Transcript Ch. 22 Renal 1

Ch. 22 Renal 1
Evaluation of Renal Disease
 Incidental discovery
 ‘Renal’ presentation:
HTN/EDEMA/NAUSEA/HEMATUREA
 Evaluation: ?Duration (acute/Chronic)/
Urinalysis/GFR
 Anatomical location of disease:
Pre-renal/ Post Renal/ Intrinsic -
2
Type
Table 22–1. Significance of specific urinary
casts.
Significance
Hyaline casts
Concentrated urine, febrile disease, after strenuous exercise, in the course of diuretic therapy (not
indicative of renal disease)
Red cell casts (1)
Glomerulonephritis
White cell casts
Pyelonephritis, interstitial nephritis (indicative of infection or inflammation)
Renal tubular cell
casts (3)
Acute tubular necrosis, interstitial nephritis
Coarse, granular casts
(2)
Nonspecific; can represent acute tubular necrosis
Broad, waxy casts
Chronic renal failure (indicative of stasis in enlarged collecting tubules)
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rine Test: Interpretations
Glucose
Positive in diabetes/Quantitative also
Ketones
Starvation/diabetes (fruity odor)
Bilirubin
Indicates hepatitis(conjugated)
Specific gravity
Renal capacity to concentrate/dilute urine
pH
Acidity/alkanlinity indicator
Protein
Glomerular disease/infections/blood in urine causes
proteinurea
Blood
Abnormal-except during menses
Nitrites
Conversion of nitrates to nitrites by gram negative
bacteria- UTI
Leukocyte esterase
Suggests presence of PMN -UTI
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Imaging studies
 Radionuclide perfusion scan
 Ultrasonogrphy
 IVP-?
 CT scan- stones 95%
 MRI-adrenals well imaged
 Renal biopsy
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Acute Renal Failure
Sudden increase in BUN or serum
creatinine.
Oliguria often associated.
Symptoms and signs depend on cause.
Serum creatinine concentration will typically
increase by 1–1.5 mg/dL daily
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Features
1.
2.
3.
4.
5.
6.
7.
Azotemia (Uremia) can cause nausea, vomiting, malaise, and
altered sensorium.
Pericardial effusion and a pericardial friction rub
Elevated BUN and creatinine
Hyperkalemia
ECG can reveal peaked T waves, PR prolongation, and QRS
widening
Metabolic acidosis
Anemia (EPO), platelet dysfunction
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Acute Renal Failure Features
 Pre-renal most common- mostly due to hypotension
and decreased kidney perfusion
 Post- renal – least common/ due to obstructionprostate/ drugs/stones/
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Glomerulonephritis
 Hematuria, red cell casts, and mild proteinuria.
 Dependent edema and hypertension.
 Acute renal insufficiency
 Immune complex deposition
 SLE(35% to 90%)/HCV(8% ESRD)
 Hypertensive and edematous, and have an
abnormal urinary sediment.
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Glomerulonephritis
 Dipstick and microscopic evaluation: hematuria,
moderate proteinuria (usually < 2 g/d),
cellular
elements such as red cells, red
cell casts, and
white cells.
Red cell casts are specific for glomerulonephritis
 TherapyHigh-dose corticosteroids and
cytotoxic agents such as
cyclophosphamide
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HIV Associated Nephropathy
 Can present as the nephrotic syndrome in patients
with HIV infection.
 Mostly young black men.
 More common mode of acquisition of HIV is
through injection drug use.(IVDU)
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Chronic Renal Failure
 Progressive azotemia over months to years.
 20 million Americans, or one in nine adults
 Symptoms and signs of uremia when nearing end-stage
disease.
 Hypertension in the majority.
 Isosthenuria (fixed specific gravity) and broad casts in
urinary sediment are common.
 Bilateral small kidneys on ultrasound are diagnostic.
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Chronic Renal Failure
Table 22–5. Stages of chronic kidney disease: a clinical action plan
Stage
Description
GFR
Action3
(mL/min/1.73 m2)
1
90
Diagnosis and treatment. Treatment of
comorbid conditions.
Slowing of progression.
Cardiovascular disease risk reduction.
2
60–89
Estimating progression.
3
30–59
Evaluating and treating complications.
4
15–29
Preparation for kidney
replacement therapy.
< 15 (or dialysis)
Replacement (if uremia is present).
5
GFR
Kidney
failure
70% due to diabetes/hypertension
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Table 22–7. Symptoms and signs of uremia.
Organ System
Symptoms
Signs
General
Fatigue, weakness
Sallow-appearing, chronically ill
Skin
Pruritus, easy bruisability
Pallor, ecchymoses, excoriations,
edema, xerosis
ENT
Metallic taste in mouth, epistaxis
Urinous breath
Eye
Pale conjunctiva
Pulmonary
Shortness of breath
Rales, pleural effusion
Cardiovascular
Dyspnea on exertion, retrosternal pain on
inspiration (pericarditis)
Hypertension, cardiomegaly, friction
rub
Gastrointestinal
Anorexia, nausea, vomiting, hiccups
Genitourinary
Nocturia, impotence
Neuromuscular
Restless legs, numbness and cramps in legs
Neurologic
Generalized irritability and inability to
concentrate, decreased libido
Isosthenuria (fixed specific gravity)
Stupor, asterixis, myoclonus, peripheral
neuropathy
BUN and Creatinine elevated
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Complications
 Hyperkalemia
 Metabolic acidosis
 Hypertension
 Pericarditis
 CHF
 Anemia/petichiae/purpura
 Uremic encephalopathy
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Treatment
 Protein restriction 1g/kg/day
 Sodium and water restriction
 Potassium restriction
 Phosphorus restriction
 Magnesium restriction
 Peritoneal/Hemo dialysis
 Renal transplant 50% eligible
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Nephrotic Syndrome
 Proteinurea > 3.5 g/1.73 m2 per 24 hours.
 Low albumin (albumin < 3 g/dL).
3.2-4.5 is normal.
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Hyperlipidemia occurs in over 50%
Peripheral edema.
Systemic disease: diabetes mellitus, amyloidosis, or SLE
Type 2 DM proportion is slowly increasing
Single most common cause
 Deficiency: vitamin D, zinc, and copper from loss of binding
proteins in the urine; they are prone to infection, in part from
urinary losses of immunoglobulins.
 Increased risk of coagulation
Clotting problems due to liver involvement – worse with heavy metal exposure – cadmium,
gold, lead, zinc, nickel, mercury, etc.
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Analgesic Nephropathy
 Large quantities of- acetaminophen (Tylenol), Aspirin-NSAIDs
(>1g/day for >3 years)
 Aminoglycosides, gentamicin antibiotics, cancer meds
Urinalysis Hematurea
 Proteinurea
 Anemia
 PMN
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Heavy Metals Nephropathy
 Lead, Cadmium
(welders/ moonshiners)
 Increased SUA-Gout
Damaged ki  uric acid levels up
 Mercury and Bismuth can do the same
Peptobismol contains bismuth – too much can cause increased bismuth levels.
 Complain of polyuria
Can’t concentrate urine, so flows out quickly
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Renal artery stenosis
 Atherosclerosis/ (67-95%)/
 Fibromuscular dysplasia (young women )
 Risk factors include renal insufficiency
 diabetes mellitus
 tobacco use
 hypertension
 Doppler ultrasonography, captopril renography, and magnetic
resonance angiography (MRA )
 Therapy-?Angioplasty/Stenting/Bypass/Medicines
Also drugs to keep the blood thin and flowing.
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The Structure of the Kidney
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Cystic Disease of Kidneys
 Simple cysts -50% over the age of 50 years
Not considered a problem if you find a couple over the age of 50. Over 5 cysts is bad.Blood
leaking into the cysts causes a colicky type of pain.
 Rarely symptomatic
 No clinical significance
 Generalized cysts scattered throughout the cortex
and medulla of both kidneys and can progress to
ESRD
Produces KI failure
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 65–70% of all renal masses
Simple cysts
Painless hematuria is a marker for this
 Differentiate them from malignancy, abscess,
or polycystic kidney disease
Abscess = fever, heat sx.
 Sonographic criteria to be considered
benign:
 (1) echo free,
 (2) sharply demarcated mass with smooth walls,
and
