical role has not been defined
Treatment of CKD
- ACE inhibitors and ARBs
- Managing comorbid conditions, including tight hypertensive control, tight glycemic control in diabetic patients, cholesterol-lowering therapy, tobacco cessation, and weight control
- Erythropoietin, iron supplements, and antiplatelet therapy should be considered to maintain hemoglobin and bleeding time as needed
- Medical therapy requires careful drug dosing to adjust for decreased renal function
- Need for hemodialysis, peritoneal dialysis, or kidney transplantation should be coordinated with nephrology service
- Pneumococcal vaccination is recommended
Dietary management of CKD
- Restriction of protein intake
- Adequate caloric intake
- Calcium and vitamin D supplements
- Limitation of water, sodium, potassium and phosphorus
Glomerulonephritis (GN) general characteristics
- Generally refers to damage of the renal glomeruli by deposition of inflammatory proteins in the glomerular membranes as a result of an immunologic response.
- The severity of disease is dictated by the degree of glomerular injury
Causes of focal glomerulonephritis in children
- Benign hematuria
- Henoch-Schonlein purpura
- Mild postinfectious GN
- IgA nephropathy
- Hereditary nephritis
Causes of focal glomerulonephritis in adults
- IgA nephropathy
- Hereditary nephritis
- SLE
Causes of diffuse glomerulonephritis in children
- Postinfectious GN
- Membranoproliferative GN
Causes of diffuse glomerulonephritis in adults
- SLE
- Membranoproliferative GN
- Rapidly progressive GN
- Postinfectious GN
- Vasculitis
Clinical features of glomerulonephritis
- Hematuria; urine is often tea or cola colored
- Oliguria or anuria is present
- Edema of the face and eyes is present in the morning, and edema of the feet and ankles occurs in the afternoon and evening
- HTN is also common, but not essential, clinical finding
Diagnostic studies in glomerulonephritis
- Antistreptolysin-O titer is increased in 60-80% and should be considered if there is a possibility of a recent streptococcal infection
- UA
- Serum complement (C3) levels
- Renal biopsy
What does the UA reveal in glomerulonephritis?
Hematuria, RBC casts and proteinuria (1-2 g/24 hr)
What will be the serum complement levels be in glomerulonephritis?
Decreased
Treatment of glomerulonephritis
- Steroids (methylprednisolone) and immunosuppressive drugs (cyclophosphamide). These are not needed in PSGN
- Dialysis should be performed in symptomatic azotemia is present
- Medical therapy: ACEI and medications that are appropriate for hyperkalemia, pulmonary edema, peripheral edema, acidosis, and hypertension
Dietary management for glomerulonephritis
Salt and fluid intake should be decreased
What is nephrotic syndrome?
Defined as excretion of more than 3.5 mg of protein per 1.73m2 of body surface in 24 hours
Nephrotic syndrome manifests with what?
Hypoalbuminemia, lipiduria, hypercholesterolemia, and edema
Nephrotic syndrome can predispose to thrombosis secondary to what?
Loss of proteins S and C and antithrombin III
Causes of nephrotic syndrome: primary renal disease (9 total)
- Focal GN
- Focal glomerulosclerosis
- IgA nephropathy
- Membranoproliferative GN
- Membranous glomerulopathy
- Mesangial proliferative GN
- Minimal change disease
- Rapidly progressive GN
- Congenital nephrotic syndrome
Causes of nephrotic syndrome: secondary renal disease (8 total)
- Poststreptococcal GN
- SLE
- Malignancy
- Toxemia of pregnancy
- Drugs and nephrotoxins
- Lymphomas and leukemias
- Diabetic glomerulosclerosis
- Amyloidosis
Diagnostic studies in nephrotic syndrome
- U/A
- Microscopic examination of urine
- Blood chemistry
- C3 levels
What does the UA show in nephrotic syndrome?
Proteinuria, lipiduria, glycosuria, hematuria, and foamy urine
What does the microscopic examination of urine show in nephrotic syndrome?
RBC casts, granular casts, hyaline casts and fatty casts
What is the key finding in microscopic urinalysis in nephrotic syndrome?
Oval fat body, which is a renal tubular cell that has reabsorbed some of the excess lipids in the urine
What does the blood chemistry show in nephrotic syndrome?
Hypoalbuminemia, azotemia, and hyperlipidemia
Why does hyperlipidemia form in nephrotic syndrome?
It is secondary to the liver producing increased lipoproteins due to hypovolemia from the loss of intravascular volume (edema)
What does the C3 levels show in nephrotic syndrome?
