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A Comprehensive Review for the Certification and Recertification Examination for Physician Asistants > Nephrology and Urology > Flashcards

Nephrology and Urology Flashcards

1
Q

What does RIFLE mean in classification of acute renal failure (ARF) or acute kidney injury (AKI)?

A
  • 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)
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2
Q

Risk of renal dysfunction

A

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

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3
Q

Injury to kidney

A

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

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4
Q

Failure of kidney function

A

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

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5
Q

Loss of kidney function (persistent ARF)

A

Complete loss of kidney function for more than 4 weeks

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6
Q

End-stage kidney disease (ESKD) or end-stage renal disease (ESRD)

A

Complete loss of kidney function for more than 3 months

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7
Q

Prerenal causes of ARF (60-70%)

A
  • Hypovolemia
  • Hypotension
  • Ineffective circulating volume (CHF, cirrhosis, nephrotic syndrome, early sepsis)
  • Aortic aneurysm
  • Renal artery stenosis or embolic disease
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8
Q

Intrinsic renal causes (25-40%)

A
  • Acute tubular necrosis
  • Nephrotoxins (NSAIDs, aminoglycosides, radiologic contrast)
  • Interstitial diseases (acute interstitial nephritis, SLE, infection)
  • Glomerulonephritis
  • Vascular diseases (polyarteritis nodosa, vasculitis)
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9
Q

Postrenal causes (5-10%)

A
  • Tubular obstruction

- Obstructive uropathy (urolithiasis, BPH, bladder outlet obstruction)

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10
Q

Diagnostic Studies to order in ARF

A
  • GFR
  • Serum creatinine and BUN
  • Urinalysis
  • Serum cystatin C
  • Urine biomarkers (IL-8 and kidney injury molecule-1 [KIM-1])
  • Renal U/S
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11
Q

BUN in diagnosing ARF

A
  • 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
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12
Q

Urinalysis in diagnosing ARF

A
  • 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
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13
Q

Serum cystatin C and urine biomarkers in diagnosing ARF

A

-These are new biomarkers that shows promise for detecting AKI

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14
Q

Prerenal causes blood and urine studies

A
  • 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
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15
Q

Intrinsic renal causes blood and urine studies

A
  • 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
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16
Q

Postrenal causes blood and urine studies

A

Urine sodium, FENa osmolality, and BUN-to-Cr ratio can vary depending on how long the obstruction has been present

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17
Q

What on the renal U/S would indicate a chronic problem in ARF?

A

A kidney smaller than 10 cm

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18
Q

What are other laboratory findings associated with a loss of renal function?

A
  • Azotemia
  • Decreased creatinine clearance
  • Metabolic acidosis
  • Hyperkalemia
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19
Q

Treatment of ARF involves correction of the underlying problem. What are some examples of that?

A
  1. Achievement of normal hemodynamics in prerenal states (IV fluids, improving cardiac output)
  2. Adjustment and avoidance of medications and nephrotoxic agents in intrarenal states
  3. Relief of urinary tract obstruction (ureteral stents, urethral catheter) in postrenal states
  4. Consideration of early intervention under the supervision of a nephrologist or intensivist for management of potential renal replacement therapy
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20
Q

What are some indications for short-term dialysis?

A
  1. When serum creatinine exceeds 5-10 mg/dL
  2. Unresponsive acidosis
  3. Electrolyte disorders
  4. Fluid overload
  5. Uremic complications
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21
Q

What is chronic kidney disease (CKD)?

A
  • 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
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22
Q

Stages of CKD: Stage 1

A

Kidney damage with normal GFR greater than 90 mL/min/1.73 m2 body surface area (BSA) and persistent albuminuria

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23
Q

Stages of CKD: Stage 2

A

Kidney damage with mild decrease in GFR 60-89 mL/min/1.73 m2 BSA

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24
Q

Stages of CKD: Stage 3

A

Moderate decrease in GFR 30-59 mL/min/1.73 m2 BSA

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25
Q

Stages of CKD: Stage 4

A

Severe decrease in GFR 15-29 mL/min/1.73 m2 BSA

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26
Q

Stages of CKD: Stage 5

A

Kidney failure with GFR less than 15 mL/min/1.73 m2 BSA

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27
Q

What generally occurs in stages 1 and 2 of CKD?

A

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

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28
Q

What generally occurs in stage 3 of CKD?

A

He or she may still remain asymptomatic; however, serum creatinine and BUN increase. In addition other hormones (PTH, erythropoietin, calcitrol) become abnormal

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29
Q

What generally occurs in stage 4 of CKD?

