Benign Prostatic
Hyperplasia:
MC benign tumor in men
and directly related to age.
D/D:
 Urinary tract infection
 Urethral stricture
 Ureterolithiasis /
Nephrolithiasis
 Prostate carcinoma
Erectile Dysfunction:
consistent inability to
maintain an erect penis w
sufficient rigidity to allow for
sexual intercourse.
Symptoms:
 Obstruction
-Urinary hesitancy
-Decreased force and caliber of the urinary stream
-Sensation of incomplete emptying of the bladder
-Straining/Dribbling
 Irritative-Urgency, Frequency, Nocturia
Signs:
 Enlarged prostate on DRE
 Smooth, firm, elastic enlargement
 Size does not correlate with symptom severity
 Normal neurological exam with good rectal tone and negative stool Hemoccult.
 Prostatic induration or Nodules
 Not a typical finding in BPH
 High index of suspicion for cancer
Labs:
 Urinalysis- Evaluate infection or hematuria
 Renal function studies- Renal insufficiency present in 10% of patients
 Serum Prostate-Specific Antigen (PSA)- Concern in levels > 4.0 ng/ml for cancer
Treatment:
 Watchful waiting- Mild symptomatic disease may spontaneously resolve.
 Medical therapy
 Alpha Blockers (Tamsulosin/Flomax) or (Terazosin/Hytrin)
 5 alpha Reductase Inhibitors (Finasteride/Proscar)
 Phosphodiesterase-5 inhibitor (Tadalafil/Cialis)
 Surgery
 Transurethral Resection of the Prostate (TURP)
 Transurethral Incision of the Prostate (TUIP)
 Open Prostatectomy
Loss of erections:
 Caused by Arterial, Venous, Neurogenic, and Psychological problems
-Hyperlipidemia
-HTN/Renal Failure
-Depression
-Diabetes
 Pharmacologic
-Excessive recreation drug and alcohol use
-Central acting sympatholytics (Methyldopa or Clonidine)
Loss of Libido:
 Caused by androgen deficiency from hypothalamic, pituitary, or testicular dz.
- Serum studies of testosterone and gonadotropin help to isolate problem
 Drug side effects- Beta Blockers, spironolactone, and many others
Clinical Evaluation:
 Complete History and Physical- Determine the presence of a underlying cause
 Laboratory analysis:
 Complete Blood Count
 Lipid profile
 Glucose
 Serum testosterone and prolactin: Serum FSH and LH
 Urinalysis
Treatment:
 Treat any underlying causes appropriately
 Hormonal Replacement- Testosterone injections
 Vacuum Constriction Device- Useful in venous disorders
 Vasoactive Therapy- Oral medications or direct injections
 Penile Prosthesis
 Vascular reconstruction- Helpful in patients with arterial disorders that do not respond to
vasoactive therapy
Urinary Incontinence
Stress Incontinence: urine leakage associated w/ increased abdominal pressure weakness
(sneezing, coughing, or physical exertion)
- Impaired urethral support from pelvic floor muscle
- Intrinsic sphincter deficiency caused by pelvic surgery
- Normal PVR
Urge Incontinence: involuntary urine loss accompanied by a sudden desire to pass urine. Usually
involves urgency, frequency, and nocturia (Overactive Bladder Syndrome)
- Caused by uninhibited bladder contraction from detrusor muscle hyperactivitiy.
- Little PVR; increased contraction on refilling
Mixed Incontinence: involuntary loss of urine associated w/ urgency as well as exertion and
increased abdominal pressure. (MC type of UI in women)
-Caused by detrusor overactivity w/ impaired urethral function
Overflow Incontinence: small volume leakage associated w/ a weak urinary stream, dribbling,
hesitancy, frequency, and nocturia.
-Caused by an incomplete bladder empyting secondary to impaired detrusor contractility or bladder
outlet obstruction. (pelvic organ prolapse or enlarged prostate, spinal cord injuries, or bladder
neuropathy)
- Increased PVR
Clinical Work-up
 Urinalysis and urine culture
 Post Void Residual (PVR): Determine functional status
 Hematuria
 Serum electrolytes (Calcium)- Glucose
 Ultrasound- Evaluation of hydronephrosis, hydroureter, and most urinary tract stones
 MRI- Most accurate technique for visualizing pelvic floor defects
Treatment:
 Identify and treat reversible causes. Discontinue potentially offending medications
 Anticholinergics (if this was the offending factor)
 Calcium Channel Blockers
 Underlying medical conditions/Behavioral Approaches
 Bladder outlet obstruction
 Diabetes
 Prostate disease
 Urinary tract infections
 Provide a commode or urinal to patients with limited mobility-Useful in Functional
Incontinence
 Pharmacotherapy:
- Anticholinergic/Antimuscurinics agents:
- Oxybutinin, Tolterodine, Fesoterodine, Trospium, Solifenacin, and Darifenacin
- Promote bladder relaxation
- Decrease urgency. With behavioral therapy
- Alpha adrenergic agonists: MOA- Relax smooth muscle and Decrease urine flow
resistance
- Selective 1 agents (Prazosin, Alfuzosin)
- Long-acting 1 agents (Terazosin, Doxazosin)
- Long-acting 1a subtype selective agents (Tamsulosin aka Flomax) –effective for
BPH
- Estrogens: Little/No evidence to support use
- Serotoninergic/Norepinephrine drugs
- 5-alpha-reductase inhibitors: Finasteride, Dutasteride
 Surgical Options:
-Electrical stimulation of detrusor muscles
- Urinary diversion
- Artificial sphincter
- Bladder neck elevation
- Urethral stricture dilation
Hernias: a protrusion,
bulge or projection of an
organ or a part of an organ
through the body wall that
normally contains it.
Abdominal Hernias: umbilical and epigastric hernias
Groin Hernias:
o Inguinal:
- Indirect inguinal hernia is the most common groin hernia in both sexes. Protrude at the
internal inguinal ring. More frequently on the right side in both sexes.
- Direct inguinal hernia are more common in men than women and they protrude medial to
the inferior epigastric vessels within Hesselbach's triangle, which is formed by the inguinal
ligament (Poupart's ligament) inferiorly, the inferior epigastric vessels laterally, and the rectus
abdominus muscle medially.
o
Femoral: less common compared to Inguinal. More common in women than men. Occur later
in life than inguinal hernias (usually >70yo). Femoral hernias are located inferior to the
inguinal ligament and protrude through the femoral ring, which is medial to the femoral
sheath and lateral to the lacunar ligament
Hernias are classified by etiology:
o Congenital inguinal hernia: due to failure of the processus vaginalis to close.
o
Acquired Hernias: due to weakening or disruption of the fibromuscular tissues of the body
wall allowing intra-abdominal contents to protrude through the acquired defect. Acquired
groin hernias can develop as a result of inherent connective tissue abnormalities, chronic
abdominal wall injury, or possibly drug effects
Treatment:
The definitive treatment of all hernias, regardless of their origin or type, is surgical repair.
Urgent/emergent repair is indicated for patients who develop complications (eg, bowel obstruction,
bowel perforation) related to an inguinal or femoral hernia.
Nephrolithiasisspecifically refers to calculi
in the kidneys.

Geographic Factors
- Increased incidence in areas of high humidity and elevated temperatures
- Significant increase of incidence during the hot summer months
Diet/Lifestyle Factors
- Sedentary occupation
- High protein, calcium, and salt diet
- Oxalate rich foods- Green leafy veggies, nuts, tea, coffee
- Frequent use of calcium-containing antacids (i.e. TUMS)
- Loop diuretics can lead to increased urinary calcium concentrations
- High doses of Vitamin C- Results in hyperoxaluria from ascorbic acid oxidizing into oxalate.