Low or normal, depending on the cause
Medical therapy in nephrotic syndrome
ACE-I should be used early in the course of the disease
Judicious use of loop diuretics is recommended to reduce fluid accumulations
Dietary management in nephrotic syndrome
- Sodium and fluid intake may be restricted for management of edema
- Dietary protein and potassium intake can be normal but not excessive
Other treatment in nephrotic syndrome
- Infectious should be treated aggressively
- Anticoagulants should be used if thrombosis are present
- Nephrotoxic drugs (e.g., NSAIDs, aminoglycoside antibiotics) should be avoided
- Children seem to respond to steroid therapy better than adults
- Frequent relapsers or steroid nonresponders may be treated with cyclophosphamide, cyclosporine, tacrolimus, or mycophenolate mofetil
What are the cysts made up of in polycystic kidney disease (PKD)?
Epithelial cells from the renal tubules and collecting system. The cysts replace the mass of the kidneys, reducing function and leading to kidney failure
Autosomal dominant PKD (ADPKD)
Most common form and almost always is bilateral. Symptoms typically develop during the fourth decade of life
Autosomal recessive PKD (ARPKD)
- Begins in utero and can lead to fetal and neonatal death.
- Surviving infants have significantly reduce life expectancy due to renal and hepatic failure
Acquired PKD (ACKD)
- Occurs in individuals with long-term renal disease or ESRD
- It is more common in AA men than in other ethnicities
PKD Diagnostic Studies
- Anemia may be noted on CBC
- UA shows proteinuria, hematuria, and pyruria and bacteriuria
- Imaging
- Genetic studies for PKD 1 and PKD 2. This can detect the mutation before symptoms start and can forestall loss of kidney function through diet and BP control
Imaging studies done in PKD
- The diagnostic method of choice is U/S, which shows fluid-filled cysts
- Plain-film radiography of the abdomen shows enlarged kidneys
- Excretory infusion urography reveals multiple lucencies
- Angiography shows bending of small vessels around cysts
- CT shows large renal size and multiple thin-walled cysts
Treatment of PKD
- There is no cure for ADPKD; treatment is supportive to ease symptoms and prolong life
- General measures should include management of pain, control of HTN (<130/80 through ACEI or ARB), high intake of fluids, and low-protein diet
- Dialysis or transplantation should be considered when renal insufficiency becomes life threatening. Transplantation has been successful, and non-PKD kidneys do not develop cysts
Infections in the setting of PKD
-Infections should be treated vigorously with antibiotics (Bactrim, fluoroquinolones like Cipro, chloramphenicol, or vancomycin) that can penetrate the cyst wall
What are the four types of kidney stones?
- Calcium
- Uric Acid
- Cystine
- Struvite
Calcium kidney stones
75-85% of stones are formations of calcium crystals; these stones are radiopaque
Uric acid kidney stones
5-8% are formed by precipitation of uric acid; these stones are radiolucent. These stones form in individuals with persistently acidic urine with or w/o hyperuricemia
Cystine kidney stones
<1% of stones are caused by an impairment of cystine transport; these stones are radiolucent. They occur in autosomal recessive cystinuria
Struvite kidney stones
10-15% of stones are formed by the combination of calcium, ammonium, and magnesium and are radiopaque.
-Formation is increased by UTI with urease-producing bacteria; therefore, this type is common in patients with abnormal urinary tract anatomy and urinary diversions and in those who require frequent catherization
Diagnostic studies in nephrolithiasis
- Serum chemistries
- Urinalysis
- Non-contrast helical (spiral) CT. In children and pregnant patients, U/S is the imaging modality of choice
- X-rays
- Renal U/S
- Intravenous pyelogram (IVP)
What do serum chemistries show in nephrolithiasis?
they are usually normal; however, there may be a leukocytosis from infection or stress
What does a UA show in nephrolithiasis?
Usually reveals microscopic or gross hematuria and may show leukocytes and/or crystals. Urine culture should be performed to rule out infection
What does plain-film radiography show in nephrolithiasis?
It can identify radiopaque stones (calcium and struvite); unfortunately, it may miss a small stone even if radiopaque
What can a renal u/s show in nephrolithiasis?
It can only identify stones in the kidney, proximal ureter, or UVJ
When is an intravenous pyelogram (IVP) indicated in nephrolithiasis?
In the treatment and evaluation of a patient with nephrolithiasis. If an IVP is considered, remember to make sure that the patient has normal renal function.