 (3) an enhanced back wall
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ADPKD
 Affects 500,000 individuals
 1 in 800 live births.
 Fifty percent get ESRD by age 60
End Stage Renal Disease
 ADPKD1 on the short arm of chromosome 16 (85–90% )
Faster progression than chrom 4.
 ADPKD2 on chromosome 4 (10–15%).
Slower progression
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APKD Features
Abdominal/Flank pain- ?infection/bleed
Hematuria
UTI/Stones 20%
Repeat infections
FH (75%)
HTN(50%)
Palpable large kidneys
Cerebral aneurysms (10-15%)
MVP & aortic aneurysms (25%)
Mitral valve prolapse – 2ndary reasons for this.
Colonic diverticula more common
U/S:2 or more cysts by age 30 diagnostic
CT scan highly sensitive
Tx is symptomatic mgmt. Treat the above stuff and watch for other signs listed above. In
other words, just throw more drugs at it. Pts often come for pain.
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Analgesic Nephropathy:
Renal Papillary Necrosis
Kidney damage due to meds. Will eventually need dialysis, KI transplants.
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Uric acid Stones
Stones consist of the following from most common to
least common:
1. Calcium
2. Struvite
3. Uric Acid
4. Homocysteine
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APKD
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Renal Cancer
Young children are likely to have – painless
hematuria. Catch it early and can cure.
Less commone for adults.
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Chronic Glomerulonephritis (ESRD)
No cortex left here.
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Staghorn Calculus
Colicky pain, UTI repeats. Will kill off the kidney in time.
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Atrophy of Kidney
You only need 1/8 of a kidney to
keep living.
atrophied kidney
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Know this!
RAAS
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Ch.23-Urology
UROLOGICAL
CONDITIONS
EVALUATIONS
MANAGEMENT
Urology Evaluations
Pain- major factor. Determine where it is, what it refers to:
1.
Renal: ipsilateral, costovertebral angle, n/v
2.
Ureteric: ‘colic’- dull ache
Commonly related to tip of penis.
3.
Bladder: Suprapubic discomfort or related to micturition
4.
Prostatic: Perenial-radiates to-lumbosacral inguinal, or lower limbs and voiding
irritation.
5.
Penile:
a) STD related (dischg/pain)
b) phimosis (uncircumcised, narrowing of foreskin – can cause urinary retention, backs up when
severe, can affect KI. Can also be common in diabetes. )
c) Peyronie’s disease
6.
Testicular: Trauma/torsion/epidydimitis- scrotal pain radiates to groin
Painless swelling can often = cancer, esp age 15-35.
Always do a belly exam. Listen to the aorta for aneurism, listen to the Lungs, look for
heart/evidence of pericarditis, feet/face for edema, ascites for abdomen. Check breath for
uremia. Check mental status for confusion (MMSI).
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Hematuria
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Initial- at beginning of urination and clears during the stream suggests anterior urethral
source
Terminal- at the end of stream implies bladder neck/ prostatic source
Penile fracture could cause this.
Total- Throughout Urination - bladder or upper tract source
Age:
Young women –cystitis. Do gynecological review too.
Older - ?renal cancer/ ?stones/GN/PKD
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Irritative Voiding Symptoms:
Something is irritating the plumbing
1.
Urgency
2.
Dysuria
3.
Frequency
4.
Nocturia
Shouldn’t have to get out of bed
to pass urine!
Obstructive Voiding Symptoms:
Blockage of urethra
1.
Hesitancy
2.
Decreased force of stream
Stream should be parabolic in shape.
3.
Intermittency
4.
Post void dribbling
All seen in patients with enlarged prostate. Rarer
in women, but not during preggers when
the bladder is squeezed.
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Incontinence
‘Involuntary’ loss of urine
1.
2.
3.
4.
Total- all the time in all positions
Urine is irritating to the skin – can cause all kinds of irritative problems in
the local area.
Stress- activity associated- coughing/lifting/sneezing/exercising
Urge-strong urge followed by loss of urine
Overflow- chronic retention results in overflow incontinence
What feels like a normal voiding, but isn’t emptying enough.
Be able to describe incontenence with these types.
Anticholinergic drugs are most popular to block relaxation of sphincter and deal
with incontinence.
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‘Systemic’ symptoms
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‘High’ fevers in women –acute pyelonephritis
Repeat fevers, chills, occ flank tenderness. Urine tests w/presence of nitrities, leukocytes
found. Both measured with dipstick. Suggests infection. May need antibiotics IV then oral
antibiotics.
Men fevers- acute pyelonephritis/ acute prostatitis/epididymitis
Fevers with cancer kidney/bladder/testes
Weight loss
Points to cancer.
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Other symptoms
Hematopsermia- blood in ejaculation-?prostate/?seminal vesicle
 Tests: urine/DRE/Cystoscopy
 Pneumaturia- air in urine fistulas(diverticulitis/Crohn’s/radiation
Fistula is an unnatural connection between UB and other like rectum – causes air
pockets in urine, might look like little soap bubbles.
Fistulas can also cause urine to spill out of the wrong orifice. Fecal mix in urine can
cause big bacterial problems.
 Urethral discharge- STD/ elderly-cancer
 Cloudy urine-UTI / Chyluria (filariasis/ tb)
Rule out UTI first.
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Scrotal Contents
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Epidydimitis- tender testcilces
Hydrocele- collection of fluid in scrotal sac
Varicocele- retroperitoneal tumor/obstruction of spermatic vein
Torsion of testis- 10-20 yrs/ acute pain and swelling, testicle elevated
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When to test for Hematuria
Always a red flag!
 Timing
 Colic/voiding/constitutional
 Anticoagulants
Even aspirin can do this
 Drugs- analgesics/cyclophophamide
 Diabetes Mellitus/Sickle Cell Disease/Stones
 Urinalysis
 Cystoscopy / Imaging/ MRI
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Manage Acute Cystitis
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Irritative voiding symptoms (frequency/urgency/dysuria/suprapubic pain/ postcoital
dysuria-hematuria)
Afebrile/ no systemic symptoms
Many docs won’t even do a test, just give antibio’s if this is the 1st time.
Positive urine culture
Most common E. coli
Urinalysis: pyuria/bacteriuria/hematuria
DD: F- vulvovaginitis/ PID
M- prostatitis/ urethritis
Tx:Short-term abx (1-3 days)
 Bactrim Ⓡ - most common treatment
 Quinolones (TequinⓇ)
 Pyridium
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Manage Acute Pyelonephritis
Symptoms
 Fever
 Flank pain
 Irritable voiding symptoms
 Positive urine culture
 Gram –ve:
E.coli/ Proteus/ Klebsiella/
Enterobacter/ Pseudomonas
Tests
 CBC: WBC Increased/
 Renal u/s
 DD: Appendicitis/
Risks
 Lower Lobe pneumonia
 Sepsis/Shock/Abscess
 Treatment:
 IV abx- ampicillin
 Gentamicin
 quinolones
Prompt diagnosis and treatment essential
Fever, flank pain, positive urine test - pyelonephritis
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Manage Acute prostatitis
 Fever
 Irritative voiding symptoms
 Perineal/suprapubic pain
 Tender DRE / + ve urine culture
 E.coli/Pseudomonas
 WBC increased/ Pyruria/
 Bacteriuria / Hematuria
 TX:
IV abx- ampicillin / gentamicin
Oral quinolones-4-6 weeks
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Manage Acute Epididymitis
 Fever
 Irritative voiding symptoms
 Painful enlarged epidydimitis/
scrotal swellings
 STD under 40 (Chlamydia/GC)
Most common cause
 Over 40- urethritis/cystitis
 IMAGING Scrotal ultrasound
 Treatment: Abx-10-21 days
 Delayed or inadequate treatment may
result
in epididymo-orchitis, decreased fertility, or
abscess formation.
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Diabetic Nephropathy
Issues
And
Management
Facts about Diabetic Nephropathy
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