Ureterothiasis- specifically
refers to calculi in the
ureter. These calculi almost
always originate in the
kidney but become lodged
in the ureter. Stones form
as a result of growth of
crystalline components in a
supersaturated urine.
Ureteral Stones:
- Renal calculi exit the kidney and become lodged in the ureter
- Typically lodge at 3 sites:Ureteropelvic junction, Crossing of the ureter over the iliac vessles,
and
Ureterovesical junction
- Stones < 5mm frequently pass spontaneously
Types of Urinary Stones:
 Radiopaque (85%)
- Calcium oxalate *most common
- Calcium phosphate
- Struvite (magnesium ammonium phosphate)
 Radiolucent
- Cystine – smooth edged, ground glass appearance
- Uric acid- Most common in children
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Signs and Symptoms
Acute onset of SEVERE unilateral flank pain
Remember “Loin to groin distribution”
N/V
Patients tend to be “on the move” and anxious
Stone size does not correlate with severity of symptoms but does relate to the ability of the
patient to pass the stone.
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Diagnostic Evaluation
Urinalysis/CBC/Chemistry/
Hematuria and infection
Elevated WBC’s = Systemic infection
Assessment of renal function
Serum Calcium (if elevated, check PTH level)
Sodium = Elevated Sodium
If history of multiple stones, check PTH level to r/o Hyperparathyroidism
24-hour urine
Calcium, Oxalate, and Uric acid levels
Imaging studies:
- Plain radiograph (KUB)
- Renal Ultrasonography
- Intravenous pyelogram (IVP)
- Helical CT without contrast *Best test
Nephrolithiasis Imaging:
 Non-contrast Helical CT Urogram (preferred, gold standard)
- All non-pregnant patients
- Preferred over intravenous pyelogram
- Findings : Identifies small stones anatomical location and Determines size, shape,
and position
 Imaging: Intravenous Pyelogram (IVP)
- Nonpregnant patients where CT is not available
- Findings: Functional renal and ureter study and Determines location but not size
 Abdominal ultrasound
- Pregnant patients
- Cholecystitis suspected
- Gynecologic process suspected
- Findings: Hydronephrosis and Renal Stones
- Difficult to identify stones < 5mm
 Abdominal X-Ray (KUB)
- History of prior radiopaque stones
- Findings:
- Radiodense (radiopaque) stones: Calcium Oxalate Stones and Struvite Stones
- Intermediate stone lucency : Cystine Stones
- Radiolucent stones (not visible on X-Ray): Uric Acid Stones
Treatment Guidelines
 Hydration and Analgesia
 Maintain adequate circulating volume
 Opiate analgesia
 Morphine sulfate
 Hydromorphone (Dilaudid)
 NSAIDS: Ketorolac (Toradol)
 Anti-emetics
 Metoclopramide (Reglan)
 Promethazine (Phenergan)
 Prochlorperazine (Compazine)
 Medical Expulsive Therapy
 Off label use of medications: Calcium Channel Blockers and Alpha Blockers
 Extracorporeal Shock Wave Lithotripsy (ESWL)
 High energy sound waves break larger stones into pieces so that they will pass more
easily
 Surgery
 Ureteroscopy
 Endoscope passed up the ureter for manipulation of the stone
 Urethral stent placement
 Percutaneous nephrostolithotomy
 Fragmentation and removal of large stones from the kidney
Hydrocele- collection of
serous fluid that results
from a defect or irritation in
the tunica vaginalis of the
scrotum.
(less commonly may arise
in the spermatic cord)
Communicating
Hydroceles: Fluid has the
ability to move bw the
abdomen and the tunica
vaginalis in the scrotum.
Caused by failed closure of
the processes vaginalis.
Non-Coummnicating
Hydroceles: Serous fluid is
contained w/in the tunica
vaginalis. Caused by
pathologic closure of the
processes vaginalis.
Varicocele: abnormal
dilation of the venous
plexus and the internal
spermatic vein.
CAUSES:
 Congenital
 Orchitis or epididymitis
 Tumors
 Trauma
 Radiation therapy
 Testicular torsion
 Most hydroceles are asymptomatic and present with an acute painless, enlarged and pearshaped scrotum.
 Generally located anterior and superior to the testes.
 Their size can vary with the position of the patient.
 May become uncomfortable with epididymal irritation.
Diagnostic studies
 Laboratory
 CBC with differential- Infection or inflammation (? Epididymitis)
 Urinalysis- Proteinuria or pyuria
 Imaging
 Inguinal-Scrotal Ultrasound with Doppler Flow Study
 Identifies testicular abnormalities (? Solid mass) and assesses
perfusion
 Procedures
- Transillumination: Not diagnostic of hydrocele but makes a solid mass less likely.
- Hydrocele aspiration: Not therapeutic because fluid reaccumulates quickly.
Should
produce a clear amber colored fluid
Treatment
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Surgical correction of underlying abnormality is the processes vaginalis
BEWARE:
- 1. 10% of testicular tumors have a reactive hydrocele.
- 2. An inguinal hernia with a loop of bowel in it will transilluminate as well.
- 3. Hydroceles are almost NEVER symptomatic.
 Occur in the left testicle 80-90%, but may be bilateral
 Pt c/o scrotal pain or a heaviness.
 Palpated as a “Bag of Worms” which is the twisting and dilation of pampiniform plexus.
Diagnostic studies
 Color flow Doppler Ultrasonography
 Follow up evaluations with U/S or CT
TREATMENT
 Surgery: No medical therapy is indicated. Significant impairment of sperm
production and function is likely.
Testicular Torsion: twisted
spermatic cord.
•
Urologic EMERGENCY!! Prompt surgical care w/in 6-12hrs from onset of s/s or infarction will
occur
Often see in males less than 30 yo
May present w/ sudden episode of intermittent testicular pain and 50% of torsions occur
during sleep.
•
•
CLINCAL FEATURES:
• Acute scrotal pain and edema (< 24 hours)
• Nausea and Vomiting
• Abdominal pain
• Fever
• Urinary frequency
•
High position and transverse lie of affected testicle
•
Abnormal cremosteric reflex
Diagnostic studies:
• Laboratory
• Urinalysis = normal
• CBC = Increased WBC’s
• Imaging
• Color Doppler Ultrasonography- Consult Urology STAT, then proceed with
ultrasound.
Balanitis- An inflammation
of the glans penis.
Treatment:
• Urologic consultation and prep for surgery
• If seen within first few hours of onset, then manual detorsion can be attempted using an
“Open Book” manipulation. Use Doppler u/s once completed to confirm the state of
testicular vasculization.
In patients with testicular torsion, the affected testis generally is twisted inward (medially). The
clinician can easily recall which direction to rotate a torsed testicle (depending on which side is
affected) by comparing the action to opening the spine of a book.
Causes:
 Poor hygiene (pediatrics)
-Uncircumcised
 STD’s (adolescents/adults)
 Candidal Infections (elderly, diabetics)
 Hx of penile discharge, inability to retract foreskin, difficulty controlling the stream of the
urine.
 Chaffing from lined swim trunks may mimic a balanitis in males.
Work-up:
 H&P- Trauma?STD?DM or immunocompromised?
 Labs- Serum glucose, culture of penile discharge, syphilis serology, wet mount, KOH for
candida, HIV and HPV for populations at risk
Treatment:
 Retract foreskin daily to wash/soak w soap and water
 Apply bacitracin daily
 Apply topical Clotrimazole if candida present
 Evaluate penile/urethral cultures
 Consider urology consult
***Most common complication is Phimosis (inability to retract distal prepuce over the glans penis)
Phimosis- in ability to
retract distal prepuce over
the glans penis
Paraphimosisentrapement of a retracted
foreskin behind the coronal
sulcus that cannot be
reduced.
Hair Tourniquets!!
Causes:
 Congential
-MC in young children.
-Nml into the teenage yrs as long as it does not cause urinary obstruction.
 Acquired
-Caused by poor hygiene, chronic balanitis, or forceful retraction on a congenital phimosis.
Treatment:
 No Tx unless urinary obstruction
 Proper hygiene
If urinary obstruction is present: Surgical Preputial plasty
Causes:
 Uncircumcised
 Hair tourniquets
S/S:
 Pain, erythema, edema of the uncircumcised penis
 If constriction is severe, then the edema causes venous engorgement of the glans leading
to arterial compromise w subsequent tissue necrosis.
 Beware of Hair Tourniquets!!
Treatment:
 Emergent Reduction!
 Noninvasive
-Manual reduction
 Invasive
-Puncture technique
-Dorsal slit Procedure
***Refer to Urology for circumcision even if reduced.
Cystitis
Infectious/Inflammatory Conditions
Acute Cystitis:
 Coliform bacteria, gram negatives or gram positive organisms.(E. coli, Staph
saprophyticus, other Enterobacteriaceae).
 S/S: Irritative voiding symptoms (urgency/freq/dysuria), Afebrile, hematuria,
suprapubic tenderness or normal exam.
 Urinalysis: Degree of pyuria/bacteriuria may not correlate with severity of sx.
 Urine culture is positive: Indicated if recurrent infections or diagnosis in question.
 DDx: Vulvovaginitis, pelvic inflammatory disease or gyn conditions in females. Urethritis,
prostatitis in males.
 Tx: 1-3 day antibiotics (Fluoroquinolones (Cephalexin 250-500mg q6hrs or Cipro 250500mg q12hrs) and Nitrofurantoin 100mg q12hrs) for uncomplicated acute cystitis. Urinary
analgesics for symptom relief.
 Complicated cystitis should be treated for 7 days
Interstitial Cystitis (Painful Bladder Syndrome):
• Pain with bladder filling, relieved by emptying.
• Irritative voiding symptoms (urgency/freq/dysuria)
• Diagnosis of exclusion. Negative w/u. Unknown etiology.
• Not common, female>male, hx of bladder problems in childhood.
• Cystoscopy may show submucosal hemorrhage with bladder distension (glomerulations).
• Spontaneous resolution 50% at 8 months.
• TX: No cure. Symptom relief. Hydrodistension (at the time of cysto) may provide relief (2030%). Anticholinergics/calcium channel blockers (Amitriptyline 10-75mg/d PO often used
as first line therapy) /other therapies/TENS
• Hallmark: Persistent and bothersome symptoms in the absence of identifiable
cause.
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Epididymitis: inflammation
or infection of the
epididymis.
Commonly affects male 19-40yo.
Age dependent pathogens:
- Prepubertal males: Escherichia coli-Retrograde extension of bacteria
- Males <40 yo: Chlamydia trachomatis (60%) and Neisseria gonorrhoeae
- Male >40yo: Escherichia coli- underlying obstructive urinary dz
Physical Examination
o Gradual scrotal pain and edema
o Urinary frequency
o Nausea
o Fever / Chills
o Urethral discharge
o Abdominal or flank pain
o Patient may waddle
o Prehn’s sign = elevation of the affected hemiscrotum above the symphysis pubis improves
pain from epididymitis. ** this may be helpful but is not reliable.
Diagnostic studies
o Laboratory
 Urinalysis, Urine C&S
 CBC
 Urethral discharge culture and wet prep
o Imaging
 Color Doppler Ultrasound (Scrotum)
Treatment
 Must r/o torsion and testicular tumor
 Bed rest with scrotal elevation/support
 ABX therapy
- Age < 35 yo = Ceftriaxone 250mg IM + Doxy 100mg PO TID x 10-21 days
- Age > 35 yo or MSM = Levofloxacin 500mg IV/PO or Cipro 500mg PO BID x 14 days
 Analgesics
Orchitis-inflammatory rxn
of the testis secondary to
infection.
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Most cases are associated with a viral mumps infection; however, other viruses and bacteria
can cause orchitis.
Viral orchitis is associated with the abrupt onset of scrotal pain and swelling and is primarily
unilateral. When associated with mumps infection, orchitis generally appears four to seven
days after the development of parotitis.
STD form in younger age group (<40), associated with urethritis. N. gonorrhea or chlamydia.
First affects tail of epididymis, then spreads over body and head of epididymis. Orchitis
develops in 20-40% of cases (via direct spread of infection)..
May have symptoms of urethritis, irritative voiding symptoms, scrotal pain which may radiate
to flank. Fever and scrotal pain evident. May be difficult to differentiate epididymis from
testes. Prostate may be tender.
Prehn’s Sign: Pain with edididymo-orchitis relieved with elevation above symphysis pubis, not
relieved with testicular torsion..
Imaging: Scrotal U/S may be indicated to r/o hydrocoele, torsion.
DDx: Tumors (painless), Testicular torsion.
Treatment: supportive and should include bed rest and the use of hot or cold packs for pain.
Antibacterial medications are not indicated for the treatment of viral orchitis, and most cases of
mumps-associated orchitis resolve spontaneously after three to 10 days.
Epididymoorchitis requires appropriate antibiotic coverage, as with epididymitis.
o
Age < 35 yo. N. gonorrhea/Chlamydia: Scrotal elevation, ceftriaxone (Rocephin), a single
250--mg dose intramuscularly, and doxycycline (Vibramycin), 100 mg orally twice daily for
10 days. Consider evaluation of urinary tract afterwards.
Age > 35 yo./Homosexuals who engage in anal insertive sex. Enterobacteriaceae. FQ for 1014 days or AM-SB, Ceph-3rd, TC-CL, PIP-TZ.
Prostatitis
Acute Prostatis
• Usually caused by Gram negative organisms (E. coli, Pseudomonas), may also be gram
positives (enterococci).
• Infection is usually ascending in origin with reflux into prostatic ducts.
• Perineal, sacral, or suprapubic pain, fever, and irritative voiding symptoms.
Obstructive symptoms usually present. Warm, tender prostate on exam. Prostate
massage contraindicated.
• Pyuria, bacteriuria, and hematuria. CBC with leukocytosis. Urine culture is positive.
• DDx: Epididymitis, diverticulitis,urinary retention from other process.
• Tx: IV antibiotics (Ampicillin 1g q6hrs and gentamicin 1mg/kg q8hrs) until afebrile x2448hrs then Fluquinolones (Cipro 750mg q12hrs) x 4-6wks. Bladder catherization if urinary
retention develops may need to be done by suprapubic route. Should avoid transurethral
catheterization (trauma, septicemia). F/U urine culture after treatment.
• Prognosis: With effective treatment, chronic prostatitis is rare.
Chronic Bacterial Prostatis (CBP)
 Similar organisms/route of infection as acute prostatitis (AP). Previous history of AP risk
factor, may have history of UTI, but most have no history of infection.
 Asymptomatic, varying degrees of irritative voiding symptoms, low back pain, perineal
pain are common. Prostate exam may be normal, boggy, or indurated.
 U/A may be normal. Prostatic secretions show leukocytes (lipid-laden macrophages).
Culture is positive. Imaging not indicated.
