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GI/GU EXAM #2 – 9/30/08

PROSTATE

Prostate Anatomy

Firm, elastic gland

Beginning of urethra passes through it

Between pubic bone and rectum

Peri-urethral and peripheral zones

Secretes acid phosphatase and prostate specific antigen

Prostate Cancer

Nodular prostate cancer feels like your first MCP joint. Typically, prostate cancer is not painful, and that is troubling.

Prostate Exam

Typically a palpation exam, that needs to be trained and refined.

Prostatitis

50% of men will experience prostatic inflammation at some time in life

Only 5% of all prostatitis is due to bacterial infection

Bacterial infections m/c due to retrograde infection of the prostate from prior urethral infection

Condition Divided into 4 Categories

1. Acute Bacterial Prostatitis

2. Chronic Bacterial Prostatitis

3. Non-bacterial Prostatitis

4. Prostatodynia

1. Acute Prostatitis

Most common in 20-40 year olds

Rapid Onset of systemic symptoms:

Fever/Chills

Lethargy

Pain (Low back, perineal, and suprapubic): Low back pain that you cannot reproduce, except with DRE.

Voiding Problems:

Dysuria: Problems peeing due to great enlargement of gland in the short amount of time that constricts gland, forcing greater holding of material in the bladder. The bladder can’t contract fully to empty. The infection of the prostate leads to cystitis because of incomplete void. Static urine due to the incomplete void leads to bladder infection (cystitis).

Urgency

Frequency: More trips to the bathroom are needed. This is not diuresis, but increased frequency. They are still not above 2L per day.

DRE:

Gland is irregular and enlarged

Warm

VERY TENDER

Palpation ---- Leads to copious purulent discharge

Fluctuating Region ---- Possible and Vigorous

Palpate Carefully: Painful and vigorous massage is contraindicated possibly causing septicemia or secondary epididymitis.

We can use a triple catch urine study. The discharge from the prostate into the prostatic urethra is flushed into Cup #3. Cups 1 and 2 aren’t normal, but Cup 3 is more abnormal than the other 2 cups.

Prostatic massage can draw the organism deeper. The deeper the organism, the more difficult to handle medically and mechanically. Prostatic massage can lead to secondary epididimytis as well.

Treatment:

Patient very ill/Hospitalization frequently

Obstruction and urine retention may necessitate catheterization

IV antibiotics

Increase Hydration

Oral Antibiotics for 4-6 Weeks after Acute Episode

In the history, ask men about cystoscopy. Cystoscopy is usually the mechanism by which the organism is carried past the body’s defenses and is implanted.

2. Chronic Prostatitis

Signs and symptoms similar to acute form but less severe, intermittent, and recurrent

Fever and urethral discharge are uncommon

Dull LBP and perineal pain

Mild Dysuria/frequency

DRE: Enlarged, Soft/Boggy, Slightly Tender

Treatment

Difficult to treat

Eradication with antibiotics only successful 30-50% of time

Suppressive antibiotic therapy may be necessary and leads to symptomatic relief

3. Non-bacterial Prostatitis

Signs and Symptoms similar to chronic form

Cultures are (-). Elevated WBC in secretions

4. Prostadynia

Signs and symptoms similar to chronic form

Cultures are (-). WBC numbers are normal.

Prostatodynia is a fancy name for prostate pain and the reason for this is idiopathic. We don’t know why this happens.

Both (non-bacterial and prostatodynia) may show symptomatic relief with antibiotic treatment.

GONOCOCCAL URETHRITIS

Pain is part of the picture but it is not severe. The copious discharge of Gonococcal Urethritis that drips is the most notable aspect. Gonoccocal urethritis is very easy to transmit. Females don’t have much pain or discharge vs. men which have more discharge and slightly more pain. Longer urethras will show more discharge (males).

Issues of Absorbance

Women don’t notice discharge because they wear pads or other absorptive devices that often absorb the discharge.

Anonymous Reporting of Gonorrhea

You are supposed to report the finding to public health officers. Discharge with urination or drainage, requires a culture and sample. If the sample is positive for gonorrhea, it requires a phone call to the public health official/office looking at the sexual history. Others can get infected, particularly females because the symptoms are less well established. Gonococcal pyelonephritis is devastating to the kidney. The system to notify patients is set up anonymously.

Key Findings

Copious Discharge is a key finding differentiating gonococcal urethritis from other UTI’s.

Differentiating features in male (more discharge and more pain than females)

Complications

Endocarditis

Meningitis

Polyarticular Arthritis (general aches, pains and synovitis)….Arthritis that is not typical is an indicator

Gonococcal Urethritis is the reportable Illness (bacterial irritation of the urethra) VS Gonorrhea (the actual bacteria and subsequent infection) which requires a different test than gonococcal urethritis.

CYSTITIS

Classic cystitis follows urethritis. Burning urination, that hurts before, while and after urination. This pattern is classic cystitis. As the bladder stretches, the infected wall notes the stretch and the patient notes discomfort. The patient recognizes bladder fullness earlier than usual (urgency). The contraction squeezes irritated mucosal tissue causing discomfort during urination. The bladder wall stretches, compresses and the patient has post-void ache. Hurts with filling, hurts with emptying and hurts after urination = CYSTITIS!

The patient may present with a profile of “acute abdominal inflammation” or appendicitis. AS you continue to work the case through, you rule out those conditions and ask for lab testing. The testing is a culture (looking for over 1000,000 colonies per type) and sample.

RBC’s are likely to be in the urine, but not a requirement. Chemotherapy is a common cause of cystitis reproducing RBC’s in the urine. The chemotherapeutic agents are cytotoxic and pass through glomerulus. The molecules are stored in the bladder till elimination causing increased contact time inflaming the bladder wall (cystitis that is not organism based). Patients on chemotherapy should increase fluid intake to reduce the chance for cystitis. The recommendation is filing a bottle with a goal level/mark of fluid and having the patient reach the mark on the bottle.

UPPER TRACT INFECTION - PYELONEPHRITIS

The basement tissue or interior of the kidney (medullary kidney) is the source of the problem. This is an ascending problem. The organism can get into the renal pelvis and other areas. This is the classic condition, where the infection ascends into the interior of the kidney.

Outlet stenosis occurs. Hard compression against resistance causes relief points at the Ureter and renal pelvis.

Hematogenous spread is concentrated in the cortex and is called nephritis.

Treatment and Care

Conservative care should be an adjunct to Antibiotics

Consult an MD/DO (primary care or urologist)

Antibiotics should be ordered based on culture and sensitivity testing.

In some cases, broad spectrum antibiotics are used.