Treatment of kidney stones measuring less than 5 mm
- All stones should undergo chemical analysis as the type of stone may dictate additional treatment
- Many are likely to pass spontaneously and, in an otherwise healthy individual, may be managed on an outpatient basis
- The patient should drink plenty of fluids
- Strain urine to catch the stone and save it for analysis
- Use an adequate supply of analgesics (NSAIDs, narcotics)
- An alpha-blocker (tamsulosin, terazosin) or CCB (nifedipine) may facilitate passage
- F/U weekly or biweekly to monitor progress. Most stones that pass do so within 2-4 weeks of onset of symptoms
Treatment of kidney stones measuring 5-10 mm
- All stones should undergo chemical analysis as the type of stone may dictate additional treatment
- These are less likely to pass spontaneously; patients should be considered for early elective intervention if no other complicating factors (e.g., infection, high-grade obstruction, solitary kidney, anatomic abnormality preventing passage, and intractable pain) are present
- Increased fluids and analgesic are needed
- Elective lithotripsy or ureteroscopy with stone basket extraction may be used.
Treatment of kidney stones measuring greater than 10 mm
- These are not likely to pass spontaneously; these patients are more likely to have complications
- The patient should be treated on an inpatient basis if he or she is unable to maintain adequate oral intake.
- Vigorous hydration should be maintained
- Ureteral stent or percutaneous nephrostomy (gold standard) should be used if renal function is jeopardized
- Urgent treatment with extracorporeal shock wave lithotripsy (ESWL) can be used for renal stones less than 2 cm or for ureteral stones of less than 10 mm; urteroscopic fragmentation also may be used. Ureteroscopy is more effective than ESWL for ureteral calculi
- Percutaneous nephrolithotomy can be used for stones greater than 2 cm
Appropriate analgesics that can be used in nephrolithiasis
Appropriate analgesics include morphine, meperidine, or ketorolac. Combination of morphine and ketorolac is found to be more effective than single-agent use
Treatment of nephrolithiasis that depends on stone makeup
- Antibiotics (e.g., ampicillin, gentamicin, ticarcillin/clavulanic acid, ciprofloxacin, levofloxacin, ofloxacin) if signs of infection are present
- HCTZ to decrease urine calcium excretion
- Allopurinol to decrease urine uric acid excretion
- Alkali to increase urine citrate excretion
Treatment of hypernatremia
- Should be treated on an inpatient basis
- Identify the underlying cause and treat accordingly
- Free water may be administered orally, which is the preferred route, or IV or SQ, as a 5% dextrose solution in water or saline
- Hypovolemia should be treated first (with isotonic saline or lactated Ringers) and the hypernatremia second
- Dialysis should be implemented if sodium is greater than 200 mEq/L
Why would you not want to correct hypernatremia rapidly?
Because it can cause pulmonary or cerebral edema, especially in patients with diabetes mellitus
What is the most common electrolyte disorder in the general hospital population?
Hyponatremia secondary to the use of hypotonic fluid administration
Hyponatremia with hypervolemia occurs with what?
In the setting of CHF, nephrotic syndrome, renal failure, and hepatic cirrhosis
Hyponatremia with euvolemia occurs with what?
Hypothyroidism, glucocorticoid excess, and SIADH
SIADH definition
Hypotonic hyponatremia; urine osmolality of greater than 100 mOsm/kg; normal cardiac, hepatic, thyroid, adrenal, and renal function; and absence of extracellular fluid volume deficit. Urine sodium is usually greater than 40 mEq/L
Hyponatremia with hypovolemia occurs with what?
Renal or nonrenal sodium loss
What should be done in terms of diagnostic studies if SIADH is suspected?
-CT may be done to r/o a CNS disorder and CXR may be done to r/o lung pathology
Treatment of hyponatremia with hypovolemia
Treat on an inpatient basis, especially if symptomatic or if serum sodium is less than 125 mEq/L. Also consider consultation with a nephrologist and/or endocrinologist
-Isotonic saline (do not give with euvolemic or hypervolemic)
Treatment of severe symptomatic hyponatremia with a sodium of less than 120 mEq/L
- Hypertonic saline may be used very cautiously
- Overly rapid correction can cause central pontine myelinolysis, resulting in neurologic damage
- Serum sodium levels should be checked hourly and neurologic status closely monitored
Treatment of chronic hyponatremia unresponsive to fluid restriction
Demeclocycline may be used to induce nephrogenic DI but may cause nephrotoxicity in patients with cirrhosis. Vasopressin antagonists (conivaptan) may be considered in euvolemic or hypervolemic hyponatremia
What is the cause of neurogenic (or central) DI?
Deficient secretion of arginine vasopressin (antidiuretic hromone [ADH]) from the posterior pituitary
What is the cause of nephrogenic DI?
Caused by kidneys that are unresponsive to normal vasopressin levels. It may be an inherited X-linked trait or acquired as a result of lithium therapy, hypokalemia, hypercalcemia, or renal disease.