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
Number one cause for ESRD
45% of all dialysis patients
Early diagnosis of diabetes and proper therapy of diabetes helps prevention of renal
issues
Diagnosed by proteinuria
Serum Creatininine progressively increases
More common in Type 1 Diabetes Mellitus
After 10-15 years of Type 1 Diabetes Mellitus
After 20 years of Type 2 Diabetes Mellitus
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Diabetes
Type I
Type II
0.85-1.7 million
15.3-16.2 million
(estimated 5.9
million
undiagnosed)
microalbuminuria at
end of 15 years†
21%
28%
macroalbuminuria at
endof 15 years†
21%
14%‡
Progression to ESRD 10
years after onset of macroalbuminaria†
50%
10%‡
Prevalence of
disease*
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Etilogy of diabetic nephropathy
 Angiotensin II (ATII) itself contributes to the
progression
 An inflammatory process with evidence of
macrophage infiltration in glomeruli with early
diabetic sclerosis
 ACE inhibitors block this macrophage induced
inflammation
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Diagnosis of diabetic nephropathy
 Albuminuria greater than 300 mg/day
THERAPY:
 tight glycemic control
 tight glycemic control
 Check HbA1c (<7%)
 Pancreatic transplants in Type 1 Diabetes patients
helps reduce seriousness of diabetic nephropathy
 Good BP control if needed
(130/80 or lower)
51
Dietary Changes
 Avoid protein supplements such as protein shakes
or powders, but do not otherwise restrict protein
from the diet.
 Protein intake reduction to 0.8 g/kg/day
 Maintain a low-sodium diet
 2.3 grams (5.8 grams of NaCl) or 100 mEq daily
(very low salt)
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Avoidance of Nephrotoxins