Kidney Function

There is often damage with lasting effects that may not be measurable on kidney function tests

Recurring Pyelonephritis

This is the 2nd episode of pyelonephritis. A second episode doesn’t bother the older fibrotic areas but goes after healthy areas. There is reduction of renal capacity that is still within reserve capacity and there is still no measurable functional deficit.

Multiple Recurrences/Chronic Pyelonephritis (3 or more times)

A third episode (3 or more) is called multiple recurrences or chronic pyelonephritis. We think a broad spectrum antibiotic has killed enough, so that another flora (often the first bug) has developed in its place. We have now killed the 2nd bug leading to another non-competitive situation in the body. The patient contracts an infection from the flora present because they don’t have other bacteria to compete against. The treatment for this is a broad spectrum antibiotic chosen to kill multiple flora.

Chronic conditions can be very dangerous, as they can cause loss of the kidney.

*** THIS WILL BE ON THE TEST ***

ASYMPTOMATIC BACTERURIA

Typically, they’ve had instrumentation or been in hospital with catheterization. A greater percentage of these patients now have UTI’s. The patient can bring this to your attention and give you their lab result. Ask the patient for information and what do they want to do about this? If they want to do something, ask for a lab profile (expected lab profile).

Treatment includes water, cranberry juice. You truly have to do nothing except watchful waiting and possibly lab testing to check if levels have gone down to normal.

10/6/08

MISCELLANEOUS DISEASE

Glomerulonephritis

Nephrotic Syndrome = Membranous glomerular nephritis

Glomerular Nephritis

Scleroderma

SLE

Sickle Cell Anemia

Miscellaneous

*** All the above diseases can lead to Nephrotic Syndrome due to loss of proteins and water leakage ***

1. SLE

Common Complaints with Lupus

SLE is an idiopathic disease. The most common complaint is myalgia. Pain motivates people to seek help. Butterfly or malar rash is present. Widespread swollen lymph nodes occur. Pericardial tissue can be inflamed along with pleural membrane inflammation/swelling.

Lupus Nephritis

SLE fits in with LUPUS NEPHRITIS. Lupus nephritis is a systemic problem seen with SLE. There is general/non-specific impact to the kidney. Breakdown of the glomerular basement membrane occurs. The holes get bigger in the kidney as the membranes breakdown allowing higher weight proteins through. As the proteins flow through, water is also lost. The patient diuresis due to large amount lost of protein.

Nephrotic Syndrome

Nephrotic syndrome occurs when 2.5 grams to 3.0 grams of protein are lost. Tamm Horsefall loss occurs at .2 grams. Loss of mass amounts of proteins makes them a “puffy weight loser.” The proteins are lost (so they get puffy) and water is lost (so they lose weight)

We can offer palliative care. We can ease discomfort and manage musculoskeletal symptoms.

Lupus Syndrome

Can be due to medications (arrhythmia drugs, anti-seizure drugs, and anti-hypertensive drugs). The good news is that they usually don’t have kidney problems with Lupus syndrome.

Overview of SLE

1. Myalgia

2. Butterfly/Malar Rash

3. Multiple Swollen Nodes

4. Pericardial or pleural tissue inflammation

5. SLE can cause Lupus Nephritis

a. Lupus Nephritis presents with diuresis

6. SLE can lead to Nephrotic Syndrome = Loss of protein

a. Nephrotic Syndrome creates Puffy Weight Losers

Overview of Lupus Syndrome

1. Due to medications

2. Kidney is not affected in Lupus syndrome (it is affected in SLE)

** Be able to separate Lupus Syndrome from SLE…SLE does impact the kidney but lupus syndrome does not affect the kidney ***

*** The effect on the kidney of SLE is loss of proteins, loss of water & diuresis ***

2. SCLERODERMA

A collagen problem that presents as a skin disease hardening which also affects the skeleton as an arthritide and a destroyer of bone (acroosteolysis). We see sclerosis of the kidney as a dystrophic pattern.

We need to do renal function testing and/or UA to appreciate the damage to the kidney. The damaged tissue affects the holes of the Glomerulus. Large proteins make it through, water follows and diuresis occurs.

The patient ends up with an oliguria form as the kidney becomes more non-functional in the end stages. So we start with diuresis, progress to oliguria and end up on dialysis with scleroderma. End stage of kidney damage by scleroderma shows the kidney is abnormally shaped on imaging. Nephrotic syndrome occurs due to leaky glomerulus.

Scleroderma tissue can also affect the GI system and swallowing. The patient can lose the ability to produce a coordinated peristaltic wave. They can also present with Reynaud’s phenomenon (1 out of every 2 with scleroderma get Reynaud’s). Cold drinks can trigger Reynaud’s in the esophagus leading to problems with swallowing.

Overview of Scleroderma

1. Skin Hardening

2. Arthritide Formation

3. Destroyer of Bone (acroosteolysis)

4. Damage to Kidney

a. Diuresis

b. Oliguria

c. Dialysis

5. Leads to nephrotic syndrome

6. Swallowing problems

7. Reynaud’s: ½ with scleroderma have it

3. SICKLE CELL ANEMIA

It causes problems of infarct in the kidney. Multiple small infarcts give polka dot appearance on IVP with black spots and areas of white surrounding the black polka dotted infarcts. In bigger vessels, the damage can show as wedge shaped, due to under perfusion. IVP is the best test to screen for sickle cell. The contrast dye may never enter the areas where sickle cell infiltrates.

Sickle cell triggers infarct. Infarct leads to death by hypoxia. The cells may never be replaced. This condition causes holes in the Glomerulus to get bigger allowing protein and water leakage from the system. Nephrotic syndrome transpires.

Overview of Sickle Cell Anemia

1. Causes infarct in the kidney

2. Best tested with IVP

a. Can present with black polka dots or wedge shaped areas

3. Damages the Glomerulus

a. Leads to water and protein leakage (nephrotic syndrome)

4.MISCELLANEOUS

A). PREGNANCY

Eclampsia or pre-eclampsia can occur. Both conditions show high pressure that creates hydrostatic pressure to increase in the Glomerulus. The size of the hole gets bigger and large proteins move through with water following. Nephrotic syndrome can occur with loss of water and proteins. Waxing and waning protein and water loss ensues.. There is s direct relationship with the mothers’ BP to amount of fluid and proteins lost.

Overview of Pregnancy

1. Eclampsia/Pre-eclampsia can affect hydrostatic pressure

2. Nephrotic Syndrome

a). Loss of water and protein

3. Correlates with Mother’s BP

B). DIABETES MELLITUS

The most common cause of nephrotic kidney is diabetes mellitus. Typical is a white spec calcification pattern of the kidney. Punctate calcification is consistent with late stage DM.