 DDx: Chronic urethritis, other prostatitidies, anal disease, other UTI.
 Tx: Goal is intraprostatic levels (trimethoprim-sulfamethoxazole best cure rate but
increasing resistance). Carbenicillin, erythromycin, cephalexin and quinolones also
effective. Must treat for 6-12 weeks. Analgesics (antiinflammatories, hot sitz baths).
 Prognosis: Chronic, difficult to cure, relapses, recurrences are common. Consider longer
therapy or suppressive antibiotic therapy.
Nonbacterial Prostatitis
• Most common of the prostatitidies.
• Cause is unknown? (chlamydiae, mycoplasmas, ureaplasmas, viruses)
• ? Infectious, noninfectious, autoimmune.
• Diagnosis of exclusion.
• Same symptoms as CBP. Similar history, except no history of UTIs.
• Increased WBCs on prostatic secretions, but negative culture.
• DDx: CBP, malignancy.
• Tx: Trial of antibiotics that target above organisms. Erythromycin 250mg PO QID x 14days
Consider dietary restrictions: alcohol, caffeine, etc..
• Prognosis: Recurrence is common. “Annoying”, but few, if any, serious sequelae.
Treatment of Prostatitis:
• Acute: <35yo; N. gonorrhea, C. trachomatis. Ceftriaxone 250mg IM (or cefixime 400mg
PO), one dose, then Doxycycline 100mg BID for 10 days.
• Acute: >35yo; Enterobacteriaceae. FQ (Cipro/Levo) or TMP/SMX DS BID for 10-14 days
(some authorities recommend 4 weeks of tx. Urine NAAT if ?.
• Chronic bacterial: Enterobacteriaceae, Enterococcus, Pseudomonas. FQ for 4-6 weeks or
TMP/SMX DS BID for 1-3 months. Treatment failures are common.
• Chronic prostatitis/chronic pain syndrome (abacterial/prostadynia): Unknown etiology, ?
Infectious. Consider alpha blockers (controversial). Antibiotics/alpha blockers, no benefit.
Prostadynia
• Pain w/ noninflammatory condition, affecting young and middle age men. Prostate is
normal.
• Symptoms similar to CBP, but no irritative voiding symptoms. May have obstructive
symptoms. Chronic symptoms. Exam reveals normal prostate, but increased anal
sphincter tone.
• Labs are normal. May have dysfunctional voiding (bladder, sphincter dyssynergia).
• DDx: Other prostatitidies.
• Tx: Consider alpha blockers (terazosin 1-10mg PO QD or doxazosin 1-8mg PO QD),
benzodiazepines, biofeedback. Sitz baths may provide relief.
Pyelonephritis
Acute Pyelonephritis
• Involves kidney parenchyma and renal pelvis. Usually ascending infection.
• Gram-negatives: E. coli, Proteus, Klebsiella, Enterobacter, and Pseudomonas.
• Gram-positives: Enterococcus faecalis. Staph aureus (think hematogenous spread)
• Fever, flank pain, chills, irritative voiding symptoms, nausea/vomiting, diarrhea,
dehydration, tachycardia, and CVAT.
• Urinalysis: Pyuria, bacteriuria, WBC casts, hematuria.
• Urine culture is positive. Blood culture may be positive.
• Leukocytosis with left shift on CBC.
• Consider ultrasound to r/o obstruction or abscess (particularly if Temp. >72hours on
therapy).
• DDx: Can be broad. Appendicitis, diverticulitis, pancreatitis, cholecystitis, pneumonia,
epididymitis, prostatitis, cystitis.
• Complications: Sepsis, shock. Impairment of renal function with scarring, particularly if
underlying disease. Abscess formation may occur.
• Tx: IV antibiotics, hospitalization for supportive care in severe cases. IV antibiotics
generally given until afebrile for 24 hours, then complete at least 7 day course of therapy.
Risk Factors for Acute Pyelonephritis (women)
• Frequent sexual activity
• UTIs within the previous 12 months
• DM
• Stress incontinence, recent
• New sexual partner within the previous year.
• Recent spermicide use.
• History of UTIs in patient’s mother
Indications for Hospitalization:
• Comorbid conditions
• Hemodynamic instability
• Male sex
• Metabolic derangement, acute. (AKI, acidosis)
• Pregnancy
• Toxic appearing, severe pain.
• Not able to hydrate orally
• Temperature > 103
Treatment:
- Acute Uncomplicated Pyelonephritis
• Moderately ill (outpatient), oral therapy. Fluoroquinolone (FQ) for 5-7 days (cipro 500mg
BID, Cipro-ER, levo,oflox, and ? moxi). AM-CL, cephalosporin, or TMP/SMX for 14 days.
• Hospitalized. IV therapy until afebrile for 24-48 hours. Should complete a 14 day course
of antibiotics. FQ or ampicillin plus either gentamicin/ceph 3rd generation/AP penicillin.
Alternatives: TC/CL,AM/SB, PIP/TZ, ERTA, or DORI.
• Prompt imaging if hypotensive to r/o obstructive uropathy (ECHO or CT)
- Complicated UTI: Pregnant, DM, recent urinary tract instrumentation, CKD, Urinary tract
abnormalities, immunosuppression.
•
Obstruction, reflux, transplant, azotemia, foley catheter related, predisposing medical
condition.
• Greater risk of complications, types of organisms, and resistant organisms.
• Higher incidence of Enterobacteriaceae, Pseudomonas, Enterococci, and rarely S. aureus.
IV AMP-Gent, PIP-TZ, TC-CL, IMP, DORI, MER, or FL as an alternative.
• Complete 14-21 days of treatment.
• Convert to oral when clinically indicated base on culture/sensitivities.
• Need to R/O obstruction with imaging (U/S or CT).
Urethritis-urethral
inflammation caused by
infectious and
noninfectious.
Infectious:
• Neisseria gonorrhoeae
• Chlamydia trachomatic
• Herpes Simplex Virus
• Mycoplasma genitalium
• Ureaplasma urealyticum
• Trichomonas vaginalis
Noninfectious:
• E.Coli and other bacteria present in stool
• Reactive arthritis (Reiter syndrome)
S/S:
•
•
•
•
•
•
•
Gonorrhea Gram Stain
Dysuria
Frequency
Difficulty starting urination
Dysparuria
Purulent Urethral Discharge
Blood in semen or urine
Itching, pain or discomfort when not urinating can also occur
Diagnostic Evaluations:
Chlamydia Non-Amplified Tests
• Enzyme Immunoassay (EIA), e.g. Chlamydiazyme.
• Nucleic Acid Hybridization (NA Probe),
• detects chlamydial ribosomal RNA.
• able to detect gonorrhea and chlamydia from one swab.
DNA amplification assays:
• polymerase chain reaction (PCR).
• ligase chain reaction (LCR).
Gonorrhea:
• Urethritis: male Incubation: 1-14 d, (usually 2-5 d).
• Sx: Dysuria and urethral purulent discharge (5% asymptomatic).
• Dx: Gram stain urethral smear (+) in > 98% of those with a (+) culture.
• 46% co-infected with C. trachomatis.
Complications: dissemination, conjunctivitis.
Urogenital infection – female (Incubation : unclear: symptoms usually in 10d)
• Endocervical canal primary site.
• Sx: majority asymptomatic; may have vaginal discharge, dysuria, pain on urination,
labial pain/swelling, abdominal pain.
• Dx: Gram stain smear (+) 50-70% with (+) culture.
• Complications: PID, dissemination.
Treatment: Ceftriaxone 250mg IM + Azithromycin 1g single dose
•
Nongonococcal Urethritis:
• Etiology:
• 40% Chlamydia trachomatis.
• 30% genital mycoplasmas (Ureaplasma urealyticum, Mycoplasma genitalium).
• 13% Trichomonas vaginalis, HSV.
• Unknown in ~50% cases.
• Sx: Mild dysuria, mucoid discharge.
• Dx: Urethral smear  5 PMNs (usually 15/OI field). Urine microscopic  10 PMNs/HPF.
Leukocyte esterase (+).
Treatment: Azithromycin 1g single dose or Doxycycline 100mg BIDx7days
• Mycoplasma genitalium – more responsive to azithromycin.
• Chlamydia are more responsive to doxycycline than azithromycin;
• Suspect Mycoplasma genitalium in relapse of NGU; can retreat with Azithromycin x 5 days
or moxifloxacin x 10 days.
Recurrent /Persistent Urethritis should be re-treated with initial regimen in non-compliant or reexposure occurs.
Vaginitis
Physical Exam:
◦ Inspection- Vulva, vagina and cervix
◦ Test/Culture - Suspected organisms based on Hx and PE
◦ Bimanual Exam- Evidence of pelvic infection
Noninfectious Vaginitis:
 Chemical vaginitis: Topical irritants (soaps, scented detergents) or Allergens (latex)
◦ Symptoms: Pruritis, irritation, burning, discharge
◦ Tx
- Stop offending agent
- Corticosteroid treatment
- Sodium bicarbonate sitz baths
Infectious Vaginitis:
1.) Bacterial vaginosis ** most common
- Overgrowth of Gardnerella vaginalis, Mobiluncus species
- Overall prevalence ~ 30% of women, rare in those who are not sexually active
- Marked decrease in lactobacilli acidophilus that maintains vaginal pH. Allows for
overgrowth of Gardenerella and other species
- Risk Factors: Pregnancy, IUD, Frequent douching(killing the good normal flora), Sex with
another woman (prevalence increases to 45%)
- Symptoms: Copious watery, malodorous (“fishy”, rotten smell), white-grey discharge,
Pruritus, No associated lesions -non-painful (thus termed vaginosis, not vaginitis)
- May be asymptomatic (50%)
- Diagnosis – 3 of 4 must be present:
- White adherent discharge
- Vaginal pH > 4.5
- (+) Whiff test with 10% KOH very strong odor
- “Clue Cells” on wet prep and marked decrease of lactobacilli
- Potential Complications:
-Increase in preterm delivery
- Pelvic inflammatory disease
- Post-abortion infection
- Postpartum Endometritis
- D/D should include cervicitis and cervical CA
- Treatment:
-Metronidazole (flagyl) 500 mg po bid x 7d
- Metronidazole gel 0.75% 1 full applicator (5g) intravaginally qd x 5 d
- Clindamycin cream 2% 1 full applicator qhs x 7d
- AVOID douching – promotes loss of vaginal lactobacilli
- Unclear if sexually transmitted
- Treating partners not necessary
- Use of condoms may reduce risk of recurrence
- Consider screening female partners
2.) Candidiasis: Caused by Candida albicans (90% of cases)
- Risk Factors:
- Young age at 1st intercourse
- Increased frequency intercourse
- Diabetes
- HIV / immunocompromised
- Pregnancy
- Antibiotics
- Oral contraceptives
- Corticosteroid use
- Obesity
- Inactive/bedriddened
- Symptoms
◦ Intense vulvar pruritus
◦ “Cottage cheese” like discharge
◦ Vulvar erythema
◦ “burning” with urination
- Diagnosis:
◦ Wet prep: shows hyphae and budding yeast
◦ KOH: hyphae and budding yeast, whiff test (-)
◦ pH: <4.5
◦ Culture (rarely)
Treatment:
- Over-the-counter intravaginal antifungal creams (many available).:
- Miconazole (Monistat-7) vaginal cream, 100 mg, 1 application in the vagina q.d. x 7 nights;
may be used during 2nd and 3rd trimesters.
- Clotrimazole (Gyne-Lotrimin, Mycelex-G) vaginal cream or 100 mg vaginal tabs q.d. x 7
to14 nights; may be used during 2nd and 3rd trimesters
-RX:
Intravaginal
- Single-dose regimens: miconazole, 200-mg vaginal suppository; tioconazole, 6.5%, 5 g
vaginally; or sustained-release butoconazole, 2% cream, 5 g vaginally.
- Three-day regimens: butoconazole (2% cream, 5 g once daily), clotrimazole (two 100-mg
vaginal tablets once daily), terconazole (0.8% cream, 5 g, or 80-mg suppository QD), or
miconazole (200 mg vaginal suppository once daily).
- 7-day regimens: once daily: clotrimazole (1% cream or 100-mg vaginal tablet), miconazole
(2% cream, 5 g, or 100-mg vaginal suppository), or terconazole (0.4% cream, 5 g).
- Fourteen-day regimen: nystatin (100,000-unit vaginal tablet once daily).
Oral
- Fluconazole (Diflucan) 150 mg single dose (commonly used)
- Recurrent Disease: Oral ketaconazole, 100 mg daily for 6 months or less, does prevent
symptoms, as does weekly or monthly dosing with oral fluconazole
- Infectious Disease Society of America
-Uncomplicated – topical agent or Diflucan 150 mg x1
-Complicated – topical agent x 7d or Diflucan 150 mg q 72 hours x3
-Recurrent – control contributing factors + topical or po med x 10 – 14 days + follow with
suppressive Diflucan 150 q week x 6 mos.
3.) Trichomonas vaginalis:
- Caused by Trichomonas vaginalis (protozoan)
- Sexually transmitted
- Symptoms:
-Asymptomatic (20 – 50%)
-Vaginal discharge
-Frothy yellow or green
-Dysuria (20%)
-Pruritus (25
- Physical Exam:
◦ Vulva and vagina may be erythematous or edematous
◦ Cervical vaginal hemorrhages (petechiae) “Strawberry Cervix”
◦ Clinical Diagnosis: unreliable
- Diagnosis:
- Wet prep – visualization of flagellated protozoans and large number WBCs
- pH usually 5.0 –7.0
- Culture
- Treatment:
◦ Metronidazole 2g po x 1 dose
◦ Tinidazole 2g po x 1 dose
◦ Alternate
◦ Metronidazole 500 mg po bid x 7d
◦ Must treat partner: Definitive evidence that it is transmitted
4.) Condyloma:
- Can occur anywhere in lower genital tract from vulva and perianal area to cervix
- Sexually transmitted
- Caused by Human Papilloma Virus (HPV)
 High risk strains
◦ Types 16, 18, 31, 33, 35, 51 and 56 (Type 6 and 11 are mc)
◦ 85% of population has HPV by age 45
 Most types cause an asymptomatic infection.. However, certain strains can be associated
with Cervical dysplasia and neoplasia.
 Postcoital bleeding can occur
 Massive proliferation seen in immunosuppression and treatment is often difficult.
 Treatment
◦ Electrocautery
◦ Cryotherapy
◦ Podophyllin
◦ Podophilox
◦ Imiquimod
◦ Laser Ablation
 Prevention
◦ Immunization
 Quadrivalent HPV Vaccine (Gardasil)
 Protects against HPV 16, 18, 6, and 11
 Recommended for females and males 9 – 26
 Bivalent HPV Vaccine
 Protects against HPV 16 & 18
 Recommended for females 9 – 26
 Prior to exposure
Pelvic Inflammatory
Disease
PID=”pus in der”
Polymicrobial infectious disease of the upper genital tract (i.e. uterus, fallopian tubes, ovaries,
pelvic peritoneum)
 Strongly associated with N. gonorrhoeae and C. trachomatis, other microbes may be
present.
 Most common in young, nulliparous, sexually active women with multiple partners.
 IUD’s, smoking, and frequent douching may increase risk
S/S:
 Lower abdominal / pelvic pain
 Chills
 Fever (+/-)
 Menstrual changes
 Cervical/vaginal discharge
 CMT and adnexal tenderness
 Presence of RUQ abdominal tenderness may signify:
Fitz-Hugh Curtis Syndrome** need to know
* perihepatitis
* most often chlamydia
Workup:
List a differential diagnosis for PID and Pelvic pain (starting with the most severe)
1. Ectopic pregnancy (need to do Preg- test first, then U/S)
2. Appendicitis
3. Septic abortion
4. Hemorrhagic or ruptured ovarian cyst
5. Ovarian torsion
6. Degeneration of a myoma
7. Acute enteritis
Diagnostic Evaluation:
 CBC (r/o infection, anemia)
 Serum Pregnancy
 Wet mount (wet prep)
 Cervical cultures for GC and Chlamydia- Obtain cultures of purulent discharge from os
 Pelvic exam -Look for CMT / chandelier's sign
 Pelvic Ultrasound
Cervicitis: Inflammation
of t he cervix.
Treatment:(outpatient)
 1. Have all sexual partners examined and treated
 2. Ceftriaxone (Rocephin) 250mg IM + Doxycycline 100mg BID x 14 days
 May add metronidazole 500mg BID x 14 days to cover bacterial vaginosis/
Trichomonas
Causes
◦ Trauma
◦ Radiation
◦ I nfection
◦ Malignancy

