Knowledge Base

Overactive Bladder Syndrome

Last Updated on Tuesday, 21 January 2014 12:13

overactive-bladder-slide1 overactivebladdersyndgetty.jpg_e_80e120e8d9501686f40a51477471da69 349756-57625-44

(Highly Prevalent but Underdaignosed Problem)

Definition:

Overactive Bladder(OAB) is a symptom syndrome of Urgency(With or Without Urge incontinence), Frequency and Nocturia. This term on be  if there is no proven injection or other obvious pathology.

Overac2

Prevalence:

in US & Europian countries prevalence of OAB is above 16.5% in population and increases markedly with age in both men and women. In asian population the incidence of OAB is much higher 53% and treatment rate is very low-only 21% get treated. When compared with western world.

OAB is as common as Arthritis and Sinusitis and Much more prevalent than Heart Disease, High Cholesterol, Asthama, Chronic Bronchitis, Diabetes.

 


Impact of OAB on Quality of Life:

There is limitation and in some patients cessation of Physical activity. These patients have increased Abscentism from work and have low productivity affecting Occupational Aspect of life. They tend to avoid Sexual Contact and Intimacy affecting their Sexual life. On psychological front there is guilt, depression, loss of self esteem and fear of being burden to the family. They restrict social interactions, mixing and limit and pkn their travel, activity around toilet accecibility. On domestic front they need special garments, bedcovers, sleeping arrangements near toilet etc.

Co-Morbidity with OAD:

Hospitalization in women increases by 30% and men by 50%. There is significantly increased frequency of UTI(Urinary Tract Infection) and Skin lesions in introital region and private parts. There is increased risk of fall by 35% and fractures by 45%. In menopausal women there is 50% increase in fracture neck femur. Overall 60% of patients suffer from depression.

Pathophysiology of OAB:

Overactive-Bladder

This is illunderstood or partly understood. There is increased afferent activity of impulses going to Brain from Detrussor Muscle of Bladder. Normally there is tonic inhibition in Suprapontine region. There excess impulses which in OAB is impaired and decreases. Hence there is increased contraction mediating transmitter i.e. Acetylcholine, which works on Cholinergic receptors in Bladder.

Also in OAB there is increased sensitivity of Cholinergic receptors in Detussor to tevis contraction mediating transmitter Acetylcholine.

Due to this there are Uninhibited detrussor contractions & Urgency, Frequency and Nocturia.

Management Stratigies:

77% of OAB patients never receive any kind of therapy. Many patients consider it part of Normal Aging. Many feel too embarrassed to discuss with doctor and have impression that treatment is unlikely to help. Approach to OAB management is twofolds

  1. Nonpharmacological or Behavioral Therapy

Behavioral Therapy:

this essentially involves asking patient to keep voiding diary, Monitor fluid and dietary intake, have timed voiding. Patient is asked to avoid items which are likely to irritate bladder like Coffee, Tea, Colas, Citrus Fruits and Juices, Sodas, Alcohol and Spices. He is advised to have more of bladder friendly Fluids and Solids like Water, Apple juice, Cranberry juice, Grape juice, Pear, Banana etc He is asked to add more time between the toilet visit and train bladder. Pelvic Floor Exercises(Kegal’s Exercises) are highly effective which strengthen the muscles controlling micturation.

Pharmacotherapy: 

Drug therapy is currently the mainstay in managing OAB. Various pharmacological agents being used are

  1. Antispasmodics
  1. Estrogens(Post menopausal females)

Amongst these Antimuscarinic agents are Gold standard and highly effective.

Antimuscarinic agents, currently available are

  1. Oxyhutynin
  1. Tolterodine
  1. Darifenacin
  1. Solefenacin
  1. Trospium

The selectivity of the drug for M2 and M3 muscarinic receptors in bladder vary and needless to say it has effect on Muscarinic receptors present all over the body in various organs. Thses receptors are present in various places in body like 1. Ciliary body(Iris), 2. Lachrymal gland, 3. Salivary gland, 4. Heart, 5. Stomach, 6. Colon, 7. Bladder, 8. CNS(Central Nervous System). Hence these agents affect function of these organs and this causes

  1. Dry mouth
  1. Constipation
  1. Cognitive impairment
  1. Blurring of Vision

However Judicious use of these agents with close monitoring of patients they give extremely rewarding results.

 

Summary: 

  • · OAB is highly prevalent condition but is Underdiagnosed
  • · As our population grows, ages, incidence will rise
  • · It affects both males and females
  • · OAB has large impact on patient’s Quality of life
  • · Patients perceive great benefit with Therapy and improvement in Quality of life is significant
  • · 
Sanctura_Trospium_Chloride
 

Information on Chronic kidney disease (CKD), The Magnitude of the Problem:

Last Updated on Sunday, 27 February 2011 18:40

mkfkinderThe two kidneys lie at the back of the body cavity, one on either side of the spinal column, with their upper portions behind the lower ribs. Each Kidney is 10 - 12.5cm (4 - 5 inches) long & contains about 1 million nephrons. Each nephron is a filtering unit made up of a filter, called glomerulus, attached to a long collecting tube. There is a constant flow of blood through the kidneys which is filtered by these nephrons.