Diabetes insipidus diagnostic studies
- Neurogenic (central) and nephrogenic DI can be distinguished by water deprivation and desmopressin testing. If the test results in reduce urine output and resultant increase in urine osmolality, central DI is diagnosed. If little or no change in urine osmolality resutls, it is most likely nephrogenic DI
- Urine osmolality of <250 mOsm/kg, despite hypernatremia, indicates DI
Treatment of DI
- Neurogenic or central DI is best treated with parenteral or intranasal desmopressin
- Diuretics, chlorpropramide, or carbamazepine can be used in patients with mild disease
- Nephrogenic diabetes can be treated with HCTZ or amiloride diuretics or indomethacin. Adequate water intake is essential to prevent dehydration
Dietary measures that can be taken in nephrogenic DI
Limiting salt and protein intake
Most common causes of hyperkalemia
Renal failure, ACE inhibitors, hyporeninemic hypoaldosteronism, cell death, and metabolic acidosis
ECG changes with hyperkalemia
- Earliest ECG manifestation is peaking of the T waves (>6.5 mEq/L)
- Flattening of the P wave, prolongation of the PR interval, and widening of the QRS complex are seen with more severe hyperkalemia (>7.0 mEq/L)
- A final event is a sine wave pattern with cardiac arrest (8.0-10.0 mEq/L)
What can be given for severe hyperkalemia with ECG changes?
-Calcium gluconate should be given IV to antagonize the effects of hyperkalemia on the heart. Strict monitoring is required
What can be given to drive potassium back into the intracellular compartment?
Sodium bicarbonate, glucose (D50) and insulin (10 units)
-The onset of action is rapid, but the duration is short; therefore serial potassium levels should be followed until correction is complete.
What can be given when potassium levels are extremely high?
Sodium polystyrene sulfonate (Kayexalate), which is a cation-exchange resin.
- Nebulized inhaled albuterol has been used to reduce serum potassium levels; however, the evidence is inconclusive
- Hemodialysis may be required if the above therapies fail
Common causes of hypokalemia
Use of diuretics, renal tubular acidosis, or GI losses
ECG changes with hypokalemia
It may reveal flattened or inverted T waves, increased prominence of U waves, depression of the ST segment, and ventricular ectopy
When is IV replacement indicated in hypokalemia?
In emergent situations where the serum potassium <2.5 mEq/L or arrhythmias are present
When is more aggressive potassium replacement in hypokalemia required?
When hypokalemia potentiates the effects of cardiac glycosides on myocardial conduction and leads to digitalis intoxication
Common causes of hypercalcemia
Malignancy, vitamin D intoxication, hyperparathyroidism, and sarcoidosis
Most patients with hypercalcemia are asymptomatic until what level?
> 12 mg/dL
Diagnostic studies with hypercalcemia
Serum calcium, CXR, UA, ESR, 24-hour urine collection, serum vitamin D levels
Serum calcium levels must be corrected for what?
Albumin levels
Corrected calcium equation
Measured total calcium + [0.8 x (4-albumin)]
What may an CXR reveal in hypercalcemia?
Underlying pulmonary mass
Why would a UA be performed in hypercalcemia?
For signs of hematuria, an early sign of RCC
In hypercalcemia, ESR may be elevated in what?
Monoclonal gammopathy. Protein electrophoresis of serum or urine may be needed to confirm the diagnosis
Elevated urine calcium in an 24 hour urine collection in hypercalcemia suggests what?
Malignant neoplastic or paraneoplastic process or hyperparathyroidism
A decreased urine sodium in an 24-hour urine collection suggests what?
Primary hyperparathyroidism
Treatment of hypercalcemia
- Isotonic saline should be used for volume repletion. Loop diuretics should be used if the patient is hypervolemic after volume repletion
- Bisphosphonates can also be considered in severe hypercalcemia
- Manage the underlying cause
Common causes of hypocalcemia
Usually results from a chronic disease (most common cause is CKD) or hypoparathyroidism
Classic neurologic findings in hypcalcemia
- Trousseau sign (carpal tunnel spasm after BP cuff applied for 3 minutes)
- Chvostek sign (spasm of facial muscle after tapping facial nerve in front of ear)
Treatment of emergent or severe hypocalcemia
- Treat any emergent cardiovascular states
2. Severe hypocalcemia should be replaced (IV calcium gluconate or calcium chloride)
Treatment of mild hypocalcemia
It can be treated on an outpatient basis with oral calcium and vitamin D supplements.
Hyperphosphatemia common causes
Secondary to CKD or excessive use of phosphate containing laxatives or enemas
Hypophosphatemia is secondary to what?