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NSAIDs
(Low dose aspirin is OK – ischemic heart disease i.e.) Nothing above 650mg
No Contrast studies! Can’t excrete the dyes.
Possibly will help:
 ? Aldosterone blocking
 ? Statins
GFR (creatinine clearence) is steadily declining or is already below 60-70 ml/min requires nephrology
consult
53
To conclude
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Tight glucose control and tight blood pressure control (140 max)
ACEinhibition
Avoid nephrotoxins
Lipid control
Stop smoking
Exercise and wt. reduction
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Manage Hematurea
Hematuria
 Initial- at beginning of urination and clears
during the stream suggests anterior urethral
source
 Terminal- at the end of stream implies bladder
neck/ prostatic source
 Total- Throughout Urination - bladder or upper
tract source
 Age: young women –cystitis/ older - ?renal
cancer/ ?stones/GN/PKD
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Fictitious ‘bloody’ urine!
•Rhubarb
•Blackberries
•Blueberries
•Paprika
•Beets
•Fava beans
•Artificial food colorings
•Bilirubin
•Myoglobin
•Hemoglobin
•Porphyrins
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Rifampin
Nitrofurantoin
Sulfonamides
Metronidazole
Phenytoin
Prochlorperazine
Phenolphthalin
Quinine
Chloroquine
Phenazopyridine
Levodopa
Methyldopa
Adriamycin
Desferoxamine
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 Dipstick Hematuira highly sensitive/ RBC Cast:
58
Risk Factors for Significant Disease in
Patients with Microscopic Hematuria
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Smoking history
Occupational exposure to chemicals or dyes (benzenes or aromatic amines)
Age greater than 40 years
Can be bladder cancer, other disease
History of urologic disorder or disease
History of irritative voiding symptoms
History of urinary tract infection
Analgesic abuse
History of pelvic irradiation
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Demographics
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1-16%
Elderly men
Glomerular and extraglomerular bleeding, separating nephrologic and urologic disease.
With casts or without casts
malignancy, renal stones, trauma, infection and medications
60
?Polycystic Kidney Disease
 A family history of renal failure and cerebral
aneurysms suggests polycystic kidney disease
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Therapy