A

The patient may become symptomatic with anemia, acidosis, hyperkalemia, hypocalcemia, and hyperphosphatemia

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30
Q

What generally occurs in stage 5 of CKD?

A

The patient is a candidate for renal replacement therapy

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31
Q

Common causes of chronic renal failure (4 total)

A
  1. DM
  2. HTN
  3. Glomerulonephritis
  4. Polycystic kidney disease
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32
Q

Other causes of chronic renal failure (6 total)

A
  1. Primary glomerular diseases (membranous nephropathy, minimal change disease, IgA nephropathy)
  2. Secondary glomerular diseases (sickle cell anemia, SLE)
  3. Tubulointerstitial renal diseases (nephrotoxins, infection, multiple myeloma, HIV)
  4. Chronic pyelonephritis (tuberculosis)
  5. Vascular diseases (renal artery stenosis or obstruction)
  6. Obstructive nephropathies (nephrolithiasis, prostate disease, neurogenic bladder)
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33
Q

Diagnostic studies in CKD

A
  • 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
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34
Q

Cockcroft-Gault formula

A

Requires the patient age, body weight and serum creatinine

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35
Q

Modification of Diet in Renal Disease (MDRD) equation

A
  • 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
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36
Q

How to calculate GFR in children

A

Use a pediatric GFR calculator

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37
Q

What is proteinuria a marker of?

A

kidney damage

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38
Q

BUN and creatinine in CKD

A

These levels will be elevated

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39
Q

Serum biomarker cystatin C in CKD

A

It is elevated when the GFR is <88 mL/min/1.73 m2 BSA; however, its clinical role has not been defined

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40
Q

Treatment of CKD

A
  • 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
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41
Q

Dietary management of CKD

A
  • Restriction of protein intake
  • Adequate caloric intake
  • Calcium and vitamin D supplements
  • Limitation of water, sodium, potassium and phosphorus
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42
Q

Glomerulonephritis (GN) general characteristics

A
  • 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
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43
Q

Causes of focal glomerulonephritis in children

A
  • Benign hematuria
  • Henoch-Schonlein purpura
  • Mild postinfectious GN
  • IgA nephropathy
  • Hereditary nephritis
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44
Q

Causes of focal glomerulonephritis in adults

A
  • IgA nephropathy
  • Hereditary nephritis
  • SLE
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45
Q

Causes of diffuse glomerulonephritis in children

A
  • Postinfectious GN

- Membranoproliferative GN

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46
Q

Causes of diffuse glomerulonephritis in adults

A
  • SLE
  • Membranoproliferative GN
  • Rapidly progressive GN
  • Postinfectious GN
  • Vasculitis
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47
Q

Clinical features of glomerulonephritis

A
  • 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
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48
Q

Diagnostic studies in glomerulonephritis

A
  • 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
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49
Q

What does the UA reveal in glomerulonephritis?

A

Hematuria, RBC casts and proteinuria (1-2 g/24 hr)

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50
Q

What will be the serum complement levels be in glomerulonephritis?

A

Decreased

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51
Q

Treatment of glomerulonephritis

A
  • 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
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52
Q

Dietary management for glomerulonephritis

A

Salt and fluid intake should be decreased

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53
Q

What is nephrotic syndrome?

A

Defined as excretion of more than 3.5 mg of protein per 1.73m2 of body surface in 24 hours

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54
Q

Nephrotic syndrome manifests with what?

A

Hypoalbuminemia, lipiduria, hypercholesterolemia, and edema

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55
Q

Nephrotic syndrome can predispose to thrombosis secondary to what?

A

Loss of proteins S and C and antithrombin III

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56
Q

Causes of nephrotic syndrome: primary renal disease (9 total)

A
  1. Focal GN
  2. Focal glomerulosclerosis
  3. IgA nephropathy
  4. Membranoproliferative GN
  5. Membranous glomerulopathy
  6. Mesangial proliferative GN
  7. Minimal change disease
  8. Rapidly progressive GN
  9. Congenital nephrotic syndrome
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57
Q

Causes of nephrotic syndrome: secondary renal disease (8 total)

A
  1. Poststreptococcal GN
  2. SLE
  3. Malignancy
  4. Toxemia of pregnancy
  5. Drugs and nephrotoxins
  6. Lymphomas and leukemias
  7. Diabetic glomerulosclerosis
  8. Amyloidosis
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58
Q

Diagnostic studies in nephrotic syndrome

A
  • U/A
  • Microscopic examination of urine
  • Blood chemistry
  • C3 levels
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59
Q

What does the UA show in nephrotic syndrome?