Infectious Causes:
◦ Chlamydia trachomatis
◦ Neisseria gonorrhea
◦ Trichomonas vaginalis
◦ Herpes Simplex Virus
◦ Human Papilloma Virus

Risk Factors
◦ <25 years old
◦ Single
◦ Multiple partners
◦ Low awareness of STDs
◦ Limited use of protection vs STDs
S/S:
- Erythematous, edematous or easily friable cervix
- Yellow-green discharge in cervical os or on swab specimen
Diagnosis
-Gram stain and culture
-N. gonorrhea:
G- “kidney bean” diplococci in PMNs
+ urine nucleic amplification
-C. trachomatis:
+ culture
+ EIA
+ Rapid test
Treatment
- Must treat the partner!
- Based on microbiology
-Gonorrhea:
- Rocephin 250 mg IM x 1 (covers gonorrhea)
- Plus Azithromycin 1g p.o. x 1 or (covers chlamydia) Doxycycline 100 mg bid x 7 days
Cervical Dysplasia (aka
Cervical Intraepithelial
Neoplasia)
Causes: Hormonal influence and changes in vaginal pH, the squamous margin begins to encroach
on the single-layered, mucous-secreting epithelium, creating an area of
metaplasia)transformation zone).
Diagnostic Evaluation:
1.) PAP Smear
◦ Start screening within 3 years of onset sexual activity or 21 years old
◦ Test yearly until age 30: If 3 consecutive normal PAP, then every 2 – 3 years
◦ Discontinue screening after age 70 if 3 consecutive normal PAP results and no abnormalities
in the last 10 years
Possible PAP results
◦ Normal – continue routine follow-up
◦ ASC-US – low risk of invasive Ca
 Repeat PAP at 6 and 12 months
 Reflex HPV test
 If either of above abnormal – colposcopy
◦ LSIL, HSIL – colposcopy and biopsy
◦ AGC – colposcopy with endocervical and endometrial evaluation
◦ AIS, adenocarcinoma – may require excisional procedures
2.) Colposcopy
-Asc-US and negative HPV screening may f/u in 1yr.
-Positive HPV screening should have colposcopy performed.
- All pt w/ SIL or atypical glandular cells should undergo colposcopy.
3.) Biopsy Biopsy
◦ In office
◦ Colposcopically directed punch biopsy
◦ Endocervical curettage
Neoplastic Disease
Bladder Cancer
(CMDT 2013)
-2nd mc urologic cancer. (M>F) Mean age of dx is 73yo
- Risk Factors: Cigarette smoking and Exposure to industrial dyes or solvents
- 98% primary bladder cancer are epithelial malignancies, majority being urothelial cell carcinomas.
S/S:
-Hematuria (gross or microscopic) chronic or intermittent
-Irritative voiding symptoms (small percentage)
-Abdominal masses may be present on bimanual exams
-Hepatomegaly or palpable lymphadenopathy may be present w/ metastatic dz
Labs:
-Urinalysis reveals microscopic or gross hematuria
-Azotemia present in cases w/ ureteral obstruction
-Anemia
Cytology useful in detecting at initial presentation or to detect recurrence
Imaging:
-U/S
-CT or MRI
-Confirmation is done by cystoscopy and biopsy (Transurethral resection)
Prostate Cancer
(CMDT 2013)
Treatment:
-Superficial Cancers(Ta, T1)- Complete transurethral resection and selective use of intravesical
chemotherapy
-Localized, Invasive cancers(T2, T3)- radical cystectomy, irradiation, or combo of chemo and
selective surgery or irradiation.
-Muscle invasive transitional cell carcinoma (T2 or greater)- neoadjuvant systemic chemo prior to
radical cystectomy is superior to radical cystectomy alone.
-MC noncutaneous cancer deteted in American men and 2nd leading cause of cancer related death.
-Majority of prostate cancers are adenocarcinomas and arise in the periphery of the prostate.
-Gleason grading system
-Risk factors: Age, dietary fat, AA, family hx.
S/S:
-Focal nodules or areas of induration w/in prostate during DRE or elevation of PSA
-Most often asymptomatic
-Rarely: systemic symptoms (wt loss, bone pain) or urinary retention or neurologic symptoms
-Lymph node metastases can lead to LE lymphedema
- Axial skeleton is the mc site of metastases, pts may present w/ back pain or pathologic fx
Diagnostic Evaluation:
-Serum tumor markers- PSA is a glycoprotein produced only by cells of benign or malignant of
prostate gland. It is useful in detecting and staging prostate cancer, monitoring response to
treatment, and detecting recurrence.
-PSA>4.0ng/mL: abnormal
- PSA< 10ng/mL : typically organ confined
- PSA>40ng/mL: advanced dz (seminal vesicle invasion, lymph node involvement, or occult
distant metastases)
-Digital Rectal Exam
-Transrectal Ultrasound-guide biopsy is standard method for detection (not recommended for
primary screening)
Treatment:
-Radiation therapy and radical prostatectomy result in acceptable levels of local control.
Prostate CA Screening:
DRE and PSA test for men 50yo or older (starting at age 40 for AA) annually
Testicular Cancer
Wilm’s Tumor