If glomerulonephritis: medical management
Stones smaller than 4 mm are likely to pass spontaneously
while those larger than 7 mm have a low likelihood of spontaneously passing and may
block the ureters/urethra.
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Hematurea OUTCOMES



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Infections 25%
Stones 20%
Unknown 10%
Advancing age- urological malignancy is often the cause.
63
How to Manage
Renal
Stones
Presenting Symptoms



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flank pain,
gross or microscopic hematuria,
obstruction of one or both kidneys, and
urinary infections
Most common reason: parathyroid tumor causing high calcium, other reasons for calcium
65
overdose such as excessive consumption, vitamin D issues, etc.
Stone Types




(1) calcium, (70%)
(2) uric acid, (5-10%)
(3) magnesium ammonium phosphates (or struvite) (10-12%)
(4) cystine (1%)(higher in children)
66
Incidence
 1 in a 1000
 M:F - 2:1
 Pathophysiology:
Super saturation
Associated UTI
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Calcium Stones
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M>W, 50+
Hypercalciuria
Always measure how much calcium is being excreted. Hypercalcuria is >300mg in men,
>250mg in women. Worse for meat eaters, users of Lasix (excrete more Ca). Thiazides actually
reduce Ca loss.
Hyperparathyroidism related 5%
Made worse by high dietary. Worst culprits:
 sodium
 animal protein
 loop diuretics
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?Diet
 Diet with normal calcium, low sodium, and low
animal protein resulted in reduced frequency of
calcium stones compared with a low-calcium diet.
-
Borghi L, Schianchi T, Meschi T, et al. Comparison of two diets for the prevention of
recurrent stones in idiopathic hypercalciuria. N Engl J Med. 2002;346:77-84.
-
Major role in stone formation
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Diet Benefit
Patients on the normal calcium,
low sodium, low protein diet had
a 50% reduction in stone risk at 5
years.
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Role of hyperoxalurea


Increased calcium stones when there is high dietary oxalate intake due to ingestion of
foods or liquids containing large quantities of oxalate:
 Baked beans, collards, green beans, rhubarb, tea, cocoa, peanut butter, and vegetable soup
IBD patients are more likely to have this.
Oxalic acid related stones
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Other Risk Factors for
Calcium Stones