Diminished supply or absorption, increased urinary losses, or redistribution
Hypophosphatemia common causes
Vitamin D deficiency, respiratory alkalosis, burns, or hyperparathyroidism
Moderate level of hypophosphatemia
Serum level of 1.0 to 2.5 mg/dL. Usually asymptomatic
Severe hypophosphatemia
Serum level of 1 mg/dL or less
Severe hypophosphatemia may lead to what conditions?
Rhabomyolysis, paresthesia, and encephalopathy
Treatment of hyperphosphatemia
-If it is secondary to CKD, it should be treated with dietary phosphorous restriction and oral phosphate binders. Calcium carbonate tablets may also help to reduce phosphate absorption: 0.5 to 1.5 g three times daily with meals (500-mg tablets)
Treatment of hypophosphatemia of chronic origin
Oral phosphate repletion
Diagnostic studies in hypermagnesemia
- ECG shows widened QRS complex, prolonged PR interval, and prolonged QT interval
- Bleeding and clotting times are increased
Treatment of hypermagnesemia
- Administer 10-20 mL of 10% calcium gluconate IV over 10 minutes
- Saline diuresis and IV furosemide may increase excretion of magnesium
- Dialysis is effective in severe hypermagnesemia
Common causes of hypomagnesemia
Chronic alcoholism, chronic diarrhea, hypoparathyroidism, hyperaldosteronism, diuretic therapy, osmotic diuresis, and nutritional deficiencies (e.g., prolonged parenteral feeding, malnutrition)
Lab tests in hypomagnesemia
Hypokalemia, hypocalcemia, and hypocalciuria commonly are associated with causes of magnesium depletion
What does the ECG show in hypomagnesemia?
Prolonged PR and QT intervals or widening of the QRS
Treatment of chronic hypomagnesemia
- Administer oral magnesium oxide for chronic hypomagnesemia. Administer twice the estimated deficit over several days
Treatment of severe symptomatic hypomagnesemia
- A magnesium sulfate solution (1-2 g) can be administered IV followed by an infusion of 6 g of magnesium sulfate over 1 L of fluids in 24 hours to replace magnesium stores. This may repeated for up to 7 days
- Magnesium sulfate may also be given IM in four divided doses (200-800 mg/day) if IV access is difficult
Respiratory acidosis PCO2 and HCO3
PCO2= Increased
HCO3=Increased
Respiratory alkalosis PCO2 and HCO3
PCO2=Decreased
HCO3=Decreased
Metabolic acidosis PCO2 and HCO3
PCO2=Decreased
HCO3=Decreased
Metabolic alkalosis PCO2 and HCO3
PCO2=Increased
HCO3=Increased
Respiratory acidosis results from what?
The failure of the lung to excrete CO2 that is generated through normal metabolism. It can be a result of alveolar hypoventilation leading to pulmonary CO2 retention or of overproduction of CO2 or a combination of both
Primary causes of respiratory acidosis
Primary pulmonary disease, neuromuscular disease (myasthenia gravis), primary CNS dysfunction (severe brain stem injury), and drug-induced hypoventilation
Lab findings in respiratory acidosis
- Acute CO2 retention leads to an increase in blood PCO2 with a minimal change in plasma bicarbonate content
- After 2-5 days, renal compensation occurs, leading to increased hydrogen ion secretion and bicarbonate production in the distal nephron, after which the plasma bicarbonate level steadily increases
Treatment of respiratory acidosis
- Treat the underlying disorder
- A blood PCO2 of greater than 60 mm Hg may indicate the need for assisted ventilation if CNS or pulmonary muscular depression is severe
Causes of respiratory alkalosis
Include any disorders associated with inappropriately increased ventilatory rate and CO2 clearance. Most common cause is anxiety (hysterical hyperventilation)
Lab findings in respiratory alkalosis
- In acute alkalosis, increased respiratory rate leads to a loss of CO2 via the lungs, which in turn increases the blood pH
- Within hours after an acute decrease in arterial PCO2, hydrogen ion secretion in the distal nephron decreases, leading to a decrease in plasma bicarbonate. Serum chloride level becomes elevated to maintain electroneutrality
Treatment of respiratory alkalosis
- Primary goal is to correct the underlying disorder. Rebreathing techniques such as breathing into a paper bag has lost favor and reassurance and light sedation is likely more effective
- Use of CO2-enriched breathing mixtures or controlled ventilation may be required in cases of severe respiratory alkalosis (pH 7.6)
Conditions that result in increased hydrogen ions in the serum (metabolic acidosis)
- Lactic acidosis; diabetic ketoacidosis; starvation ketosis; and ethylene glycol, methanol, and salicylate intoxication. These conditions result in an increased anion gap (AG)
- Hydrogen ions may also be retained in renal tubular acidosis, renal insufficiency, and adrenal insufficiency
Conditions that may result in the loss of bicarbonate and result in metabolic acidosis
Diarrhea, pancreatic or biliary drainage, and ureteral diversion; these conditions typically have a normal AG
Clinical features of metabolic acidosis
- Hyperventilation is the earliest and most recognized sign, resulting from stimulation of the respiratory drive to blow off CO2 (pulmonary compensation)
- Ventricular arrhythmias may occur
- Neurologic symptoms
What is Winter’s formula and what does it calculate for?