The bulk of the sclerosis occurs by atherosclerosis. Protein loss can make it seem like nephrotic syndrome, but the failure is more complex. The early stage of renal damage is related to the glomerulus. The atherosclerotic pattern later involves the vascular network surrounding each tubule. Water enters the vascular network and is carried into systemic circulation. As diabetes progresses, we see a decline in tubular function, GFR decrease and urinary output decrease (oliguria) At 90% loss of output, we see end stage renal failure. They need dialysis until transplant or death.

The diabetic kidney occurs by glomerulosclerosis/atherosclerotic process. Mot common sign and symptom is nephrotic syndrome starting with diuresis, progressing to oliguria and ending with renal failure.

Overview of Diabetes Mellitus

1. Most common cause of nephrotic syndrome = Diabetes Mellitus

2. White Spec Calcification (early) & Punctate Calcification (late)

3. Glomerulosclerosis & Atherosclerosis contribute

4. Water backs up into systemic circulation

5. Decreased Tubular Function, Decreased GFR

6. Progression

a. Diuresis

b. Oliguria

c. Dialysis

7. Leads to Nephrotic Syndrome

C). TROPICAL DISEASES

Comes only with travels to tropical areas. This can be asked in the history.

5). NEPHROTIC SYNDROME

Massive proteinuria occurs. The proteinuria comes from the blood. Massive loss of protein from the blood pool occurs. Hyperproteinuria is linked with hyperproteinemia, the protein lost to urine comes from the blood.

Typically, take notice 2.5 grams of protein lost per day. The official classification for nephrotic syndrome starts at 3.0 grams. A 24 hour sample is required to make the diagnosis. Protein takes water with it and the patient sees diuresis. The patient is often dehydrated. Osmotic pressure is reduced in the vascular tree. The water goes to the tissues. They end up with edema. Edema must be present to have nephrotic syndrome.

Dependent edema is present along with edema in the small intestine. The small intestine does not absorb as well when edema is present. Proteins are taken from muscle (endogenous storage) to facilitate the body’s need. Proteins are taken from all muscle sources (cardiac, skeletal, smooth).

They are Puffy weight Losers. They are using endogenous proteins to maintain osmotic pressure in the vascular tree. These patients also have hyperlipidemia. It is the body’s attempt to keep osmotic pressure. It is not as good as protein, but is better than nothing

Descriptors of Nephrotic Syndrome

1. Hyperalbuminuria 2. Hypoalbuminemia 3. Edema 4. Protein 5. Hyperlipidemia

Clinically

They will have pitting edema due to collection of fluid in LE. Cloudy urine occurs due to protein loss. There can be ketones in the urine evident by smell. They have polyuria or diuresis. They present with dry mouth. They report being thirsty.

The RAA system is driven and stimulated. During low GFR and low tubular flow rates causes activation of the RAA system. Dehydration also stimulates the RAA system. They are peeing a lot and thirsty.

In many cases, nephrotic syndrome is the end result of numerous other renal problems. Some of these conditions are: scleroderma, diabetes, pregnancy, tropical disease, etc.

Causes

There are 2 major categories of cause for nephrotic syndrome:

1). Glomerular tissue specific

2). Systemic

Systemic Causes of Nephrotic Syndrome

Only 25% is by processes outside the kidney (DM, SLE, NSAIDS, cancer, etc). NSAID’s affect tubular cells and glomerular function. Cancers like Hodgkin’s lymphoma and leukemia, can affect the basement membrane causing nephrotic syndrome

Glomerular Tissue Specific Causes of Nephrotic Syndrome

75% is due to direct damage to the Glomerulus. If you find large proteins in urine, the only explanation is damage to the Glomerulus basement membrane.

Membranous glomerular nephritis is the single largest category causing nephrotic syndrome. We find immune cells in the basement membrane during biopsy. A strong stimulus of our immune system is the trigger. Inflammatory reactions cause basement membrane destruction. IgG pokes large holes in the basement membrane.

Treatment

Treatment depends on the cause, because nephrotic syndrome is a complication of other disease.

Pregnancy = Regulate pressure, bed rest and allow homeostatic mechanisms to occur

Diabetes = Not linked with well regulated or poorly regulated diabetes. They can do everything right and still have a kidney problem.

Membranous Glomerulonephritis = Typically get corticosteroid to disrupt inflammatory cycle. It tends to disrupt the process allowing for 5-7 days better/faster relief. The goal is to get them out of the hospital ASAP.

Multiple systems can be affected leading to accumulation of fluid can occur. Protein powders can be used to replace some of the proteins. If they are in the hospital, they will put hem on IV drip with protein. The protein will help get rid of edema (less risk for pulmonary edema and pleural effusion).

Loss of albumin causes loss of Parathormone. This is a mechanism for secondary hyperparathyroidism. We should place them on Vit D with calcium and magnesium to reduce the robbing from bone of calcium. Additionally, exercise and ambulating will help them prevent bone mineral loss.

Overview of Nephrotic Syndrome

1). Massive protein loss occurs

2). Classification occurs at 3 grams during 24 hour sample

3). Edema (Dependent Edema and Edema in other tissues – lungs, cardiac tissue, etc.)

4). Endogenous Proteins are taken from muscle to keep osmotic pressure

5). Descriptors = Hyperalbuminuria, Hypoalbuminemia, Edema, Protein, Hyperlipidemia

6). Early on = Diuresis, Dry Mouth, Increased Thirst

7). 2 Major Causes = 1). Glomerular Specific 2). Systemic

a). Glomerular Specific = Occurs most often (75%). Linked with damage to basement membrane by immune cells and inflammatory reaction.

b). Systemic = Occurs less often (25%). NSAID’s, cancer, SLE, Diabetes Mellitus can all be causes

8). Treatment

a). Depends on the cause

b). Other general treatments are:

1). Protein Powders

2). Vit D, Calcium, Magnesium for bone mineral loss from Parathormone

3). Exercise and Walking

URINARY OBSTRUCTION

Inability to move urine is broken down into 2 categories: 1). Intrinsic 2). Extrinsic.

Intrinsic Problems

The most common is stone disease (intrinsic). Other things that cause intrinsic problems are congenital hypoplasia of the Ureter, duplex kidneys and carcinoma. Congenital hypoplasia of the ureter shifts material to the other kidney. Duplex kidneys are subdivided kidneys. Subdivided kidneys are underdeveloped. Radiological studies show a pair of renal pelvis and calyces. The duplex kidneys net out to less function than a single kidney would. Carcinoma of bladder, prostate, ureter, and kidney can create obstruction. Cancer of the GU is an intrinsic problem.

Extrinsic(extrinsic problems to the GU system)

Uterine Cancer, GI Cancers, Lymphoma (lymph change in pelvis that grabs onto Ureter and causes obstruction). Large aortic aneurysm causes problem s to the left Ureter. Retroperitoneal obstruction and fibrosis can be other causes of extrinsic obstruction.