(1) chronic low urine output
(2) hyperuricosuria and
red meat and purines will cause more of this.
(3) low urine citrate
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SIGNS AND SYMPTOMS
 Episodes of colicky flank pain that radiates to the
anterior abdomen or even to the genitalia
 Microscopic or gross hematuria
 Ca Oxalate crystals in the urine
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DIAGNOSIS
 Stone analysis for
calcium oxalate/ phosphate stones
 Computed helical scan (helical CT)
 US for stones larger than 3-5 mm size
 Helical computed tomography without contrast
is the procedure of choice. Can see very very tiny
stones.
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Therapy
 High fluid intake, dietary sodium restriction, and
add thiazide diuretics to restrict amt of calcium in
the urine.
 Dietary calcium restriction is not advised
 Rule out hyperparathyroidism
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URIC ACID STONE DISEASE
 Low pH urine and concentrated urine
(?insulin resistance)
 Increased uric acid excretors
(gout, or high purine intake)
 radiolucent, but are visualized by both US and
noncontrast helical CT
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THERAPY
 Alkalinization of urine to pH >6.5 with potassium
citrate solution
 Hydration
 Reduces stones by 90%
 Use of Allopurinol
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STRUVITE SONES
 Aka: magnesium ammonium phosphate stone
 Women more likely to have than Men
 Spinal cord injury pt.
 Neurogenic bladder
 Vesicoureteric reflux
 Chronic indwelling Foley catheter
 Recurrent UTI
 CAUSE LARGE STAG HORN STONE
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THERAPY
 Eradicate UTI
 Stone removal
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CYSTINE STONES
 Autozomal Recessive disorder
 Renal tubular absorption disorder
 Urine test with sodium nitroprusside turns it purple-red
color.
 Therapy: high fluid intake
 Reduce dietary methionine- restriction of red meat, fish,
poultry, and dairy products and sodium restriction
 Alkalinization of urine pH 6.5-7
 Chelating agents – Thiol derivatives
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UTI due to
 Urea-splitting bacteria include Proteus (most
commonly), Pseudomonas, Klebsiella, some
Escherichia coli, and Staphylococcus
Nasty bugs – less common.
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Interstital Cystitis /
Painful Bladder Syndrome
Background
Epidemiology
Diagnosis
Treatment
Summary
References
Nasty disease western med can’t really help
with. Might have institial dx.
Background
Chronic urinary bladder disease features Bladder pain -excruciating
 Frequency – 60 times/24 hrs
 Urgency
 Nocturia
 90% Women
 Distressing life style
83
Epidemiology
 60 / 100,000
 Age / Gender / Family history
 Disease may wax and wane for the lifetime
 Associated increase in ‘non-bladder’ disease:
 Inflammatory bowel disease
 Irritable bowel syndrome
 Systemic lupus erythematosus
 Panic attacks, and
 Fibromyalgia
84
Etiology
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Unknown cause
? Increased permeability of bladder mucosa to toxins
Abnormal bladder nerves sensitivity
Mast cell activation – inflammation
large number of mast cells
Autoimmune
Infections
Toxins in urine/diet
Antiproliferative substance in urine
protective substance that can disappear, hence the problems.
Better when bladder is empty
85
Factors Associated With Exacerbation of
Symptoms of IC*
 Sexual intercourse
 Perimenstrual
 Allergies
*Urinary
Frequency,
Urgency and
Pelvic Pain.
 Diet
 Physical, emotional stress
 Pelvic floor muscular contractions
86
Pathogenesis of IC:
Defective Urothelial Barrier
Irritating
Solutes
Urothelium
Irritated
Nerve
Glycosaminoglycan layer
GAG
Layer
Inflammation
87
IC is Characterized by a Vicious Cycle:
Increased Symptomology
With Increasing Age
Bladder Insult
More Inflammation
Epithelial Layer
Dysfunction
Mast Cell Activation and
Histamine Release
Potassium Leak Into
Interstitium
Activation of C-fibers and
Release of Substance P
Adapted with permission from Evans RJ. Rev Urol. 2002;4(suppl 1):S16-S20.
88
Differential Diagnosis of IC
 Bladder or Urinary tract
infection
 STI
 Vaginal infections
 Vulvodynia
 Uterovaginal prolapse
 Renal calculi