A

Proteinuria, lipiduria, glycosuria, hematuria, and foamy urine

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60
Q

What does the microscopic examination of urine show in nephrotic syndrome?

A

RBC casts, granular casts, hyaline casts and fatty casts

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61
Q

What is the key finding in microscopic urinalysis in nephrotic syndrome?

A

Oval fat body, which is a renal tubular cell that has reabsorbed some of the excess lipids in the urine

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62
Q

What does the blood chemistry show in nephrotic syndrome?

A

Hypoalbuminemia, azotemia, and hyperlipidemia

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63
Q

Why does hyperlipidemia form in nephrotic syndrome?

A

It is secondary to the liver producing increased lipoproteins due to hypovolemia from the loss of intravascular volume (edema)

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64
Q

What does the C3 levels show in nephrotic syndrome?

A

Low or normal, depending on the cause

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65
Q

Medical therapy in nephrotic syndrome

A

ACE-I should be used early in the course of the disease

Judicious use of loop diuretics is recommended to reduce fluid accumulations

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66
Q

Dietary management in nephrotic syndrome

A
  1. Sodium and fluid intake may be restricted for management of edema
  2. Dietary protein and potassium intake can be normal but not excessive
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67
Q

Other treatment in nephrotic syndrome

A
  • 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
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68
Q

What are the cysts made up of in polycystic kidney disease (PKD)?

A

Epithelial cells from the renal tubules and collecting system. The cysts replace the mass of the kidneys, reducing function and leading to kidney failure

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69
Q

Autosomal dominant PKD (ADPKD)

A

Most common form and almost always is bilateral. Symptoms typically develop during the fourth decade of life

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70
Q

Autosomal recessive PKD (ARPKD)

A
  • Begins in utero and can lead to fetal and neonatal death.

- Surviving infants have significantly reduce life expectancy due to renal and hepatic failure

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71
Q

Acquired PKD (ACKD)

A
  • Occurs in individuals with long-term renal disease or ESRD

- It is more common in AA men than in other ethnicities

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72
Q

PKD Diagnostic Studies

A
  1. Anemia may be noted on CBC
  2. UA shows proteinuria, hematuria, and pyruria and bacteriuria
  3. Imaging
  4. 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
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73
Q

Imaging studies done in PKD

A
  1. The diagnostic method of choice is U/S, which shows fluid-filled cysts
  2. Plain-film radiography of the abdomen shows enlarged kidneys
  3. Excretory infusion urography reveals multiple lucencies
  4. Angiography shows bending of small vessels around cysts
  5. CT shows large renal size and multiple thin-walled cysts
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74
Q

Treatment of PKD

A
  • 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
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75
Q

Infections in the setting of PKD

A

-Infections should be treated vigorously with antibiotics (Bactrim, fluoroquinolones like Cipro, chloramphenicol, or vancomycin) that can penetrate the cyst wall

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76
Q

What are the four types of kidney stones?

A
  1. Calcium
  2. Uric Acid
  3. Cystine
  4. Struvite
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77
Q

Calcium kidney stones

A

75-85% of stones are formations of calcium crystals; these stones are radiopaque

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78
Q

Uric acid kidney stones

A

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

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79
Q

Cystine kidney stones

A

<1% of stones are caused by an impairment of cystine transport; these stones are radiolucent. They occur in autosomal recessive cystinuria

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80
Q

Struvite kidney stones

A

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

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81
Q

Diagnostic studies in nephrolithiasis

A
  1. Serum chemistries
  2. Urinalysis
  3. Non-contrast helical (spiral) CT. In children and pregnant patients, U/S is the imaging modality of choice
  4. X-rays
  5. Renal U/S
  6. Intravenous pyelogram (IVP)
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82
Q

What do serum chemistries show in nephrolithiasis?

A

they are usually normal; however, there may be a leukocytosis from infection or stress

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83
Q

What does a UA show in nephrolithiasis?

A

Usually reveals microscopic or gross hematuria and may show leukocytes and/or crystals. Urine culture should be performed to rule out infection

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84
Q

What does plain-film radiography show in nephrolithiasis?

A

It can identify radiopaque stones (calcium and struvite); unfortunately, it may miss a small stone even if radiopaque

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85
Q

What can a renal u/s show in nephrolithiasis?