*** Know intrinsic and extrinsic….Know examples of each…Intrinsic must be within the tissue or of the tissues…Everything else is extrinsic….Focus on subsets ***

Bladder Obstruction

Males and females can both have this. There are intrinsic and extrinsic causes of bladder obstruction with stone disease the most likely cause.

Stones enlarge in the bladder. The keyword is supersaturation, which leads to stone formation. The net effect is precipitation. The solutes aggregate growing in size in the bladder. The stretch signal comes from the bladder wall and increases parasympathetic tone. The Detrussor contracts and pushes the stone, lodging it into the bladder or urethral walls.

We have an unsatisfied contraction called retropubic pain. The overly full bladder is a firm rounded dome over the edge of the pubic bone that may be felt with palpation. Pushing on it will increase discomfort. Patients can even wet themselves with pressure from palpation on the bladder during low grade obstructions.

Ureter& Urethral Obstruction

Ureters can also experience unsatisfied contraction. This will present as bilateral flank pain. Hydrostatic pressure resists the inflow from the Glomerulus. Acute renal failure can develop. The patient that ignores the signs of acute renal failure jacks up pressure so high that blood won’t enter the kidney. The kidney will die (ischemic necrosis). The condition is called Autonephrectomy, occurring from ischemic necrosis. A plugged urethra thus has serious consequences on the kidney.

10/7/08

Obstruction Review (Continued from previous day’s lecture)

Low grade obstruction can occur from scarring of the tissue. Patients have problems completely emptying the bladder. They also experience increased incidence of UTI’s due to static urine. Another cause of obstruction can be stone formation. Patients not drinking enough water can cause stone formation in the bladder. The stone lingers during dehydrated states. People with inflammatory bowel disease are more likely to have stones (all types of stones: gallstones, kidney stones, bladder stones).

Autonephrectomies

Patients who empty their bladder regularly can dump the stone into the system. During high grade obstruction of the system, backs up the urinary system towards the kidney. Kidney filtration is impaired when net flow of urine is severely decreased. Increased pressure causes hypoxia in one kidney and anoxia in the other kidney. Bilateral autonephrectomy manifests from loss of blood flow and lack of nutrients to both kidneys. This is a worst case scenario with a stone (autonephrectomy), but it is possible.

Residual Capacity of the Bladder

Stones are not painful till the physiologic limit is met. Worrisome is 300-500 mL that cannot get out of the bladder. Over 400 mL retained in the bladder can lead to permanent increase in size by tearing the muscular integrity of the bladder. The person will then always have this residual capacity and increased chances for UTI’s.

Pushing the Stone Out

Pushing on the stone with the intent of pushing the stone out, can lead to rupture and bladder failure. Symptoms of bladder failure and rupture are: pain & peritonitis. This can provoke bursting and surgery (particularly with large obstructions).

Overview of Obstruction

1. 2 Forms: Intrinsic and Extrinsic

a. Most common is stone formation = intrinsic reason

2. 2 Common Places: Bladder and Ureters

3. Bladder Obstruction

a. Affects males and females equally

b. Supersaturation and precipitation occur in the bladder

c. Increased Parasympathetic tone lodges the stone in the bladder or urethra

d. Unsatisfied Contraction and retropubic pain can occur

e. Bladder may be evident upon palpation

4. Ureter and Urethral Obstruction

a. Bilateral Flank Pain can occur when both Ureters are blocked

b. Patient can experience autonephrectomy due to ischemic necrosis when the Ureters back up

i. Autonephrectomies are the worst case scenario with stones

5. Overall Increased chances of UTI with stones due to static urine and increased residual capacity

6. Pushing on a stone with the intent to flush it out can cause rupture

URETERITIS & URINARY TRACT OBSTRUCTION

Ureteritis often begins with a high back pain pocket. The condition tends to move with low grade obstruction. Obstruction tends to form in the medullary part of the kidney in the concentrating tubules (Thin Loop). The situation progresses to and because of the thick loop, but first forms in the Thin Loop.

Site of Obstruction Formation

#1. The most common site of obstruction is the Uretero-Pelvic Junction. (#1 Top of the Ureter or bottom of the renal pelvis).

#2. The second most common site is the uretero-vesicle junction (vesicle = bladder).

#3. The third most common site is where it tips over the sacrum until it gets to the sacral promontory, the direction change it the culprit.

Low grade obstruction shows movement of the stone. The stone is small enough to move through the system and large enough to lodge. Dilation causes hydronephrosis in the kidney. Stretching and decompression of the urinary tract causes stone movement downward. Urine backs up behind the stone. The process is repeated as stretch and decompression occur moving the stone further and further down till it either lodges or passes. As the stone passes, pain occurs. Pain often follows along with passage of the stone/obstruction and pressure build up. Pain starts up high and moves down the system as the stone moves.

Renal Colic

Renal Colic occurs with unsatisfied contraction. Renal colic tells us that the motor and neurological system is intact.

Pain Pattern

Pain often begins in the flank and remains in the flank as the stone passes. Secondarily, the stone pain pattern moves down a little more and a little more, eventually projecting into the body core. The pain goes anterior and wraps around as it gets to the sacral promontory.

The whole system dilates and works to move the stone further until it backs up. The patient will point from the TL area, down to LS area and wrap around spiraling down and anterior to indicate their pain pattern. If the pain pattern descends, the stone is passing.

Overview of Ureteritis/Urinary Tract Obstruction

1. These stones tend to form in the Thin Loop in the medullar part of the kidney

mon Areas of Obstruction

a). Uretero-Pelvic Junction (#1 spot)

b). Uretero-Vesicle Junction (#2 spot)

c). Tip of the Sacrum/Sacral Promontory

3.Pain pattern follows the passage of the stone

a). Pain begins typically in the flank and travels as the stone progresses down the tract

4. Renal colic can occur with unsatisfied contraction

TREATMENT OF STONES

1. Management of Stone: A). Let it pass on its own B). Surgical Removal

2. Prevention of next stone: We can teach patients about anti-stone behavior.

Obstruction – Patient Characteristics

The condition is often very painful. Patients often vomit with obstruction/stone. They state they have a “different type back pain. The patients are often on pain medication, seeking relief.

Management

1. If the stone is moving, doctors let the stone pass on its own.

2. If the stone is stuck, there is no widespread agreement. If there is failure to enhance on IVP, that is a surgical emergency. Failure of contrast entering an area (failure to enhance), means that you are losing blood flow to the area.

High grade obstruction can lead to removal within 4-18 hours. For the 4-18 hours, they wait and check for signs of migration. Migratory or non-migratory is important. Non-migratory stones, you want to have them go to the hospital. At the hospital, they will document, triage, pain medicate and hydrate them to force the stone through the kidney.