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Cystocele/Rectocele
Endometriosis
Sterile urine culture
Urethral diverticula
Pelvic floor dysfunction
Overactive bladder
89
DIAGNOSIS
 At least one of the cardinal symptoms: bladder pain,
frequency, urgency, and/or nocturia
 Women for whom UTI has been ruled out or treated
yet who have persistent or recurrent urinary
symptoms in whom IC / PBS (painful bladder
syndrome) should be considered.
Might look like D/H in TCM, but likely a deficient condition.
90
Diagnostic features
 Suprapubic pain (anywhere between the
umbilicus and the upper thighs )
 Pain worsens with bladder filling and diminishes
with bladder emptying
 Certain foods or drinks may exacerbate their pain
:
91
Aggravating FOOD ITEMS
 Alcoholic beverages
 Apples, Apple juice
 Aspartame
 Avocados
 Bananas
 Cantaloupes
 Carbonated drinks
 Cheese (except:
American, cottage,
ricotta, cream)
 Chicken livers
 Chilies / spicy foods
 Chocolate
92
Aggravating FOODS
 Citrus fruits (lemons, limes,
grapefruits, oranges, and their
juices)
 Coffee (except no-acid type)
 Corned beef
 Cranberries
 Grapes, grape juice
 Guava
 Lentils
 Lima beans
 Mayonnaise
 Nuts (almonds, peanuts, and pine
nuts are tolerable)
 Onions
 Peaches
 Pickled herring
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Pineapple
Plums
Prunes
Raisins
Rye bread
Saccharine
Sour cream
Soy sauce
Strawberries
Tea (except sun tea)
Tomatoes (except low-acid types)
Vinegar
Vitamins buffered with aspartate
Yogurt
93
?Tests
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Physical examination non specific
Imaging procedures unrewarding
Abnormality in their urinary tract:
Urinalysis- hematuria, pyuria
Cystoscopy- petechial hemorrhages
Urodynamics- small bladder
Potassium chloride instillation induces pain/ urgency
94
Treatment
 Diagnosis is by symptoms and exclusion
 Empirical therapy
 Education
 Diet
 Analgesics and specific oral medications
95
 Education websites:
 http://www.ichelp.com
 http://www.ic-network.com/
 Identify food items to avoid
 NSAIDs
96
Drug
Number
RCTs
% Patients Improved
Drug
Comparator
P Value
Oral
Amitriptyline[13]
1
63%
4% (placebo)
< .001
Pentosanpolysulfate[14-19]
5
approx.
30%
approx. 15%
(placebo)
Values range from
NS to .01
Hydroxyzine[19]
1
31%
20% (placebo)
NS
Cyclosporine A[20]
1
75%
19% (PPS)
.001
40%
18% (placebo)
"significant"
Intravesical
Dimethylsulfoxide[21]
1
PPS = pentosanpolysulfate; RCT = randomized controlled trial.
Amitriptyline increases pain threshhold.
97
Drugs
 Amitryptaline very effective
 Pentosanpolysulfate (Elmiron®) protects GAG
layer -25-35% effective (100 mg 3 times a day)
 Intravesical:
 dimethylsulfoxide / heparin / lidocaine / and/or
corticosteroids into the bladder
 ? Sacral nerve stimulation
98
CAM Therapies for IC



Dietary Modification:
IC diet, fluids, bowel regimen, Urinary alkalinization
Nutraceuticals:Calcium glycerophosphate , L-arginine
Mucopolysaccharideshyaluronic acid, chondroitin sulfate, aloe vera
Bioflavinoids-quercitin
Chinese herbs
Bladder Training
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Neuromodulation
Physical therapy: of external pelvis (manual therapy) / of internal pelvis (Thiele massage)
Biofeedback/electrical stimulation
Acupuncture
Stress Reduction
Sex Therapy
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Don’t try to hold it – don’t retain too much urine at a time.
99
MALE UROLOGY
Disorders of Prostate, Testes
Infertility


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
Affects 15–20% of couples
Rule of 3’s:
 One-third of cases due to male factors
 One-third due to female
 One-third due to combined factors
Following 6 months of unprotected intercourse
Simultaneous evaluation of both partners critical
101
102
Infertility History
 Prior testicular insults (torsion, cryptorchidism,
trauma)
 Infections (mumps orchitis, epididymitis)
 Environmental factors (excessive heat, radiation,
chemotherapy)
 Medications :
(anabolic steroids, cimetidine, and spironolactone
may affect spermatogenesis; phenytoin may lower
FSH;
sulfasalazine and nitrofurantoin affect sperm
motility), and drugs (alcohol, marijuana)
103
Semen Analysis
Performed after 72 hours of abstinence
Analyzed within 1 hour after collection
Abnormal sperm concentrations are less than 20 million/mL.
Normal semen volumes range between 1.5 and 5 mL (volumes < 1.5 mL
may result in inadequate buffering of the vaginal acidity and may be due to
retrograde ejaculation or androgen insufficiency).
 Normal sperm motility and morphology demonstrate 50–60% motile
cells and more than 60% normal morphology.
 Abnormal motility may result from antisperm antibodies or infection.
 Abnormal morphology may result from a varicocele, infection, or