A

It can only identify stones in the kidney, proximal ureter, or UVJ

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86
Q

When is an intravenous pyelogram (IVP) indicated in nephrolithiasis?

A

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.

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87
Q

Treatment of kidney stones measuring less than 5 mm

A
  • 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
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88
Q

Treatment of kidney stones measuring 5-10 mm

A
  • 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.
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89
Q

Treatment of kidney stones measuring greater than 10 mm

A
  • 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
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90
Q

Appropriate analgesics that can be used in nephrolithiasis

A

Appropriate analgesics include morphine, meperidine, or ketorolac. Combination of morphine and ketorolac is found to be more effective than single-agent use

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91
Q

Treatment of nephrolithiasis that depends on stone makeup

A
  • 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
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92
Q

Treatment of hypernatremia

A
  • 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
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93
Q

Why would you not want to correct hypernatremia rapidly?

A

Because it can cause pulmonary or cerebral edema, especially in patients with diabetes mellitus

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94
Q

What is the most common electrolyte disorder in the general hospital population?

A

Hyponatremia secondary to the use of hypotonic fluid administration

95
Q

Hyponatremia with hypervolemia occurs with what?

A

In the setting of CHF, nephrotic syndrome, renal failure, and hepatic cirrhosis

96
Q

Hyponatremia with euvolemia occurs with what?

A

Hypothyroidism, glucocorticoid excess, and SIADH

97
Q

SIADH definition

A

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

98
Q

Hyponatremia with hypovolemia occurs with what?

A

Renal or nonrenal sodium loss

99
Q

What should be done in terms of diagnostic studies if SIADH is suspected?

A

-CT may be done to r/o a CNS disorder and CXR may be done to r/o lung pathology

100
Q

Treatment of hyponatremia with hypovolemia

A

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)

101
Q

Treatment of severe symptomatic hyponatremia with a sodium of less than 120 mEq/L

A
  • 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
102
Q

Treatment of chronic hyponatremia unresponsive to fluid restriction

A

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

103
Q

What is the cause of neurogenic (or central) DI?

A

Deficient secretion of arginine vasopressin (antidiuretic hromone [ADH]) from the posterior pituitary

104
Q

What is the cause of nephrogenic DI?

A

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.

105
Q

Diabetes insipidus diagnostic studies

A
  • 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
106
Q

Treatment of DI

A
  • 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
107
Q

Dietary measures that can be taken in nephrogenic DI

A

Limiting salt and protein intake

108
Q

Most common causes of hyperkalemia

A

Renal failure, ACE inhibitors, hyporeninemic hypoaldosteronism, cell death, and metabolic acidosis

109
Q

ECG changes with hyperkalemia

A
  • 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)
110
Q

What can be given for severe hyperkalemia with ECG changes?

A

-Calcium gluconate should be given IV to antagonize the effects of hyperkalemia on the heart. Strict monitoring is required

111
Q

What can be given to drive potassium back into the intracellular compartment?

A

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.

112
Q

What can be given when potassium levels are extremely high?

A

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
113
Q

Common causes of hypokalemia

A

Use of diuretics, renal tubular acidosis, or GI losses

114
Q

ECG changes with hypokalemia

A

It may reveal flattened or inverted T waves, increased prominence of U waves, depression of the ST segment, and ventricular ectopy

115
Q

When is IV replacement indicated in hypokalemia?

A

In emergent situations where the serum potassium <2.5 mEq/L or arrhythmias are present

116
Q

When is more aggressive potassium replacement in hypokalemia required?

A

When hypokalemia potentiates the effects of cardiac glycosides on myocardial conduction and leads to digitalis intoxication

117
Q

Common causes of hypercalcemia

A

Malignancy, vitamin D intoxication, hyperparathyroidism, and sarcoidosis

118
Q

Most patients with hypercalcemia are asymptomatic until what level?

A

> 12 mg/dL

119
Q

Diagnostic studies with hypercalcemia

A

Serum calcium, CXR, UA, ESR, 24-hour urine collection, serum vitamin D levels

120
Q

Serum calcium levels must be corrected for what?

A

Albumin levels

121
Q

Corrected calcium equation

A

Measured total calcium + [0.8 x (4-albumin)]

122
Q

What may an CXR reveal in hypercalcemia?

A

Underlying pulmonary mass

123
Q

Why would a UA be performed in hypercalcemia?

A

For signs of hematuria, an early sign of RCC

124
Q

In hypercalcemia, ESR may be elevated in what?