IVP

If things aren’t progressing, demand an IVP. IVP tests function. Failure to enhance on IVP, forces the physician/surgeon to act.

Migratory Stone Treatment

Cautious Hydration (be cautious because over hydration can cause hydronephrectomy and hydronephrosis)

Pain Management

NSAIDS, COX-2 inhibitors, narcotics

Other pain control methods

Acupuncture, Basic, Resistive Heating Blanket

Examples of Surgical Treatment Options for Non-Migratory Stones

1. Extracorporeal Lithopathy; The patient sits in a warm bath and undergoes fluoroscopy while an sound like device sends sound waves to break up the stone from the outside-in (sound waves are directed towards the skin with the hope that they will penetrate and cause the stone to break apart allowing easier passage). The more brittle the stone, the easier it is to remove. The softer the stone, the harder it is to remove as it absorbs energy.

2. Basket Retrieval: A surgeon enters the urinary tract via the urethra heading into the bladder and Ureters. They expand the vessel and the stone pops into a basket for retrieval. They remove device slowly. Basket retrieval is a quick, well documented retrieval approach with minimal complications. The patient is given pain meds during and after retrieval.

3. Ultrasound Lithotraphy

They use ultrasound to remove the stone from the inside. The device is inserted via the urethra to the site of the stone and the ultrasound sends sound waves to break the stone apart.

4. Laser

The same approach is used as the previous conditions. A laser deep heats, causing vaporization and expansion of the vessels and crystals of the stone. The instrument requires venting, because it is a bigger product. This may be detrimental to the patient.

“Breaking it up, Blowing it up, or burning it up.”

Cancer

Ovarian & Uterine Cancers can also cause ureteral obstruction

Diagnostic Imaging

Plain film with a white spec in the correct area along with patient history matching the condition is a stone until proven otherwise. Another method is diagnostic ultrasound. You often get a better view of the R kidney due to the liver window on diagnostic

Prevention Techniques of the Next Stone

Lifestyle changes: For people with history of kidney stones

For Calcium stones, which are often a combination of calcium and oxalate; recommend restricting foods rich in oxalates.

Calcium and oxalate based foods are rhubarb, star fruit, beets, beet greens, collards, okra, refried beans, spinach, Swiss Chard, Sweet potatoes, sesame seeds, almonds, and soy products

What’s more, studies show that an overall diet low in salt and very low in animal protein can greatly reduce the chance of developing kidney stones.

As a general rule, restricting the intake of calcium doesn’t seem to lower the risk

In fact, researchers have found that women with the highest calcium intake are the less likely to develop kidney stones than are women who consume less calcium

Why? Dietary calcium binds with oxalates in the GI tract causing less stones to form in the GU system

Overview of Treatment Options

1). Choices/Options

a). Manage the Stone

1). Let it pass on its own

2). Surgical removal

a). The only immediate surgical indication is failure to enhance on IVP

b). Educate the Patient about the next stone

2). Surgical Options

a). Extracorporeal Lithopathy

b). Basket Retrieval

c). Ultrasound

d). Laser

3). Corresponding history along with white spec in the correct location on film = Stone until proven otherwise

GENERAL STONE INFO & STONE FORMATION

Over ½ the stones are radio opaque. A white spec anywhere in the area with colicky pain is stone until proven otherwise.

Calcium stones are 50% of the stones. 15% of the stones are Cysteine (6 sided crystals). Uric acid crystals can be star shaped (pointy edged). Crystals can impale the ureteral wall causing tissue swelling. Influx of white cells to the area of trauma forces greater obstruction as more space is taken up. Damage to the ureteral wall and edema can actually seal the stone in the area.

Stones can be formed in acidic or basic environments. It is important to know the environment of stone formation to recommend the appropriate measures (either acidifying or alkalizing the local environment). If you don’t know the pH of the local environment, recommend hydration with water.

Uric acid is the #2 stone and is radiolucent on KUB exam.

Staghorn calculus typically presents on very sick kidneys.

Mechanisms of Stone Formation

1). Overwhelming the system with solute (supersaturation)

2). Dehydrated system: Concentrated urine is left behind due to ADH causing water to be retained.

3). Medications: Ex. Sulfa drugs precipitate stones. Sulfa drugs are used with UTI’s. Sulfa drugs must be taken with water to prevent stone formation.

Pathophysiology of Stone

Urinary tract stone disease is likely caused by 2 basic phenomena.

Supersaturation and renal tubular dysfunction.

Frequency

Lifetime prevalence of urinary tract stone disease in the US is approximately 10-12%

50% will get a second stone

The annual incidence of urinary tract stones in the industrialized world is .2%

The likelihood that a white male will develop stone disease by age 70 years is 1:8

TYPES OF STONES

Calcium Based Stones

The most common type of stone is calcium stones.

A). 2nd Hyperparathyroidism is the most common cause for calcium stones. You may want to check for Parathormone levels is you suspect calcium stones. 2nd HPT occurs because of kidney damage and wasted calcium. Calcium leaks into urine. We can’t recover the calcium in urine due to poor tubular function. Hypocalcemia and hypercalcuria results from 2nd hyperparathyroidism. Calcium is robbed form the skeleton. We don’t produce active Vitamin D Dehydration along with increased calcium in urine allow for stone formation.

B). Neoplasia; Widespread lytic mets can drive enough calcium out of bone and into blood Ex. -- Multiple Myeloma causes inhibition of the osteoblasts presenting as cold on bone scan. The disease overwhelms the kidneys with calcium causing stone formation/excess solute load.

C). Milk Alkali Syndrome: Milk alkali syndrome can be due to ulcer. Calcium based products like TUMS neutralize acid and grant temporary relief. This is the patient that takes significant high ingestion of calcium antacids. The milk component can be due to a ”cumulus cloud” aggregation. Drinking a lot of milk daily can also lead to accumulation.

D). Renal Tubular Acidosis: Toxins….Cleaning products (alkalinization agents) can lead to stone formation. Calcium is born in alkaline environments. We need to acidify the diet to treat the problems. Increased hydrogen load drops pH below 7, keeping stones from aggregating. Another treatment is to recommend hydration flushing stones out. Hydration recommendations call for ½ ounce per lb of body weight.

3 Simple Treatments to Help Patients with Calcium Stones and Prevent Future Stone Formation

1. Change the diet 2. Hydrate the patient 3. Acidify the patient

Calcium Based Stones (Explanation of the Interventions)

Increase hydration

Acidify the body & urine (lemon water can be used to hydrate and acidify)

Proper Calcium intake, not too much, but not too little

Restrict oxalate intake – spinach, nuts, rhubarb, instant coffee, tea, chocolate all contain oxalate

Search for metabolic disorders, renal tubular acidosis, hyperuricuria (increased uric acid in urine), and urinary citrate levels

Cysteine Stones

Cysteine stones are the second most common stones. They are radiopaque. Cysteine stones are a product of the AA pathway. Lysine, ornithine and arginine are some of the AA’s that contribute to stone formation. Cysteine stones form in acid urine. The management advice is to alkalinize urine and hydrate.