PCO2 = (1.5 × [HCO3-]) + 8 ± 2; it allows for calculation of the expected PCO2 compensation in metabolic acidosis
Anion gap formula
Na+ - [HCO3- + Cl-]
Normal anion gap
8 ± 4 mEq/L
Normal anion gap in metabolic acidosis (also called hyperchloremic metabolic acidosis)
Normal AG renal tubular acidosis can be divided into cases of the kidney failing to reabsorb bicarbonate or secrete acid
Causes of normal AG metabolic acidosis
Ureteroenterostomy Small bowel fistula Endocrinopathies/extra chloride Diarrhea Carbonic anhydrase inhibitors Ammonium chloride Renal tubular acidosis Pancreatic fistula *Remember the mnemonic: USED CARP
How is the anion gap adjusted for hypoalbuminemia
For each 1.0 g/dL decrease in serum albumin, the AG should be increased by 2.5 mEq/L
Elevated AG metabolic acidosis 4 categories
Lactic acidosis, ketoacidosis, toxins/drugs, and kidney failure
Common causes of elevated AG metabolic acidosis
Carbon monoxide/cyanide Alcoholic ketoacidosis Toluene Methanol Uremia Diabetic ketoacidosis Paraldehyde Infection/iron/isoniazid Lactic acidosis Ethylene glycol Salicylates *Remember the mnemonic CAT MUD PILES
Formula used in metabolic alkalosis for calculation of expected CO2 compensation:
Expected PCO2= (0.7 x HCO3-) + 20 ± 2
Metabolic alkalosis and increased serum bicarbonate can be caused by what?
Loss of hydrogen (vomiting), addition of bicarbonate (hyperalimentation therapy), or disproportionate loss of chloride (diarrhea)
Treatment of metabolic alkalosis
- Intervention to increase renal excretion of bicarbonate are the most effective therapy for metabolic alkalosis
- Chloride-responsive conditions (e.g., gastric fluid loss, diuretic therapy) are treated with solutions containing sodium chloride to repair the sodium and chloride deficits
- Chloride-resistant conditions (e.g., mineralcorticoid excess) can be successfully treated by removing an adrenal adenoma, if present or by using spironolactone
Treatment of uncomplicated cystitis in women
- The suggested regimen is a fluoroquinolone or nitrofurantoin for 3-5 days
- Resistant E. coli is common, but Bactrim can be used as an alternative to a quinolone in susceptible strains
Patient education for cystitis
Fluids should be encouraged. Preventive measures include proper hygiene, urine acidification, and voiding after intercourse
-Hot sitz baths or urinary analgesics (phenazopyridine) may provide symptomatic relief. Patients should be warned that phenazopyridine will discolor the urine (dark orange or reddish)
In complicated pyelonephritis, renal U/S may show what?
Hydronephrosis secondary to obstruction
Outpatient treatment of pyelonephritis
-Treatment with a fluoroquinolone (Cipro) or Bactrim for 1-2 weeks has shown to be effective in immunocompetent patients. Immunocompromised patients should be treated for a longer duration.
When is hospital admission required for pyelonephritis?
It is required for patients with severe infections or complicating factors, such as older age, comorbid conditions, signs of obstruction, or inability to tolerate oral antibiotics
Inpatient pyelonephritis treatment
IV fluoroquinolones or ampicillin and gentamicin should be initiated while waiting for sensitivity results. IV antibiotics should be continued for 24-48 hours after the patient becomes afebrile; oral antibiotics are then given to complete a minimum of 2 weeks of therapy
What is required if failure to treatment occurs in complicated pyelonephritis?
Ultrasound imaging to exclude complicating factors such as stones or possible abscess formation that may require prompt intervention
Chronic prostatitis
- It is the most common of the prostatitis syndromes, and its cause is unknown
- It may represents a noninfectious inflammatory disorder, perhaps with an autoimmune origin and is a diagnosis of exclusion
- It is often associated with the term chronic pelvic pain syndrome
What is a potential complication of acute bacterial prostatitis?