A

Monoclonal gammopathy. Protein electrophoresis of serum or urine may be needed to confirm the diagnosis

125
Q

Elevated urine calcium in an 24 hour urine collection in hypercalcemia suggests what?

A

Malignant neoplastic or paraneoplastic process or hyperparathyroidism

126
Q

A decreased urine sodium in an 24-hour urine collection suggests what?

A

Primary hyperparathyroidism

127
Q

Treatment of hypercalcemia

A
  1. Isotonic saline should be used for volume repletion. Loop diuretics should be used if the patient is hypervolemic after volume repletion
  2. Bisphosphonates can also be considered in severe hypercalcemia
  3. Manage the underlying cause
128
Q

Common causes of hypocalcemia

A

Usually results from a chronic disease (most common cause is CKD) or hypoparathyroidism

129
Q

Classic neurologic findings in hypcalcemia

A
  • 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)
130
Q

Treatment of emergent or severe hypocalcemia

A
  1. Treat any emergent cardiovascular states

2. Severe hypocalcemia should be replaced (IV calcium gluconate or calcium chloride)

131
Q

Treatment of mild hypocalcemia

A

It can be treated on an outpatient basis with oral calcium and vitamin D supplements.

132
Q

Hyperphosphatemia common causes

A

Secondary to CKD or excessive use of phosphate containing laxatives or enemas

133
Q

Hypophosphatemia is secondary to what?

A

Diminished supply or absorption, increased urinary losses, or redistribution

134
Q

Hypophosphatemia common causes

A

Vitamin D deficiency, respiratory alkalosis, burns, or hyperparathyroidism

135
Q

Moderate level of hypophosphatemia

A

Serum level of 1.0 to 2.5 mg/dL. Usually asymptomatic

136
Q

Severe hypophosphatemia

A

Serum level of 1 mg/dL or less

137
Q

Severe hypophosphatemia may lead to what conditions?

A

Rhabomyolysis, paresthesia, and encephalopathy

138
Q

Treatment of hyperphosphatemia

A

-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)

139
Q

Treatment of hypophosphatemia of chronic origin

A

Oral phosphate repletion

140
Q

Diagnostic studies in hypermagnesemia

A
  1. ECG shows widened QRS complex, prolonged PR interval, and prolonged QT interval
  2. Bleeding and clotting times are increased
141
Q

Treatment of hypermagnesemia

A
  1. Administer 10-20 mL of 10% calcium gluconate IV over 10 minutes
  2. Saline diuresis and IV furosemide may increase excretion of magnesium
  3. Dialysis is effective in severe hypermagnesemia
142
Q

Common causes of hypomagnesemia

A

Chronic alcoholism, chronic diarrhea, hypoparathyroidism, hyperaldosteronism, diuretic therapy, osmotic diuresis, and nutritional deficiencies (e.g., prolonged parenteral feeding, malnutrition)

143
Q

Lab tests in hypomagnesemia

A

Hypokalemia, hypocalcemia, and hypocalciuria commonly are associated with causes of magnesium depletion

144
Q

What does the ECG show in hypomagnesemia?

A

Prolonged PR and QT intervals or widening of the QRS

145
Q

Treatment of chronic hypomagnesemia

A
  1. Administer oral magnesium oxide for chronic hypomagnesemia. Administer twice the estimated deficit over several days
146
Q

Treatment of severe symptomatic hypomagnesemia

A
  1. 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
  2. Magnesium sulfate may also be given IM in four divided doses (200-800 mg/day) if IV access is difficult
147
Q

Respiratory acidosis PCO2 and HCO3

A

PCO2= Increased

HCO3=Increased

148
Q

Respiratory alkalosis PCO2 and HCO3

A

PCO2=Decreased

HCO3=Decreased

149
Q

Metabolic acidosis PCO2 and HCO3

A

PCO2=Decreased

HCO3=Decreased

150
Q

Metabolic alkalosis PCO2 and HCO3

A

PCO2=Increased

HCO3=Increased

151
Q

Respiratory acidosis results from what?