Uric Acid Stones.

High protein diets place people more at risk for uric acid stones. Another issue is lack of hydration when on protein based diets. The stones enlarge and may not be seen on X-ray. They can be seen on ultrasound. Thoroughly stuck stones cause hydronephrosis. IVP, CT/IVP can help visualize the stone.

Uric Acid Stones – Specific Treatments

Increase hydration

Increase Urinary pH – sodium bicarbonate, potassium citrate

Decrease intake of purine-rich foods

Shellfish

Wine

Cream sauces

Miscellaneous Stones

A). Proteus: Can cause UTI”s and ammonia phosphate stones. Proteus creates urease which is an enzyme that breaks waste molecules. Urease leads to production of ammonia phosphate stones. You need to address the infection (proteus) to get rid of the stones.

B).Drugs: Glaucoma patients or “mountain sickness” patients are prescribed drugs that create damage to tubules. These patients acquire renal tubular acidosis. The pH changes causing stone formation. The stones are acid based.

C). Bactrin/Septa Drugs: Drugs for UTI’s that interferes with the stone clearing properties of the kidney The only effective management is to stop the medication or to adequately hydrate.

Chart of Most Common Stones

Most common Stones = 1). Calcium 2). UA 3). Cysteine 4). Everything else

Radio opaque (Most Common) = 1). Calcium 2). Cysteine

Radiolucent (Most Common)= 1). UA

DDX of Opaque Stones

Opaque Stone = Calcium or Cysteine

Check urinary pH

Acid = Cysteine

Basic = Calcium

Overview of Stone Types

1). Calcium Stones are the most common, radio-opaque and due to alkalinization

2). Types of Calcium Stones

a). 2nd Hyperparathyroidism (most common)

b). Cancer

c). Milk Alkali Syndrome (excess Tums or Milk)

d). Renal Tubular Acidosis (Toxins)

3). Treatment for Calcium Stone = a). Change Diet 2). Acidify 3). Hydrate

4). Cysteine Stones are second most common, radio-opaque and due to acidification

a). Treatment = Alkalinization and Hydrate

5). Uric Acid Stones = Radiolucent, linked with high protein diets and dehydration

6). Miscellaneous

a). Proteus = Makes urease and ammonia phosphate stones

b). Drug induced

X-RAY PRESENTATIONS OF STONES

*** AP Pelvis ***

The stone in the view takes up the shape of the Ureter. The stone is 1/3 to ½ the way down the Ureter. The L kidney shows residual contrast. The kidney is rounded and under pressure, hydronephrosis.

*** IVP ***

On the right, the contrast is a narrow, normal band. On the L side, we see delayed enhancement. WE don’t see much contrast on the L kidney. The ureter appears very dilated. The patient will be in lots of pain.

*** IVP ***

Ureterovesicle stone…A little white speck is present. Every centimeter of movement, the patient could feel the stone move. This area is the 2nd most common site.

*** X-Ray ***

Staghorn calculus is present. The patient came in with non-mechanical back pain. The kidney is in trouble and the odds are that the kidney needs to be removed. Refer to a nephrologist. A nephrologist will do a contrast study. If dye doesn’t pass, they may try to remove the bad kidney.

*** X-ray ***

Duplex Ureter = Pair of kidneys with 2 drainage points. There is a high drainage point and low drainage point. Duplex Kidneys have a wide and narrow exit point. The narrow one is the one typically obstructed.

10/13/08

INCONTINENCE

Definition of Incontinence = Involuntary loss of urine

Incidence

Less than 12 million Americans (report this condition…more may have it, but not report it)

Greater in women (approximately 38% of American Women to some degree): Over 1/3 of all women have the clinical classification to have incontinence

40% of hospitalized elderly persons

50% of nursing home residents

A leading cause of nursing home admissions: Incontinence is a powerful driver to make people seek nursing home support. Incontinence along with nursing home admission can be a big source of depression.

Costs of Urinary Incontinence

Costs exceed $10 billion/year

Greater than $1 billion in sales/year (Depends and other products to manage incontinence)

Psychological costs

Embarrassment and social inhibition

Depression, Impaired Nutrition in elderly

If we don’t manage the psychosocial component, there is little chance to reverse the condition, altogether. Interventions must both help the physiological problem and the psychosocial problem.

Cause of Urinary Incontinence

Myth: normal and expected age-related change

Age-related physiological changes in the lower urinary tract or chronic illness may predispose to urinary incontinence

Changes consist of: Decrease bladder capacity, flow rate, ability to postpone voiding, nocturnal fluid excretion, and prostate size

Urethritis can cause fibrotic repair. The patient can then have higher outlet pressure, making the bladder work harder leading to incomplete void.

Anatomy and Physiology of Lower Urinary Tract

Detrussor muscle and 2 sphincters

Detrussor mm, innervation

Pelvic Nerve via PSNS (cholinergic receptor – Ach neurotransmitter)

Bladder neck and proximal urethra

SNS (alpha-adrenergic receptor-norepinephrine neurotransmitter)

Distal urethra (skeletal mm-voluntary)

Pudendal Nerve (Ach neurotransmitter)

*** Check out the papers in the GI/GU folder in the library, by Keating, et. Al ***

The pelvic floor sphincter is under voluntary control.

Sympathetics and Bladder Filling Mode

We spend most of our time in bladder filling mode. The sphincter is under sympathetic control when the bladder fills, sympathetics keep the sphincter closed. Sympathetic tone acts to inhibit the musculature component of the bladder wall keeping urine from trickling out.

Stretch Receptors, Bladder Filling/Emptying, & Voiding

Typical, urinary events are about 250 m. More urine flows during times where the person is forced to “hold it) (300-350 mL). Stretch receptors in the bladder during filling increase stimulation. Stretch receptors send messages to the spine. Sudden stretching triggers voiding, but slow stretching on the bladder is weeded out by the cord. So the cord, offers some form of dampening effect with long filling periods. When the bladder is almost completely full or fills very quickly, the cord does not dampen and the stimulus goes to the brain, triggering the conscious action to void. Increase parasympathetics now work to relax the sphincter and push the urine out.

Second Sphincter

Somatic stimulation to the bladder wall is called the “second sphincter”

Pelvic Floor Weakness

Weakness of pelvic floor muscles enables incontinence to occur. Pelvic floor muscles are skeletal muscles that are subject to stress. Pelvic floor muscles can be strengthened to improve the quality of the sphincter.