Prostatic abscess
Diagnostic studies in prostatitis
- UA: reveals pyuria and potentially hematuria and bacteriuria
- Prostatic fluid: will reveal leukocytosis; culture the fluid
Treatment of uncomplicated acute prostatitis
Ciprofloxacin 500 mg BID or levofloxacin 500 mg once a day for 2-6 weeks or Bactrim 160 mg/800 mg twice a day for 6 weeks.
-Culture urine 1 week after conclusion of therapy
What should you suspect in prostatitis if a fever is not resolved after 36 hours?
Prostatic abscess; consult a urologist for management
Treatment of chronic prostatitis
A fluoroquinolone for 1-3 weeks is more effective than bacterium for 1-3 months
What is an effective analgesic for prostatitis?
NSAIDs
What medication may be helpful in prostatitis if lower urinary tract symptoms (LUTS) is present?
Doxazosin
What may be required in chronic, recurrent, or resistant cases of prostatitis with or without prostatic calculi?
Transurethral resection of the prostate for ultimate resolution
Clinical features of orchitis?
- Testicular swelling and tenderness, usually unilateral, occur
- Fever and tachycardia are common
Diagnostic studies for orchitis
- U/A: reveals pyuria and bacteriuria with bacterial infection
- Cultures are positive for suspected organisms
- U/S is useful if abscess or tumor is suspected and to r/o testicular torsion
Treatment of orchitis
- If mumps is the cause, symptomatic relief with ice and analgesia should be provided
- If bacteria is the cause, the orchitis should be treated like epididymitis (Ceftriaxone + Doxycycline)
- Carefully evaluate any scrotal masses
General characteristics of epididymitis
- It is an infection of the epididymis acquired by retrograde spread of organisms through the vas deferens
- In men younger than 35 yo, Chlamydia and gonococci are the most common organisms
- In men older than 35 years of age, E. coli is the most common organism
Diagnostic studies in epididymitis
- UA reveals pyuria and bacteriuria
2. Cultures show positive results for suspected organisms
Treatment of epididymitis
- In men younger than 35 years of age, ceftriaxone 250 mg IM, plus doxycycline 100 mg BID PO or azithromycin 1 g orally for 7 days, may be administered for gonococci or Chlamydia. A test for cure should be done 1 week after conclusion of therapy
- In men older than 35 years of age, ceftriaxone plus ofloxacin or levofloxacin
Supportive care in epididymitis
It would include things like bed rest, scrotal elevation, and analgesics
Clinical features of BPH
- Obstructive symptoms include decreased force of urinary stream, hesistancy and straining, postvoid dribbling, and sensation of incomplete emptying
- Irritative symptoms include frequency, nocturia, and urgency
- Recurrent urinary tract infections and urinary retention can also occur
- DRE typically reveals and enlarged prostate
Diagnostic studies of BPH
- PSA is slightly elevated
- Other tests are done to evaluate for renal damage, infection, and prostate or bladder cancer, as suspected
Treatment of BPH with mild to moderate symptoms
Watchful waiting and frequent monitoring
BPH options for medical therapy
Alpha-adrenergic agonists (prazosin, etc.), 5 alpha reductase inhibitors (finasteride, dutasteride) and phosphodiesterase 5 inhibitors (tadalafil, vardenafil), which improve prostate symptom scores for LUTS due to BPH
- Anticholinergic agents (ex: Tolterodine) may be appropriate and effective treatment alternatives for management of LUTS secondary to BPH in men without an elevated postvoid residual and when LUTS are predominantly irritative
- Tamsulosin plus tolterodine extended release reduces symptoms in men with LUTS and overactive bladder
- IM cetrorelix (60 mg then 30 mg at 2 weeks) improves International Prostate Symptom Score in men with symptomatic BPH
Behavioral strategies that can be used in BPH
Limiting of fluids prior to bedtime
Procedures that may be used to relieve obstruction in BPH
Balloon dilation, microwave irradiation, and stent placements
Surgical treatment of BPH
Transurethral resection of prostate or transurethral incision of prostate
Diagnostic studies in urinary incontinence
- UA can identify diabetes-related glycosuria or acute UTI
- Postvoid residual urine volume should be measured to identify urinary retention
- Simple urodynamic studies such as cystometry can identify bladder contractions and should be considered
- Stress test, U/S, cystoscopy, and cystographic studies may be used to determine anatomic abnormalities
Nonpharmacologic treatment of urinary incontinence
- Pelvic floor muscle training (Kegel exercises), electrical muscle stimulation, biofeedback, and bladder training can be used to improve the strength and control of the pelvic muscles
- Pessaries or implants can help decrease stress incontinence
- Catherization, either intermittent or indwelling, can be used for overflow incontinence
- Surgery for stress incontinence as last resort
Pharmacologic treatment of urinary incontinence
- Anticholinergic medications, such as oxybutynin or tolterodine, are effective for urge incontinence
- Vaginal estrogen can be used for stress incontinence. Oral estrogen may worsen urinary incontinence
- Tolterodine and oxybutynin can be used for overactive bladder
Where do the majority of prostate cancers originate?