Painless, firm testicular mass.
May present with mild to moderate pain if tumor is infarcted
Patient c/o “heaviness” to the scrotum
Often misdiagnosed as epididymitis
PEARL: Always consider testicular exam in patients with abdominal mass, chronic cough,
resistant to therapy and an unexplained supraclavicular node.
NEEDS PROMPT UROLOGY Referral !!!
-
Metastatic Testicular Cancer
Most common renal malignancy in children and the fourth most common childhood cancer.
Common congenital anomalies associated with Wilms tumor are cryptorchidism, a double
collecting system, horseshoe kidney, and hypospadias
A missing iris of the eye (aniridia) and hemihypertrophy are birth defects that is sometimes
associated with Wilm’s tumor
S/S:
• Abdominal pain
• Constipation
• Fever
• General discomfort or uneasiness (malaise)
• High blood pressure
• Increased growth on only one side of the body
• Loss of appetite
• Nausea
• Swelling in the abdomen (abdominal hernia or mass)
• Vomiting
A physical examination shows an abdominal mass. High blood pressure may also be present.
Tests include:
• Renal U/S- initial study
• Abdominal CT
• Complete blood count (CBC)
• Chemistry profile • Urinalysis
• Coagulation studies
Cytogenetics studies, including 1p and 16q deletion
Treatment:
- The first step in treatment is to stage the tumor.
-Nephrectomy
-Chemotherapy and Radiotherapy typically follows surgery.
Uterine Fibroids
•
•
The most common benign neoplasm of the female genital tract.
Benign growths that occur on the uterus.
– Develop from the uterine myometrium and lead to a round, firm and often multiple
uterine tumor composed of smooth muscle and connective tissue.
– AKA: fibromyomas, leiomyomas, or myomas
• Genetic alterations
– Many fibroids contain alterations in genes that code for uterine muscle cells.
– Hormonal
– Excess in Estrogen and Progesterone
– Additional substances
– Insulin like growth factor may be related to fibroid growth
Signs / Symptoms
– Asymptomatic to Significantly Symptomatic
– Heavy / Prolonged / Irregular menstrual bleeding
• Anemia
– Dyspareunia
– Infertility
– Pelvic pain or pressure
– Urinary incontinence
– Acute ABD/Pelvic pain
• Outgrows the available blood supply or ruptures
Diagnosis: Most commonly found during routine pelvic exam.
– Irregularly shaped uterus or masses, usually non-tender, NOT globular or spherical
– Always check serum pregnancy
– Transabdominal / Transvaginal Ultrasound: Confirms the diagnosis and determine
location and size of the fibroids.
– Hysterosonography: TVUS with saline to expand the uterine cavity
– Hysteroscopy: Easily performed during an office visit to visualize the walls of the
uterus and fallopian tubes
Uterine Cancer
(Endometrial Cancer)
Treatment:
Identification, awareness, and watchful waiting.
 Gonadotropin Releasing Hormone (GnRH) Analogs
 Depo leuprolide, 3.75 mg IM once monthly can be used preoperatively for 3-4
months to induce reversible hypogonadism, which temporarily reduces the size
of myoma, suppresses further growth, and reduces surrounding vascularity prior
to surgical intervention.
 Oral / Injectable Contraception

Typical hormonal changes shrinks fibroid tissue
 Surgical
 Myomectomy: Removal of fibroids more commonly indicated for patients of
childbearing years

Hysterectomy
 Most common GYN malignancy in U.S.
 75% are adenocarcinoma
 75% have disease confined to uterine corpus @ initial diagnosis
- Most common in women 50-70 years old
- 30% occur < 40 years old
-Suspect HNPCC (Lynch Syndrome)- Colon cancer is the most common with lynch
syndrome and the second mc is endometrial cancer however, endometrial cancer will show
up first.
 WARNING SIGN
- “Abnormal bleeding” in a postmenopausal female
o - Lower abdominal pain
-Occurs late in the disease process – metastases







Increases Risk:
Unopposed estrogen (4-8x)
Menopause after 52yo (2.4x)
Obesity( 3-5x)
Nulliparous (2-3x)
Diabetes (2.8x)
Hypertension