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exposure history.
104
ED

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10 million American men
More common than infertility
organic rather than a psychogenic cause
neurovascular phenomenon
intact autonomic and somatic nerve supply to the penis, smooth and striated musculature of the
corpora cavernosa and pelvic floor
arterial inflow supplied by the paired pudendal arteries
105
ED: ? NT



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
nitric oxide,
vasoactive intestinal peptide,
acetylcholine,
prostaglandins. Have to inject it into the base of the penis though. Ow!
Therapy:
 Testosterone injections/patches
 Vasoactive prostaglandins: alprostadil
106
ED Treatment



Decreasing the breakdown of cyclic guanosine monophosphate (cGMP)* has
revolutionized the treatment of erectile dysfunction. Sildenafil (Viagra) allows cGMP to
function unopposed.
Newer drugs including vardenafil (Levitra) and tadalafil (Cialis), have a longer half-life.
*By blocking Phospho Di Esterase (PDE)enzyme activity
Erection needs the parasympathetic, increased levels of Acetylcholine. Sympathetic is needed
for ejaculation. There’s an enzyme that is blocked by viagra like drugs – same enzyme
needed for rods and cones, hence the danger of blindness.
Can have a blinding headache, drop in the blood pressure – especially dangerous with HTN
and medications to control it. Can cause enough drop in blood pressure to kill someone.
107
Enlarged Prostate

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Most common benign tumor in men
Incidence increases with aging
25% at 55 have some symptoms
? Genetic ?ethnic
Multifactorial & endocrinal (^androgen sensitivity)
Dihydrotestosterone & age
Sensitivity to testosterone – gets very large. Dihydrotestosterone is what makes the
prostate get larger.
Hyperplasia
108
Enlarged Prostate Symptoms
Obstructive:
 Hesitancy
 Decreased force and caliber of the stream
 Sensation of incomplete bladder emptying, double voiding (urinating a second time within
2 hours)
 Straining to urinate, and
 Post void dribbling
Diagnosed with DRE and PSA.
109
Enlarged Prostate Symptoms
Irritative:


Urgency
Frequency

Nocturia
110
111
Phytotherapy for EP
 Saw palmetto berry,
 The bark of Pygeum africanum,
 The roots of Echinacea purpurea
 Hypoxis rooperi, pollen extract
 The leaves of the trembling poplar
112
Enlarged prostate Therapy
 Alpha 1 (α1)-blocker therapy
(prazosin/terazosin/tamulosin) :
excellent responses in patients with benign
prostatic hyperplasia when there is a
significant component of smooth muscle
dysfunction (sphincter)
 Epithelial Hyperplasia responds better to 5 αreductase inhibitors (finasteride Proscar®)
Blocks testosterone effects on prostate
113
Prostate Cancer
 Prostatic induration on digital rectal examination
or elevation of PSA.
 Most often asymptomatic.
 Rarely: systemic symptoms (weight loss, bone
pain).
114
Cancer
Prostate
Most common
cancer detected in American men
 Second leading cause of cancer-related death
 2005:
 over 232,000 new cases diagnosed, and
 30,300 deaths resulted
 Environmental or dietary differences prostatic
cancer growth
115
Prostate
Cancer
Large number of prostate cancers are
associated with
prostates and are
of elevations in
palpably normal
detected on the basis
serum PSA
Lymph node metastases: can lead to lower
extremity lymphedema
Axial skeleton is the most common site of
metastases: back pain or pathologic
fractures.
Imaging and biopsy
Management
116







Lab
Testscorrelates with cancer
PSA: Increases
BUN & Creatinine increase if obstructive uropathy
exists
Increased ALP and Calcium if bone metastases
exist
Prostatic biopsy
MRI/US scan
Radionuclide bone scan
“Screening Tests”: DRE, PSA testing, and
transrectal
ultrasound
117
Treatment
 Most patients with an anticipated survival in excess
of 10 years should be considered for treatment.
 Both radiation therapy and radical prostatectomy
allow for acceptable levels of local control
118
Bladder Cancer
 Irritative voiding symptoms.
 Gross or microscopic hematuria. (85-90%)
 Positive urinary cytology in most patients.
 Filling defect within bladder noted on imaging.
 second most common urologic cancer
 M:F-(2.7:1) Age 65+
 Risk factors: Cigarette smoking and exposure to
industrial dyes or solvents
 confirmed by cystoscopy and biopsy
 Papillomas
119