In the peripheral zone, followed by transitional zone and lastly the central zone
Gleason Grading System
- Used for prostate CA
- The Gleason grading system adds together the primary and secondary grades of the tumor, resulting in a final score of 2-10. The total score can be used for prognostic purposes, with a higher score indicating a worse prognosis than a lower score
Stages A and B (tumor confined to the prostate) of prostate cancer treatment
May be treated with radical retropubic prostatectomy, brachytherapy, or external beam radiation therapy
Stage C (tumor with local invasion) of prostate CA treatment
Treated similar to stages A and B but with reduced effectiveness
Stage D (distant metastases) of prostate CA treatment
Treated with hormonal manipulation using orchiectomy, antiandrogens, luteinizing hormone-releasing hormone agonists, or estrogens. Chemotherapy has limited usefulness and palliative treatment is given for advanced disease
What is the definitive diagnostic procedure in bladder cancer?
Cystoscopy while biopsy confirms the pathologic diagnosis
Radiologic diagnostic studies used in bladder cancer
IV urogram, pelvic and abdominal CT, CXR, bone scan, and retrograde pyelography for renal pelvic or ureteral tumors and staging
Superficial lesions of bladder cancer are treated with what?
Endoscopic resection and fulguration, followed by cystoscopy every 3 months. Recurrent or multiple lesions can be treated with intravesical instillation of thiotepa, mitomycin-C, or bacillus Calmette-Guerin (BCG)
When is radical cystectomy used for bladder CA?
For recurrent cancer, diffuse transitional cell carcinomas in situ, and for tumors that have invaded the muscle
External beam irradiation therapy is typically reserved for who?
Those individuals who are not surgical candidates due to significant comorbid medical conditions
Renal Cell Carcinoma paraneoplastic syndromes
Includes erythrocytosis, hypercalcemia, hypertension, and hepatic dysfunction in the absence of hepatic metastases
What is the primary treatment for localized disease (stage T1 to T3a lesions) for renal cell carcinoma?
Radical nephrectomy. Neoadjuvant or adjuvant radiation therapy has not been shown to prolong survival for early stage lesions
What is an important method of palliation in patients with disseminated disease of renal cell carcinoma to the brain, bone, and lungs?
Radiation therapy
What in Wilms tumor is associated with a poorer prognosis?
Anaplasia
What is the initial study of choice for Wilms tumor?
Ultrasonography
What is the treatment of choice for surgicaly resectable tumors?
Radical nephrectomy with lymph node sampling
What is the treatment for unresectable tumors?
They should undergo preoperative biopsy followed by chemotherapy
Wilms tumor is responsive to what chemotherapy drugs?
Dactinomycin, vincristine, and doxorubicin
When is radiation therapy added for Wilms tumor?
For higher stage tumors (stages III and IV) and for tumors with focal anaplasia
What are the subtypes of nonseminomatous testicular cancer?
Embryonal carcinoma, teratoma, mixed cell type, and choriocarcinoma
Elevated blood levels of what are diagnositc for nonseminomatous germ cell tumors?
Alpha-fetoprotein or beta-human chorionic gonadotropin; the majority of patients with seminoma have normal levels
Are seminomatous tumors radiosensitive or radioresistant?
Radiosensitive
Stage I nonseminomatous tumor (testicular CA) treatment
It can be treated with nerve-sparing retroperitoneal lymph node dissection or rigorous surveillance without surgery or chemotherapy
Stage II nonseminomatous tumor (testicular CA) treatment
Surgery or chemotherapy
Stage III nonseminomatous tumor (testicular CA) treatment
Surgery or chemotherapy
Stage I seminomatous tumor (testicular CA) treatment
Radiation therapy to the para-aortic and ipsilateral iliac nodal areas
Stage IIa and IIb seminomatous tumor (testicular CA) treatment
Increased radiation to the affected nodes
Stage IIc and III seminomatous tumor (testicular CA) treatment
Chemotherapy
What are some causes of acquired phimosis in adults?
Poor hygiene and chronic balanitis. Consider evaluation for possible diabetes in men with chronic infections
Treatment for paraphimosis
- Reduce emergently (either manual or surgically)
- After reduction, referral for circumcision is necessary because the condition is likely to recur