*** There will be question on filling, emptying, and interference in these processes ***

Bladder Function

Storing Urine

Relaxation of Detrussor muscle (bladder wall)

Contraction of sphincters

Intravesicular pressure less than the urethral pressure (leads to urine storage)

Voiding Urine

Detrussor muscle contracts and sphincters relax

Intravesicular pressure greater than urethral pressure

Stress Presentation

Prone lumbar adjustments and other drop piece adjustments can increase pressure transiently and they can leak urine. This is classic stress presentation, where patients leak following adjustment.

Causes of Reversible Incontinence

Acute illness with;

Confusion or disorientation (disorientation from medication or disease states)

Immobility (elderly, post surgical, etc.)

Lethargy

Urinary Tract Infection (reduce the threshold of the bladder, making the bladder more sensitive and requiring lower volume to void)

Fecal Impaction: Rectum shares innervation with the bladder. As the fecal column expands, it can mechanically load the bladder. Increased intra-abdominal pressure triggers a stress incontinence reaction via parasympathetic stimulation. Parasympathetics spill over into the urinary system causing voiding when the system actually doesn’t have to

Hypersensitivity reactions: Can be source of incontinence, especially in children. These allergic reactions may/may not go away with time.

CLASSIFICATION OF PERSISTENT INCONTINENCE

Persistent incontinence may result from untreated illness or arise insidiously

5 Basic Classifications:

1. Stress

2. Urge

3. Overflow/Neurogenic/Paradoxical

4. Functional

5. Mixed

1. Stress Incontinence

Loss of small amounts of urine during coughing, laughing, or other activities which increase intra-abdominal pressure

Due to weak pelvic floor muscles

Predominantly found in women

2. Urge Incontinence

Leakage of large amounts (full volume void) precipitated by involuntary bladder contractions

Inability to delay voiding once a sensation of bladder fullness is perceived

Due to various GU and CNS conditions that cause hyper-reflexia of bladder contractions

Urethritis, cystitis, stones, stroke, spinal cord injury, MS, Parkinson’s, Alzheimer’s, tumors

Subluxation can create a somatovisceral reflex. We destabilize the Detrussor balance between holding and emptying. Chiropractic analysis of the patient helps the urge patient. Examine the lumbar spine and SI joint as they are a source of urge, incontinence.

Weak pelvic floor is also part of the problem. Strengthening of the pelvic floor can help the patients. Patient education is critical for these patients. Educate the patients (urge patients), that when the get the sensation of bladder fullness, squeeze the pelvic floor. The wave of fullness can subside with retreat of strong stimulus, reasserting sympathetic tone to the sphincter and help them not pee in their pants. They can ride out the strong parasympathetic tone, but conscious firing of the pelvic floor muscles so that they can wait to use the washroom. It gets easier and easier each time they practice strengthening the pelvic floor.

Stress and urge are the two most common types of incontinence.

3. Overflow Incontinence (also called Neurogenic & Paradoxical)

Constant dribbling of small amounts of urine

Due to over-distention of the bladder

Causes include:

Anatomic Obstruction: Stone (can cause overflow incontinence)

Hypocontractile Bladder: Nerve Injury can cause hypocontraction

Use of Certain Medications: Patient can respond to strong stretch signal due to medication interference

Neurogenic/Overflow/Paradoxical incontinence may occur from cord injury, abdominal surgery (hernia repair, hysterectomy), and ovarian cysts. This patient cannot empty a full bladder. This patient mostly is at the physiological limit. They dribble due to the influence of peristaltic waves and low pressure of the outlet sphincter.

4. Functional Incontinence

Involuntary loss of urine resulting from the inability to use a toilet

May be caused by physical, psychological, or environmental factors

Occurs despite normal urinary tract function

These patients are often depressed at first. Secondarily, they don’t care and personal hygiene becomes an issue.

Another issue is drug/iatrogenic based functional incontinence. It should be noted that drug induced incontinence can occur in any category.

5. Mixed Incontinence

Combinations of the 4 previous categories

MC combo: Stress and urge incontinence

Identifying presence of greater than 1 type)

10/14/08

TREATMENT OF INCONTINENCE

Patient Evaluation

Primary goal: Identify reversible factors contributing to incontinence

History

Symptoms (frequency, volume, dysuria, urgency)…Low volume voiding repeatedly creates a stimulus to the brain.

Active and Past medial conditions

Environmental Factors and medications

Urobehavioral diary

Self-Monitoring and Feedback

Urobehavioral diary: Include food (for hypersensitivity reaction

Treatment goals

Goals in treatment of the elderly

Maintain existing continence

Improve socialization

Decrease embarrassment

Preserve Renal Function

Avoid catheterization and the need for absorbent undergarments

Ex. Paradoxical and overflow forms can impact the system with retention of urine. The bladder will be at physiological unit. Pressure in the kidneys remains high, the patient can clear waste as efficiently, GFR is affected. Catheterization and education is often the best tool for these people to keep the bladder below their physiological limit.

Conservative Treatment Options

Biofeedback Methods

Monitoring pelvic floor muscles and contraction of external urethral sphincter through reinforcement with visual and auditory signals

25% success rate (slightly higher than the placebo)

Requires expensive equipment

Exercise

Kegel’s Exercises: drawing in anal and vaginal sphincters as if to control urination or defecation, WITHOUT contracting abdominal buttock, or inner thigh musculature

Performed several times a day for greater than 3 months

Studies indicate 40-60% decrease in accidents

Kegel originally thought of the muscles as postural muscles, meaning that to be worked they needed to do hundreds a day. You have to make this manageable for the patient. Do 25-30 when you watch TV during commercials. Or if you drive a lot, do 15-20 repetitions at stoplights. These are not outrageous things to ask for.

Exercise and Biofeedback

Currently, the use pads (instead of needles) and induction for biofeedback. The cooperation rate is better today than before. The goal is to contract the pelvic floor and not to contract other muscles. If they contract globally, they cannot talk, so part of the training is the exchange of air and the ability to talk while exercising along with checking the biofeedback machine. Often larger cities have uro-rehabilitation laboratories that use both methods.

Vaginal Combs

Egg shaped devices exclusively designed for women with incontinence. The combs are of different weights. This is progressive weight training for the vaginal/pelvic floor. They hold the combs in place with squeezing of the muscle groups. Each time they succeed they gain control over the pelvic floor. The analogy is similar to progressive weight training of other muscle groups (biceps, triceps, hamstrings, etc.).