A

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

152
Q

Primary causes of respiratory acidosis

A

Primary pulmonary disease, neuromuscular disease (myasthenia gravis), primary CNS dysfunction (severe brain stem injury), and drug-induced hypoventilation

153
Q

Lab findings in respiratory acidosis

A
  1. Acute CO2 retention leads to an increase in blood PCO2 with a minimal change in plasma bicarbonate content
  2. 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
154
Q

Treatment of respiratory acidosis

A
  1. Treat the underlying disorder
  2. A blood PCO2 of greater than 60 mm Hg may indicate the need for assisted ventilation if CNS or pulmonary muscular depression is severe
155
Q

Causes of respiratory alkalosis

A

Include any disorders associated with inappropriately increased ventilatory rate and CO2 clearance. Most common cause is anxiety (hysterical hyperventilation)

156
Q

Lab findings in respiratory alkalosis

A
  1. In acute alkalosis, increased respiratory rate leads to a loss of CO2 via the lungs, which in turn increases the blood pH
  2. 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
157
Q

Treatment of respiratory alkalosis

A
  1. 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
  2. Use of CO2-enriched breathing mixtures or controlled ventilation may be required in cases of severe respiratory alkalosis (pH 7.6)
158
Q

Conditions that result in increased hydrogen ions in the serum (metabolic acidosis)

A
  1. Lactic acidosis; diabetic ketoacidosis; starvation ketosis; and ethylene glycol, methanol, and salicylate intoxication. These conditions result in an increased anion gap (AG)
  2. Hydrogen ions may also be retained in renal tubular acidosis, renal insufficiency, and adrenal insufficiency
159
Q

Conditions that may result in the loss of bicarbonate and result in metabolic acidosis

A

Diarrhea, pancreatic or biliary drainage, and ureteral diversion; these conditions typically have a normal AG

160
Q

Clinical features of metabolic acidosis

A
  1. Hyperventilation is the earliest and most recognized sign, resulting from stimulation of the respiratory drive to blow off CO2 (pulmonary compensation)
  2. Ventricular arrhythmias may occur
  3. Neurologic symptoms
161
Q

What is Winter’s formula and what does it calculate for?

A

PCO2 = (1.5 × [HCO3-]) + 8 ± 2; it allows for calculation of the expected PCO2 compensation in metabolic acidosis

162
Q

Anion gap formula

A

Na+ - [HCO3- + Cl-]

163
Q

Normal anion gap

A

8 ± 4 mEq/L

164
Q

Normal anion gap in metabolic acidosis (also called hyperchloremic metabolic acidosis)

A

Normal AG renal tubular acidosis can be divided into cases of the kidney failing to reabsorb bicarbonate or secrete acid

165
Q

Causes of normal AG metabolic acidosis

A 
Ureteroenterostomy
Small bowel fistula
Endocrinopathies/extra chloride
Diarrhea
Carbonic anhydrase inhibitors
Ammonium chloride
Renal tubular acidosis
Pancreatic fistula 
*Remember the mnemonic: USED CARP
166
Q

How is the anion gap adjusted for hypoalbuminemia

A

For each 1.0 g/dL decrease in serum albumin, the AG should be increased by 2.5 mEq/L

167
Q

Elevated AG metabolic acidosis 4 categories

A

Lactic acidosis, ketoacidosis, toxins/drugs, and kidney failure

168
Q

Common causes of elevated AG metabolic acidosis

A 
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
169
Q

Formula used in metabolic alkalosis for calculation of expected CO2 compensation:

A

Expected PCO2= (0.7 x HCO3-) + 20 ± 2

170
Q

Metabolic alkalosis and increased serum bicarbonate can be caused by what?

A

Loss of hydrogen (vomiting), addition of bicarbonate (hyperalimentation therapy), or disproportionate loss of chloride (diarrhea)

171
Q

Treatment of metabolic alkalosis

A
  1. Intervention to increase renal excretion of bicarbonate are the most effective therapy for metabolic alkalosis
  2. Chloride-responsive conditions (e.g., gastric fluid loss, diuretic therapy) are treated with solutions containing sodium chloride to repair the sodium and chloride deficits
  3. Chloride-resistant conditions (e.g., mineralcorticoid excess) can be successfully treated by removing an adrenal adenoma, if present or by using spironolactone
172
Q

Treatment of uncomplicated cystitis in women

A
  1. The suggested regimen is a fluoroquinolone or nitrofurantoin for 3-5 days
  2. Resistant E. coli is common, but Bactrim can be used as an alternative to a quinolone in susceptible strains
173
Q

Patient education for cystitis

A

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)

174
Q

In complicated pyelonephritis, renal U/S may show what?

A

Hydronephrosis secondary to obstruction

175
Q

Outpatient treatment of pyelonephritis

A

-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.

176
Q

When is hospital admission required for pyelonephritis?