PCOS
Caucasian
Tamoxifen >2 years
FHx: Colon or Gyn cancer
Decreases Risk:
 Ovulation
 Progestin
 Combo OCPs
 Normal weight
 Multiparity
 Menopause <49yo
S/S:
 Abnormal Bleeding
 Abnormal vaginal discharge
 Frequent urination (from compression)
 Pelvic pressure
 Pelvic exam may be normal in early disease; advanced disease may reveal an enlarged,
boggy uterus and even ascites with abdominal exam.
Workup:
 Serum Pregnancy (do first)
 Vaginal US
o Evaluation of endometrial thickness
o Hypertrophy or Neoplastic changes
 Diagnostic test of choice
o Endocervical and endometrial biopsy with hysteroscopy
 Papanicolaou (PAP) Smear alone is very limited !! Will not show indication
of endometrial cancer. May show atypical cells but is a very insensitive
diagnostic tool.
 CT or MRI
Definitive Treatment
 Total Hysterectomy with bilateral salpingo-oophorectomy.
 Lymph node resection
o Focus irradiation for + nodes
o Consider colonoscopy and genetic testing if (+) family history
Cervical Cancer
Cofactors
◦
◦
◦
Smoking
Decreased circulating vitamin A
Increased risk in HIV and high-risk HPV types (16 and 18)- Squamous (85%) and
adenocarcinoma (rising) etiology
◦
◦
◦
Abnormal Papanicolaou test result
Metrorrhagia, Postcoital bleeding and cervical ulceration are the mc signs.
Non-pruritic, Vaginal discomfort, malodorous discharge, and dysuria are not
uncommon
Bladder and rectal dysfunction are late findings
History
◦
Physical Exam
◦
◦
◦
◦
◦
Management
◦
Findings can be relatively normal
Abnormal appearing cervix
External rectal mass
Abnormal bimanual exam
Leg edema
Referral to Gyn-Oncology: Cervical Biopsy, Endocervical curettage, or conization
Ovarian Cancer
- 3rd most common, but leading cause of death from reproductive tract cancer
- 75% of women with ovarian cancer are diagnosed with advanced disease.
RISK Factors
 Increasing age (most cases between 50-75 y.o)
 Nulliparity
 Childbearing in later years of life (40’s)
 Caucasian
 Family Hx: BRCA gene
- BEWARE of those with personal or family history of Breast CA (male or female relatives)
 *25% w/BRCA2 gene mutation
 *45% w/BRCA1 gene mutation
 *Screening (every 6 months)
- Transvaginal US
- Ca-125
- Prophylactic oophorectomy by age 35
 Breast CA correlates w/ Ovarian CA (Colon CA correlates w/ Endometrial CA)
Protective Mechanisms
- Oral Contraceptive Pills (OCP’s)
- Breastfeeding
- Multiparity
S/S:




Typically asymptomatic
-Detected on routine pelvic examination
- Note whether the mass is unilateral or bilateral
-Premenopausal vs. postmeunopausal
-Beware of FIXED masses (doesn’t move)
Mild symptoms
-Non-specific GI related problems (nausea, change in bowel habits)
Advanced Disease
-Pain
-Bloating (although often vague, pay attention to this symptom when does it occur)
Often thru out the day rather than after eating)
-Abdominal mass
Transperitoneal dissemination is most common route of metastasis. Will often spread to
omentum, peritoneum, bowel surfaces, retroperitoneal lymph nodes.
Screening:
 Complete H&P – emphasize pelvic exam
 Check serum pregnancy
 CA 125 : >35 units indicates an increased likelihood for a malignant ovarian tumor. NOT a
screening test.
 Transvaginal Ultrasound
o Good test for high-risk women
o Able to differentiate between benign from malignant ovarian masses.

CT ABD/Pelvis
 Genetic testing (to R/O BRCA) if mass/cancer is confirmed
 Consider screening examinations for “high-risk” patient populations.
o No indications for lower risk patients
 Diagnostic testing
o Laboratory- FSH, LH, Prolactin, TSH, Ca-125
o Imaging- TVUS
Treatment:
 Benign Tumors
o Surgical removal of tumor
o +/- unilateral oophorectomy
 Early stage carcinoma
o Surgical staging of the disease
o Abdominal hysterectomy, bilateral salingo-ooporectomy
 Selective lymphadenectomy
 Advanced Disease
o Surgical tumor removal
o
Chemotherapy
Prognosis
75% of women are initially diagnosed with advanced disease.
Overall 5-year Survival
 17% with distant metastases
 36% with locally confined
 89% in early disease
Renal Diseases
Acute Renal Failure
(Acute Kidney Injury)Sudden decrease in kidney
func, resulting in an inability
to maintain acid-base, fluid
and electrolyte balance and
to excrete nitrogenous
wastes.
 0.5 mg/dl or greater rise in serum creatinine
Causes:
 Nausea, vomiting
 Diarrhea
 Decrease hydration
 Thirst
 Medications: NSAIDs,ACE inhibitors-neprhon protective causes rise in Creatiinin, Contrast,
Diuretics-don’t give to pt who are vol deprivative , Cyclosporine, Amphotericin B, Cisplatin,
Acyclovir, Indinavir
 Contrast exposure
 Rash- interstitial neprhitis
 Urinary tract infections
 Renal colic
 Recent surgery
 Falls, exercise
S/S:

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
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
Data:








altered mentation
seizures
nausea, vomiting
sleep disturbance
pericardial friction rub
arrhythmias especially with hyperkalemia
crackles on lung exam, peripheral edema
suprapubic tenderness
asterixis
‘frost’
rash
Urinalysis(absolute must), microscopy
-Proteinuria: Nephrotic syndrome
-Hematuria: Nephritic syndrome
-Greater than 3 red cell per hpf and may be caused by renal or extrarenal conditions.
- EXTRARENAL- Malignancy
- RENAL:
-Extraglomerular: Cysts, calculi, renal neoplasia
-Glomerular: Post-infectious glomerulonephritis and nephritic syndrome
-Casts:
- WBC:Pyelonephritis and Acute Interstitial Nephritis
- RBC: Glomerulonephritis
- Granular: acute tubular necrosis
- Hyaline: prerenal
BUN to creatinine ratio (20/1)
Fractional excretion of sodium
Hyperkalemia
Metabolic acidosis (anion gap)
Hyperphosphatemia
Anemia
Urine output
 Anuria less than 100 ml/24 hours
 Oliguria less than 400 ml/24 hours

Polyuria greater that 2.5 liters/24 hours
Prerenal: Azotemia-very common- accounts for the majority of AKI cases as a result of renal
hypoperfusion.

Decrease in intravascular volume-excessive fluid loss
- hemorrhage, burns, dehydration

Change in vascular resistance
- sepsis or anaphylaxis and ACE inhibitors, NSAIDs, cirrhosis (hepatorenal syndrome),
renal artery stenosis

Decreased/low cardiac output- low renal blood flow
- low EF, cardiogenic shock or pericardial tamponade
Renal: Parencymal renal dysfunction of the tubules, interstitium, vasculature, or glomeruli.
 Vascular- renal infarction, renal vein thrombosis, atheroemboli
 Tubular- hypotension, nephrotoxins, myoglobin
- Acute Tubular Necrosis- Intrinsic renal failure. 2nd mc form of AKI
– Ischemia- prolonged hypotension or hypoxia
– Toxic Nephrotoxin:
-Exogenous exposure
-Endogenous exposure
– Clinical Findings:
-Serum:
-Increased BUN:Cr
-Hyponatremia, Hyperkalemia, Hyperphosphatemia
-Urinalysis:
-Brown colored urine
-Abnormal sediment
-Muddy brown casts
– Treatment
- Avoid volume overload
- Avoid life threatening electrolyte disturbances
- Use of diuretics to maintain adequate urine output is questionable.
- Dialysis indicated for:
- Life-threatening electrolyte disorders
- Volume overload not responding to diuresis
- Metabolic acidosis (worsening or not improving)
- Severe complications of uremia
- Early clearance
 Glomerular- acute glomerulonephritis (RBC casts), Wegener’s
 Interstitium- penicillins, tumor infiltration (lymphoma)
 Interstitial Nephritis-Kidney diseases that involve structures in the kidney but outside
the glomerulus are termed tubulointerstitial.
-Primary acute and chronic etiologies:-Medications (70%)
- Penicillins, Cephalosporins, and sulfonamides
- NSAIDS
-Clinical Findings
- Fever and Maculopapular rash
- Urinalysis:
- Heavy Proteinuria (albuminuria) *hallmark of NSAIDS
- Hematuria
- WBC’s with or without bacteria
- WBC casts
- Serum: Eosinophilia
-Treatment:
-Supportive care for underlying etiology and stop offending mechanisms
- Glucocorticoid therapy
- Dialysis support if needed
Post-Renal:
 Enlarged prostate
 Neurogenic bladder
 Intraureteral obstruction
 crystals - acyclovir, uric acid, indinavir
 stones
 clots
 Retroperitoneal fibrosis
Imaging:
 Ultrasound: size, number, mass, obstruction
 Radionuclide study
 Intravenous Urography
 Computed Tomography
 Magnetic Resonance Imaging
 Arteriography and Venography
 Renal Biopsy
Indications for Renal Biopsy:
 Proteinuria + Decreased Renal Function
 Unexplained AKI or CKD
 Unexplained hematuria / proteinuria
 Plan for future therapy
 Evaluation of potential transplant rejection
AKI Pearls:
 Anemia suggests Multiple myeloma
 Thrombocytopenia-- TTP
 Coagulation abnormalities indicate liver disease or hepatorenal syndrome
 Elevated CPK is seen in Rhabdomyolysis and AMI
 Hypocalcemia and Hyperkalemia is a common finding in AKI
Acidosis: (MUDPILES)
 Methanol
 Uremia
 DKA
 Paraldehyde
 Ischemia / Iron / INH
 Lactic acidosis
 Etoh
 Salicylates / Starvation
Chronic Renal Failure:
Kidney damage or GFR
less than 60ml/min/1.73m^2
that has been present for
greater than 3 months
 Formerly known as chronic renal insufficiency
 Frequently an asymptomatic progressive disorder that develops over months to years
 Over 70% of ESRD cases are a result of diabetes or hypertension.
 Most common cause of death is cardiovascular disease
 Prediction equations based on creatinine, age, gender, race, body size
 Cockcroft Gault:
[ (140 – age) x (weight in kg) ]
-------------------------------------(serum creatinine x 72)
Multiply by 0.85 if female
Risk Factors for Development:






Older age: GFR declines at 8 ml/min/1.73m² per decade after 40
Family history
Diabetes
HTN
Low income or education-lack of accesss to healthcare
Autoimmune diseases
Risk for Progression:
 Proteinuria
 HTN, diabetes
 Type of underlying kidney disease
 African-American
 Male
 Obesity
 Dyslipidemia
 Smoking
Clinical Consequences:
 Stage 3
 abnormalities in erythropoeitin, PTH, calcitriol
 asymptomatic
 Stage 4
 mild symptoms
 hyperkalemia, hyperphosphatemia, anemia, hypocalcemia
 Stage 5

uremia, salt and water retention, HTN
Watch drug dosing with all stages!
Laboratory Findings
 Serum
 Elevated urea and creatinine
 Hyperkalemia
 Metabolic acidosis
 Normochromic normocytic anemia
 Urine
 Proteinuria
 Abnormal urine sediment
– RBC’s or RBC casts
– Pyuria
Signs and Symptoms
 General- Anorexia, nausea, and vomiting
 Neurological- Irritability, insomnia, mild memory defects
 Dermatologic- Pruritus
Imaging studies
 Renal Ultrasound- Identifies small kidneys in advanced renal failure or polycystic
abnormalities.
 CT scan

Able to define renal masses and cysts. Very sensitive for renal stones
– Contrast !!! Need to weigh risks and benefits
– Premedicate before contrast
 MRI: Watch gadolinium- risk of nephrogenic systemic fibrosis
Current Medical Care Recommendations
– Manage underlying conditions
 Anemia- Erythropoietin
 Hyperphosphatemia- Dietary phosphate binders and dietary restrictions
 Hypocalcemia- Calcium supplements
 Volume Overload- Loop diuretics or Dialysis
 Aggressive control of hypertension- ACE Inhibitors may be indicated
 Maintain tight glycemic control
-
Glomerulonephropathy:
Nephritic Syndrome





Proteinuria
Hematuria
RBC casts
Edema
HTN
 Manage hyperlipidemia
Avoid potential nephrotoxins- (IV Contrast, NSAIDS, Aminoglycoside)
Kidney Transplant- Gold standard


Acute or chronically worsening abnormalities of glomerular function that result in an
inflammatory reaction.
 The cause of the glomerular injury is best identified by the histologic pattern obtained by
renal biopsy.
– Nephritic Syndrome
– Nephrotic Syndrome
 A specific set of renal diseases that in which an immunologic mechanism triggers
inflammation and proliferation of glomerular tissue.
– Postinfectious Disorders
 Postinfectious Streptococcus
– Systemic causes
 Wegener granulomatosis
 Systemic Lupus Erythematosus
 Polyarteritis nodosa
 Henoch-Schönlein purpura
 Goodpasture syndrome
– Renal Diseases
 Membranoproliferative glomerulonephritis
 Berger disease
Nephritic Syndrome:
 Physical findings
– Hematuria, proteinuria, hypertension, and reduction of the GFR.
 Clinical findings
– Serum - Antinuclear Antibodies, complements, ANCA, etc
– Urine- Proteinuria, Red Blood Cells, RBC casts
– Renal biopsy- Specific pattern of histology helps to determine the etiology

Acute (postinfectious) Glomerulonephritis
– Commonly Streptococci
– Most commonly affects males between 5-15 as a poststreptococcal infection.
– Manifests as a sudden onset of hematuria, proteinuria, and the presence RBC
casts in the urine.
– Clinically accompanied by hypertension, edema, and impaired renal function, low
complements
– Common scenario: A young boy presents with a sudden onset of periorbital and
facial edema, has dark colored urine, and is moderately hypertensive.
– This typically follows a 1-2 week history of pharyngitis

IgA Nephropathy: Berger’s Disease and Henoch-Schönlein Purpura
- Most common GN worldwide
-Peak incidence in the second and third decades of life
-More common in Asians and Caucasians
-2:1 male to female predominance
-40-50% present with gross hematuria w/ Upper Respiratory Infection
or associated w/ exercise
-Normal complements
-Good prognosis if there is no significant proteinuria and renal function is preserved
-Pts w/ persistent hematuria, HTN, elevated creatinine have incidence of ESRD at
2030% at 20 years
-Treatment includes ACE/ARB, fish oil, statins, steroids

Rapidly Progressive Glomerulonephritis
– Systemic Lupus Erythematosus
- Active urine sediment, elevated creatinine, HTN, low complements, active
serologies suggest very active disease
- High index of suspicion in young AA female
- Check ANA and dsDNA
- May need renal biopsy to determine treatment
– Goodpasture’s Syndrome
– Wegener’s Granulomatosis
Pulmonary-Renal Syndrome:
Presentation: hematuria, RBC casts, elevated creatinine w/ hemoptysis and/or infiltrates
DDx: Goodpasture’s, Wegener’s, granulomatosis, pauci-immune GN, post streptococcal GN
Glomerularnephropathy:
Nephrotic Syndrome
o
o
o
o
o


Proteinuria
Hypoalbuminemia
Edema
Hyperlipidemia
Oval fat bodies in
urine

Polycystic Kidney
Disease
Physical findings-Peripheral edema
Clinical findings
– Urine
 Proteinuria– greater than 3.5 gm/24 hours
 Oval fat bodies = hyperlipidemia
 Bland (no cells or cellular casts)
– Serum
 Hypoalbuminemia
 Hypoproteinemia
 Hyperlipidemia
Renal biopsy- Findings determine specific classification
Causes:
 Minimal Change Disease
– Common in younger population
– Associated with NSAID use
– Found in patients with Hodgkin’s Disease
 Focal and Segmental Glomerulosclerosis
– Most common in young AA men
– Secondary causes include heroin use and HIV
 Membranous nephropathy
– More common in caucasions
– Associated with non-Hodgkin’s lymphoma
 Other causes secondary to systemic dz.- Diabetes, Amyloidosis, SLE
 HIV nephropathy
- Most characteristic form presents with nephrotic range proteinuria and on biopsy shows
collapsing FSGS with severe tubulointerstitial nephritis
- Most pts have low CD4 counts and advanced disease
- Present with edema, heavy proteinuria, hypoalbuminemia, large kidneys on renal US
Treatment:
– Protein Supplementation - Follow serum albumin
– Reduction of peripheral edema
 Dietary sodium restriction
 Diuretic therapy
– Hyperlipidemia- Pharmacologic treatment highly indicated
– Hypercoagulable state - Risk of thrombosis is elevated in hypoalbuminemia
 Very common hereditary disease that affects 1 in 800 live births.
 50% of these will develop ESRD
 Clinical findings
 History
 Significant family history present 75%
 50% of patients have hypertension


Physical
 Flank or abdominal pain
 Large easily palpable kidneys
Laboratory
 Urine
 Gross or microscopic hematuria
 Proteinuria
 Serum- Frequent renal failure
Imaging- Ultrasound can confirm diagnosis with the presence of 2 or more cysts

Treatment:
 Pain control with bed rest and analgesia
– Consider US guided decompression of cysts
– Evaluated continued hematuria for renal cell carcinoma.
– Typically resolves in 7 days with bed rest and hydration
 CT scan for worsening pain to evaluate for presence of nephrolithiasis
 Aggressively control hypertension
– Diet and Medication
Electrolyte/Acid/Base Disorders
Hyponatremia: serum
sodium less than 135
meq/L (mc lyte disorder in
hospital)