Conservative Treatment Options

Chiropractic Adjustment

Lumbosacral Plexus

Neurological Facilitation with the VSC

Changes in Vascular Tone

Habit Retraining

Scheduled Voiding (“Bladder drills”) can alter Detrussor activity

10 Case Series revealed 72% improvement

Electrical Stimulation and Reflex Techniques:

Stimulate Nerves in the perineal floor: For very weak muscles, with Russian stim (10-15% strength increase)…The patient does not learn to contract on their own (so you’ll still have to emphasize this)

Relax Bladder

Mechanisms are not clear

Medical Management

Syringe Injections

Syringe injections of collagen into the urethra are used. The collagen is resorbed by the body over time. AS a downside, collagen injection over time can actually retain urine/static urine and lead to stone formation and UTI’s. Often the patients have a little period of good control, and then the body resorbs collagen leading to the same incontinent issues.

Surgical Management

Surgeons open up the pelvic floor and tease out the fibers, stitching the fibers over and down. They try to create a muscle based stricture to limit incontinence. Besides the normal complications, surgical failure involves either loosening of the area or over-tightening of the area, both of which create problems.

Pharmacologic Treatment Options

Used to facilitate the storage and emptying functions of the lower urinary tract

Goals: Increase bladder capacity and urethral resistance and decrease uninhibited bladder contractions

Anticholinergic agents

Antidepressants

Miscellaneous Treatment options

Many surgical options are available

Absorbent undergarments

Indwelling catheters

External Collection devices

Disadvantages:

Expensive, require nursing care, increase risk of complications (UTI, sepsis, pressure sores)

NOCTURNAL ENURESIS

It is an incontinence event that mostly affects children. This is involuntary loss of urine. You must establish whether they had control and lost it or if they never had control to begin with. You need to establish the presence or absence some congenital anomalies like micro urethra (where the patient congenitally has a small urethra).

A patient that never had control, may need medical intervention/investigation. An example would be a 10 year old without control. Another issue may be inappropriate expectation by parents (ex. a 1 year shouldn’t have control).

*** Test #2 is next Tuesday 10/14/08 ***

Vrenaman’s Research

Vrenaman was a researcher in the field of nocturnal enuresis. He had a longitudinal 20 year study. His study suggested 66% of all patients with nocturnal enuresis had food sensitivities as the culprit. He found that 60% of those with food allergies had problems with cow’s milk.

The Academy of Pediatric Allergists later found out that milk was the single most potent allergen for children. The proteins of cow’s milk is a big problem as our body identifies it and tries to attack it We have identified that the IgG is in the basement membrane along the bladder. IgG may lead the immune attack. The proteins of cow’s milk have an exciting effect on the bladder triggering stretch receptors and enuresis.

Milk allergies tends to affect males. Often the condition is demonstrated on scratch test. If the scratch heals, they are not sensitive. If the scratch blisters, this is sure sign they are allergic to milk (cow’s milk). The Langherhan’s cells in the dermal layer are part of the immune system. These cells trigger an immune reaction (blister).

ENURETIC TRIAD = 1). Bedwetting male 2).Milk allergy 3).Chvosteck Reflex

Chvosteck Reflex = Tap on the zygomatic arch…Their system is so excitable they blink multiple times.

Harrison’s Research

Allergies and infection of the GI tract, create conditions for nocturnal enuresis. He was credited with intervention strategies. He wanted to identify the allergens, eliminate them, and record the results. He identified that 100% elimination of bedwetting with elimination of the allergen.

Espiranza’s Research

Found dairy products to be a culprit in nocturnal enuresis, he also found that citrus fruit can be an allergen/irritant.

Stress

Child abuse, divorce, death of close loved one, etc. can cause a child to regress and repeat stages they went through before (bedwetting). These are people who had control and lost it. You have to find a strategy to regain control.

Late Developers

In some cases, the people with nocturnal enuresis may be late developers. There can be a developmental component that you have to explain to the parents.

Urge Incontinent

The most benefit from adjustment comes in this patient. Impulse through mechanoreceptors into the CNS may help the urge incontinent patient. Osteopaths and early chiropractors left anecdotal evidence and case studies to lead us to believe that we can help urge incontinent patients. The urge incontinent patient is linked to problems at the lumbosacral plexus.

Nocturnal Enuresis Patient (Incorrect Management Strategies)

Parents may try spanking, plastic sheets, diapers, lack of giving the child water, type of fluid (do not give them caffeinated beverages), trying other health care providers, psychological counseling (tricyclic antidepressants actually induce more enuresis). Parents can reward the child for staying dry.

The child doesn’t choose to wet the bed, so rewarding them or punishing them won’t be effective. Kids do not go to bed choosing to pee in the bed. Punishing them more or rewarding them is not good, because nocturnal enuresis is not a choice, it is based on the child’s physiology/condition. The condition is mostly boys.

General Recommendations

1-2 hours before bedtime limit the fluids (reasonable restriction is advised)

No more punishment or reward

The pad (under the sheets that sets an alarm off when wet) is not a good idea

Deal with the foods and milk elimination. Soy milk may be better for the child. Try 2 weeks of elimination of milk and milk derived products.

A psychosocial evaluation may be necessary when all other measures have failed

Most of the time nocturnal enuresis can be solved with conservative management. There has to be good doctor-patient communication.

GU CARCINOMA

Prostate Cancer

Prostate cancer is the most frequent of the GU system (it is an organ that ½ of us have and it is still the most frequent carcinoma). Bladder cancer is the #2 most common GU cancer.

The concern with prostate cancer for men is whether they live long enough to get it. According to the New England Journal of Medicine, if you are over 76 and you are diagnosed with prostate cancer, they shouldn’t do anything about it.

We have 70,000 cases that represent new diagnosis per year and about 20,00 mortalities from this cancer. In males, prostate cancer is the second most common overall (next to lung cancer), but it is a less significant killer/cause of cancer death.

Bladder Cancer

Bladder cancer is the 2nd most common GU Cancer. There is a 3:2 male to female ratio of bladder cancer patients. Female bladder cancer is getting more frequent. The reasons for this are smoking, alcohol, and occupational. Women are now working in coal mines, steel/coke plants, drinking more and smoking more.

Testicular Cancer

#3 on the list is testicular carcinoma. We started looking for it and find it more often as compared to before. Testicular cancer is quick and aggressive requiring immediate treatment.

Ureteral and Renal Cancer

Ureteral and renal cell carcinoma are not common. Renal cells may be a good environment (hostile environment) for cancer cells to grow. Kidney cancer by the time of diagnosis shows 25% metastasis. The lethal complication of kidney cancer are great. Signs and symptoms are few, and that is probably why ¼ arrive with metastasis by diagnosis. Hematuria is only present 56% of the time and is the most frequent finding. This is one of the reasons why we have the hematuria algorithm. Another finding is flank pain (38% of the time). 33% have a palpable mass at the time of diagnosis. About 27% have weight loss at the time of diagnosis. Other less common findings are polycythemia and loss of liver function (due to metastasis).

______________________________________END OF TEST 2 MATERIAL______________________________________

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