A

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

177
Q

Inpatient pyelonephritis treatment

A

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

178
Q

What is required if failure to treatment occurs in complicated pyelonephritis?

A

Ultrasound imaging to exclude complicating factors such as stones or possible abscess formation that may require prompt intervention

179
Q

Chronic prostatitis

A
  • 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
180
Q

What is a potential complication of acute bacterial prostatitis?

A

Prostatic abscess

181
Q

Diagnostic studies in prostatitis

A
  • UA: reveals pyuria and potentially hematuria and bacteriuria
  • Prostatic fluid: will reveal leukocytosis; culture the fluid
182
Q

Treatment of uncomplicated acute prostatitis

A

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

183
Q

What should you suspect in prostatitis if a fever is not resolved after 36 hours?

A

Prostatic abscess; consult a urologist for management

184
Q

Treatment of chronic prostatitis

A

A fluoroquinolone for 1-3 weeks is more effective than bacterium for 1-3 months

185
Q

What is an effective analgesic for prostatitis?

A

NSAIDs

186
Q

What medication may be helpful in prostatitis if lower urinary tract symptoms (LUTS) is present?

A

Doxazosin

187
Q

What may be required in chronic, recurrent, or resistant cases of prostatitis with or without prostatic calculi?

A

Transurethral resection of the prostate for ultimate resolution

188
Q

Clinical features of orchitis?

A
  • Testicular swelling and tenderness, usually unilateral, occur
  • Fever and tachycardia are common
189
Q

Diagnostic studies for orchitis

A
  1. U/A: reveals pyuria and bacteriuria with bacterial infection
  2. Cultures are positive for suspected organisms
  3. U/S is useful if abscess or tumor is suspected and to r/o testicular torsion
190
Q

Treatment of orchitis

A
  1. If mumps is the cause, symptomatic relief with ice and analgesia should be provided
  2. If bacteria is the cause, the orchitis should be treated like epididymitis (Ceftriaxone + Doxycycline)
  3. Carefully evaluate any scrotal masses
191
Q

General characteristics of epididymitis

A
  1. It is an infection of the epididymis acquired by retrograde spread of organisms through the vas deferens
  2. In men younger than 35 yo, Chlamydia and gonococci are the most common organisms
  3. In men older than 35 years of age, E. coli is the most common organism
192
Q

Diagnostic studies in epididymitis

A
  1. UA reveals pyuria and bacteriuria

2. Cultures show positive results for suspected organisms

193
Q

Treatment of epididymitis

A
  1. 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
  2. In men older than 35 years of age, ceftriaxone plus ofloxacin or levofloxacin
194
Q

Supportive care in epididymitis

A

It would include things like bed rest, scrotal elevation, and analgesics

195
Q

Clinical features of BPH

A
  1. Obstructive symptoms include decreased force of urinary stream, hesistancy and straining, postvoid dribbling, and sensation of incomplete emptying
  2. Irritative symptoms include frequency, nocturia, and urgency
  3. Recurrent urinary tract infections and urinary retention can also occur
  4. DRE typically reveals and enlarged prostate
196
Q

Diagnostic studies of BPH

A
  • PSA is slightly elevated

- Other tests are done to evaluate for renal damage, infection, and prostate or bladder cancer, as suspected

197
Q

Treatment of BPH with mild to moderate symptoms

A

Watchful waiting and frequent monitoring

198
Q

BPH options for medical therapy

A

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
199
Q

Behavioral strategies that can be used in BPH

A

Limiting of fluids prior to bedtime

200
Q

Procedures that may be used to relieve obstruction in BPH

A

Balloon dilation, microwave irradiation, and stent placements

201
Q

Surgical treatment of BPH

A

Transurethral resection of prostate or transurethral incision of prostate

202
Q

Diagnostic studies in urinary incontinence

A
  1. UA can identify diabetes-related glycosuria or acute UTI
  2. Postvoid residual urine volume should be measured to identify urinary retention
  3. Simple urodynamic studies such as cystometry can identify bladder contractions and should be considered
  4. Stress test, U/S, cystoscopy, and cystographic studies may be used to determine anatomic abnormalities
203
Q

Nonpharmacologic treatment of urinary incontinence

A
  1. 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
  2. Pessaries or implants can help decrease stress incontinence
  3. Catherization, either intermittent or indwelling, can be used for overflow incontinence
  4. Surgery for stress incontinence as last resort
204
Q

Pharmacologic treatment of urinary incontinence

A
  1. Anticholinergic medications, such as oxybutynin or tolterodine, are effective for urge incontinence
  2. Vaginal estrogen can be used for stress incontinence. Oral estrogen may worsen urinary incontinence
  3. Tolterodine and oxybutynin can be used for overactive bladder
205
Q

Where do the majority of prostate cancers originate?