Hyponatremia usually reflects excess water retention relative to sodium rather than sodium
deficiency.
Osmolality = 2(Na) + Glucose/18 + BUN/2.8
nml=285-295mosm/kg
Serum Osmolality:
- Hypotonic Hyponatremia (<280)-Most causes of hyponatremia
- Hypertonic Hyponatremia (>295)
- GLUCOSE
- Mannitol
S/S:
Mild: N/V/HA/Lethargy/Disorientation as sodium concentration drops
Severe: Respiratory arrest/Seizure/Coma/Permanent brain damage/Brainstem herniation/Death
Treatment:
• Hypotonic hypovolemic hyponatremia
– Normal saline or lactated ringers’
• Hypotonic hypervolemic hyponatremia
– Fluid restriction
– Diuretics
Euvolemic Hyponatremia - SIADH is characterized by:
Low sodium
Low osmolality
Absence of heart, liver, kidney disease
Normal TSH and serum cortisol
Urine sodium >20 (Natriuresis occurs in response to slight increase in ECV from
ADH via increased atrial natriuretic factor and inhibition of renin-angiotensinaldosterone system)
Causes of SIADH:
• CNS (head trauma, stroke, tumor, infection)
• Lung (tumors—esp small cell which synthesizes ADH, infection)
• Drugs (seizure meds, anti-depressants, “Ecstasy”
• Other (pain, stress, postoperative)
Treatment of SIADH:
• Water restriction
– 0.5 – 1 L per day
– Demeclocycline inhibits the effect of ADH on the distal tubule
Rate and Degree of Sodium Correction:
• Changes in sodium should occur by no more than 1-2 mEq/L/h
• Otherwise, can cause changes in brain cell volume, leading to irreversible brain injury,
central pontine myelinolysis.
Hypernatremia:
Sodium concentration
>145mEq/L
•
•
•
•
•
•
Changes in sodium are due to water imbalance, not sodium.
Most cases of hypernatremia are due to inadequate water intake (THIRST)
Urine osmol helps differentiate renal from nonrenal water lost.
Low urine osm is characteristic of low ADH activity, hence diabetes insipidus
Urine Osm >400 implies high ADH and that renal water conserving ability is functioning.
Urine Osm <250 implies low ADH and is characteristic of central and nephrogenic diabetes
insipidus (seen with Lithium or demeclocycline therapy)
S/S:
Dehydrated= Orthostatic hypotension and Oliguria
Early signs: lethargy, irritability and weakness
Late signs: Hyperthermia, delirium, seizures,, and coma
Treatment:
• Hypernatremia w/ hypovolemia= isotonic .9% NS
• Hypernatremia w/ euvolemia= water ingestion or IV 5% dextrose
• Hypernatremia w/ hypervolemia= 5% dextroseor Loop diuretics to promote natriuresis and
lower Total Body Sodium
• Changes in sodium should occur by no more than 0.5-1 mEq/L/h or 12 mEq per day
• Remember the brain synthesizes idiogenic osmoles in response to hypernatremia so if
serum sodium is corrected too rapidly, water will shift into brain cells and cause edema
Hypokalemia
Calculate free water deficit:
Vol to replace (L) = TBW x (Na-140)/140
TBW men = .6 (Ideal body weight)
TBW women = .5 (Ideal body weight)
• Total body content = 50 meq/kg
• More than 95% intracellular
• K level kept in very narrow range by cellular shift and renal handling
• Abnormal potassium levels lead to life-threatening arrhythmias
• Magnesium is a cofactor for potassium uptake and should always be checked in setting of
hypokalemia
Symptoms:
• muscle weakness, muscle cramps, rhabdomyolysis, arrhythmia, ileus
• ECG U waves, PVC, depressed ST
• Hypokalemia can worsen digitalis toxicity because of its depressive effect on the Na-K
ATPase pump.
3 Main mechanisms:
• Intracellular shifts (insulin,alkalosis,trauma,periodic paralysis)
• Renal loss (aldosteronism, Cushing’s, genetic disorders- High urine K (> 40)
means renal losses
-Aldosterone
-Bartter’s syndrome
-Liddle’s syndrome
• Extrarenal loss (diarrhea, vomiting, laxative abuse, villous adenoma)- Low urine K
(<20) extrarenal losses
Treatment:
• For severe hypokalemia or EKG changes move patient to a monitored bed.
• Know patient’s GFR!—decrease replacement doses in renal disease. IF GFR is normal,
generally expect to replace 10mEq per 0.1 decrease in potassium.
• Oral K supplementation is the safest for mild to modereate deficiency.
• Avoid glucose-containing fluid to prevent further shifts of K into the cells.
• Mg deficit should be corrected
HyperKalemia: Serum
Potassium level >5.0mEq/L
(5.0mmol/L)
Causes:
 Spurious causes of hyperkalemia:
o Hemolysis
o Thrombocytosis
o Leukocytosis
o Repeated fist clenching
o Drawn above IV site where potassium is infusing
 Renal failure
 Medications (heparin, ACE, ARB, aldactone, trimethoprim, NSAIDs, cyclosporine,
tacrolimus
 Cellular shifts (acidosis, rhabdomyolysis, internal bleeding, vigorous exercise)
S/S:
Muscle weakness, flaccid paralysis, ileus
ECG: bradycardia, PR interval prolongation, peaked T waves, QRS widening, and biphasic QRS-T
complexes. BBB and AV block. VFib and Cardiac arrest.
Treatment:
• IF EKG changes (peaked T waves, widened QRS) give calcium to stabilize cardiac
membrane.
• Give diuretics and resin binders to remove potassium from body.
• Give Insulin, albuterol, bicarbonate for quick onset of action to cause cellular shifts.
• If medically refractory, dialysis.
Hypocalcemia: Serum Ca
conc <8.5mg/dL
•
•
•
•
•
Interpret abnormal calcium levels with phosphorus, Vit D, magnesium, and PTH levels
Hypocalcemia can cause arrhythmia and tetany
The mc cause is renal failure(CKD), due to decreased production of vitamin D and
hyperphosphatemia.
Low magnesium reduces the release of PTH, causing hypocalcemia.
Respiratory alkalosis, total calcium is normal, but the ionized calcium is low.
S/S:
 Spasm of skeletal muscle causes cramps and tetany
 Convulsions, perioral and peripheral paresthesias, and abdominal pain
 Chvostek’s sign- Contraction of the facial muscle in response to tapping on the facial n
anterior to the ear
 Trousseau’s sign- Carpal spasm after occlusion of the brachial artery w/ a BP cuff
 ECG shows long QT.
Treatment:
Asymptomatic Hypocalcemia: Oral calcium carbonate (1-2g) and Vit D
Severe: IV calcium gluconate
Hypercalcemia
Causes:
Outpatient- primary hyperparathyroidism.
Inpatient- malignancy via production of PTH-rp (esp lung, breast, kidney,hematologic, thyroid)
Others (familial hypocalciuric hypercalcemia, meds such as HCTZ, Paget’s, milk-alkali
syndrome)
• Hypercalciuria uslaly precedes hypercalcemia
•
•
•
Symptoms:
 neurological changes-drowisiness, weakness, depression, stupor, coma
 GI manifestations-constipation, polyuria
 ECG shows short QT interval.
 Measurement of PTH and PTHrp distinguish between malignancy-associated
hypercalcemia and hyperparathyroidism.
Treatment:
• Volume repletion is first line to increase calcium excretion.
• Bisphosphonates cannot be used in renal insufficiency, but are the mainstay of treatment
for hypercalcemia of malignancy. (May take up to 72 hours for effect)
• Dialysis can be used to lower calcium when levels are as high as 18-20
Hypomagnesemia
Metabolic Acidosis
AG= Na+ - (Cl- + CO2-)

Serum concentration of Mg may not be decreased even in the presence of Mg depletion.
Check urinary Mg excretion if renal Mg wasting is suspected.
Causes:
 Diminished absorption or intake: Alcohoism, PPI, laxative abuse
 Increased renal loss (diuretic therapy, hyperaldosteronism)
 DM
 Post-parathyroidectomy (hungry bone syndrome)
 Respiratory alkalosis
 Pregnancy
S/S:
 Similar to hypokalemia and hypocalcemia
 Weakness and muscle cramps
 Neuromuscular and CNS hyperirritability – tremors, athetoid movements, jerking,
nystagmus, Babinski response, confusion, and disorientation
 Cardiovascular response: HTN, tachycardia, Ventricular arrhythmias
Treatment:
Chronic hypomagnesium: Magnesium oxide 250-500mg orally OD or BID
Symptomatic hypomagnesemia: IV Magnesium sulfate 1-2g over 5-60mins mixed in either dextrose
or 0.9%NS
Torsades de pointes- 1-2g MgSO4 in 10mL dextrose 5% solution pushed IV over 15mins
Low HCO3- with low pH
Normal Anion Gap Acidosis: AG<12
- GI losses (diarrhea)
- Renal tubular acidosis (defect in renal acidification)
Treatment:
- Administration of alkali (either as bicarbonate or citrate) to correct metabolic abnml and prevent
nephrocalcinosis and CKD
-Thiazides may reduce amount of alkali required but could cause hypokalemia
-Potassium supplement
Increased Anion Gap Acidosis: AG>12
Methanol
Uremia
Diabetic Ketoacidosis (DKA)
Paradelhyde or Propylene Glycol
Isoniazid, infection
Lactic acidosis
Ethylene glycol
Salicylates
Treatment:
-Tx aimed at underlying disorder, such as insulin and fluid therapy for DM and appropriate volume
resuscitation to restore tissue perfusion.
Metabolic Alkalosis


High HCO3- and High pH
Check urinary chloride concentration to differentiate saline-responsive alkalosis from salineunresponsive alkalosis.
-Saline-responsive alkalosis(more common): extracellular volume contraction
-Diuretic therapy, Posthypercapnia, Vomitting or NG suction, Antacids, Transfusion,
Contraction alkalosis
Treatment:
- Correction of the extracellular volume deficit with isotonic saline.
- Discontinue diuretics.
- H2-blockers or proton pump inhibitors may be helpful in pts w/ alkalosis from NG sunction. - Acetazolaminde will increase renal bicarbonate exrection (risk of hypokalemia).
-Saline-unrespoinsive alkalosis implies excessive total body bicarbonate w/ either
euvolumeia or hypervolemia
- Bartter syndrome (renal salt wasting), Primary hyperaldosteronism, Hypercalcemia
and hypoparathyroidism, Severe potassium depletion, Liddle syndrome, Exogenous
alkali, Exogenous minerlocorticoids, Licorice
Treatment:
-Surgical removal of mineralocorticoid-producing tumor and blockage of aldosterone effect w/
ACEi or spironolactone.
- Metabolic alkalosis in primary aldosteronism can be treated only w/ potassium repletion.
Respiratory Acidosis
(Hypercapnia)




S/S:


Respiratory Alkalosis
High PCO2 and low pH
Results from hypoventilation and subsequent hypercapnia.
Acute respiratory failure associated w/ severe acidosis and only small increase in the
plasma bicarbonate.
Chronic respiratory acidosis seen in pts w/ underlying lung dz, such as COPD.
Acute onset: somnolence, confusion, mental status changes, asterixis and myoclonus.
Severe: increased cerebral blood flow, CSF and intracranial pressure. Papilledema
and pseudotumor cerebri.
Treatment:
-Relieve underlying disorder to improve ventilation
-IV naloxone administered for Opiod overdose
 Low PCO2 and High pH
Causes:
 Hyperventilation syndrome
 Bacterial Septicemia
 Cirrhosis
 Pregnancy (progesterone stimulates respiratory center)
S/S:
Acute: light-headedness, anxiety, perioral numbness, and paresthesias.
Severe: Tetany from low ionized calcium, since severe alkalosis increases calcium binding to
albumin.
Treatment:
Hyperventilation from anxiety: Discourage from breathing into a bag bc it doesn’t correct pCO2 and
may decrease pO2. Reassurance and sedation if hyperventilation persist.