A

In the peripheral zone, followed by transitional zone and lastly the central zone

206
Q

Gleason Grading System

A
  • 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
207
Q

Stages A and B (tumor confined to the prostate) of prostate cancer treatment

A

May be treated with radical retropubic prostatectomy, brachytherapy, or external beam radiation therapy

208
Q

Stage C (tumor with local invasion) of prostate CA treatment

A

Treated similar to stages A and B but with reduced effectiveness

209
Q

Stage D (distant metastases) of prostate CA treatment

A

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

210
Q

What is the definitive diagnostic procedure in bladder cancer?

A

Cystoscopy while biopsy confirms the pathologic diagnosis

211
Q

Radiologic diagnostic studies used in bladder cancer

A

IV urogram, pelvic and abdominal CT, CXR, bone scan, and retrograde pyelography for renal pelvic or ureteral tumors and staging

212
Q

Superficial lesions of bladder cancer are treated with what?

A

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)

213
Q

When is radical cystectomy used for bladder CA?

A

For recurrent cancer, diffuse transitional cell carcinomas in situ, and for tumors that have invaded the muscle

214
Q

External beam irradiation therapy is typically reserved for who?

A

Those individuals who are not surgical candidates due to significant comorbid medical conditions

215
Q

Renal Cell Carcinoma paraneoplastic syndromes

A

Includes erythrocytosis, hypercalcemia, hypertension, and hepatic dysfunction in the absence of hepatic metastases

216
Q

What is the primary treatment for localized disease (stage T1 to T3a lesions) for renal cell carcinoma?

A

Radical nephrectomy. Neoadjuvant or adjuvant radiation therapy has not been shown to prolong survival for early stage lesions

217
Q

What is an important method of palliation in patients with disseminated disease of renal cell carcinoma to the brain, bone, and lungs?

A

Radiation therapy

218
Q

What in Wilms tumor is associated with a poorer prognosis?

A

Anaplasia

219
Q

What is the initial study of choice for Wilms tumor?

A

Ultrasonography

220
Q

What is the treatment of choice for surgicaly resectable tumors?

A

Radical nephrectomy with lymph node sampling

221
Q

What is the treatment for unresectable tumors?

A

They should undergo preoperative biopsy followed by chemotherapy

222
Q

Wilms tumor is responsive to what chemotherapy drugs?

A

Dactinomycin, vincristine, and doxorubicin

223
Q

When is radiation therapy added for Wilms tumor?

A

For higher stage tumors (stages III and IV) and for tumors with focal anaplasia

224
Q

What are the subtypes of nonseminomatous testicular cancer?

A

Embryonal carcinoma, teratoma, mixed cell type, and choriocarcinoma

225
Q

Elevated blood levels of what are diagnositc for nonseminomatous germ cell tumors?

A

Alpha-fetoprotein or beta-human chorionic gonadotropin; the majority of patients with seminoma have normal levels

226
Q

Are seminomatous tumors radiosensitive or radioresistant?

A

Radiosensitive

227
Q

Stage I nonseminomatous tumor (testicular CA) treatment

A

It can be treated with nerve-sparing retroperitoneal lymph node dissection or rigorous surveillance without surgery or chemotherapy

228
Q

Stage II nonseminomatous tumor (testicular CA) treatment

A

Surgery or chemotherapy

229
Q

Stage III nonseminomatous tumor (testicular CA) treatment

A

Surgery or chemotherapy

230
Q

Stage I seminomatous tumor (testicular CA) treatment

A

Radiation therapy to the para-aortic and ipsilateral iliac nodal areas

231
Q

Stage IIa and IIb seminomatous tumor (testicular CA) treatment

A

Increased radiation to the affected nodes

232
Q

Stage IIc and III seminomatous tumor (testicular CA) treatment

A

Chemotherapy

233
Q

What are some causes of acquired phimosis in adults?

A

Poor hygiene and chronic balanitis. Consider evaluation for possible diabetes in men with chronic infections

234
Q

Treatment for paraphimosis

A
  • Reduce emergently (either manual or surgically)

- After reduction, referral for circumcision is necessary because the condition is likely to recur

A Comprehensive Review for the Certification and Recertification Examination for Physician Asistants (8 decks)

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