Read more: Information on Chronic kidney disease (CKD), The Magnitude of the Problem:

What Causes Kidney Failure?

Last Updated on Sunday, 27 February 2011 18:42

kidney_failure
  • Diabetes is the commonest cause of CRF in both, the developed and the developing countries comprising 25% of all cases.
  • Another 25% develop ESRD due to chronic glomerulonephritis.
  • 10 percentage of patients develop ESRD due to hypertension, another lifestyle disease which is correctable.
  • Some other correctable causes are allopathic drugs especially pain killers, which are consumed for trivial reasons as they are easily available OTC drugs.
  • In addition Ayurvedic products, especially those containing heavy metals in the form of BHASMAS, are an important cause of CKD.
  • Indian subcontinent is in the stone belt and stones not treated in time can lead to kidney failure if stone disease is involving both sides.
 

Prescribing Drugs in CKD

Last Updated on Sunday, 27 February 2011 18:26

HOW TO PRESCRIBE DRUGS IN A CKD PATIENT

 

How does CKD affect drug handling?drugs_1

Accumulation of drugs normally excreted. Eg- antibiotics

Accumulation of active drug metabolites. Eg- acyclovir, chloramphenicol

Changes in drug distribution – protein binding and volume of distribution. Eg- diazepam

Decreased metabolism of drugs in failing kidneys. Eg- insulin

Drug interactions. Eg- NSAIDs & aminoglycosides.

Important questions to ask before writing a prescription in a case of CKD:

Will this drug be effective in renal failure? 

Will it hurt the already failing kidneys and worsen renal failure – type A? 

Will it or its toxic products accumulate in the body because of renal dysfunction-type B?  

4. If drug is type A or B, why not find another safer substitute drug? 

5. Will renal failure modify the pharmacokinetics of this drug Eg- iron tablets 

6. Is the liver function normal eg- in ceftriaxone? 

7. If I must use an unsafe (type A or B) drug, how should I modify the drug     prescription? 

Drugs ineffective in renal failure:

Nitrofurantoin 

Nalidixic acid 

Norfloxacin 

Pyridium 

Mandelamine 

Thiazide diuretics when GFR<30 ml/min 

These drugs only work after being filtered in the glomerulus.

How do you detect worsening of renal function?

Increase in urea/creatinine

Sodium & water retention

Hyperkalemia

Acidosis

Hypoglycemia in diabetic

Hyperuricemia

Bleeding

Increase in urea alone – steroids, tetracycline

Increase in urea and creatinine - NSAIDs, ACE inhibitor, ARBs, aminoglycoside, diuretics in excess, radiocontrast agents.

Sodium & water retention - steroids, NSAIDs

Hyperkalemia – NSAIDs, ACE-I, ARB, kesol, spironolactone, tetracycline, K sparing diuretics.

Metabolic acidosis – Metformin in diabetics (creat>1.4 ), acetazolamide, NSAIDs 

Hyperuricemia – diuretics 

Bleeding – aspirin, clopidogrel, warfarin, heparin.

Hypoglycemia in diabetics – Long acting insulins,  

All oral hypoglycemics except acarbose, glipizide and gliclazide, pioglitazone, repaglinide.  

Gatifloxacin 

Drugs that accumulate in renal failure:

Antibiotics – aminoglycoside, vancomycin, tetracyclines, most cephalosporins, carbapenems

Antivirals – acyclovir, gancyclovir, indinavir, zidovudine

Anti TB – INH, ehthambutol, PZA

Antifungals – amphotericin, fluconazole.  

Cardiac – digoxin, antiarrythmics 

Hypoglycemic agents – insulin, sulfonylureas 

Opioids – morphine, codeine, meperidine 

Anticancer agents 

Sedatives – barbiturates, benzodiazepenes 

Others – allopurinol, fibrates, aluminium 

How to adjust doses:

COCKROFT GAULT FORMULA

GFR = (140 – age) X Ideal body wt

72 x S. creat

Multiply by 0.85 for females

MDRD formula

Schwartz formula in children

Reduce the dose according to GFR.

Formula for radiocontrast 

DOSE = 1 X Usual dose 

S.creat  

Eg. If S.Creatinine is 3.0, Maximum Dose of radiocontrast allowed is one-third of usual dose.

What to do when contraindicated drugs have to be used: 

Take informed consent 

Documentation of renal function 

Prepriscription investigation – renal artery doppler before prescribing RAAS blockers 

Reduce doses as per GFR

Avoid dehydration – this applies to most nephrotoxic drugs esp. Radiocontrast agents, nsaids, acyclovir, lithium, methotrexate, cisplatin

Use once daily dosing – aminoglycosides

Avoid concomitant use of diuretics when prescribing NSAIDs, aminoglycosides

Pre and post prescription antidote – acetylcysteine for radiocontrast agents

Take special care in certain situations :

-old age

-heart failure

-liver cirrhosis

-dehydration

-severe hypoalbuminemia

-while other nephrotoxic agents are being used.


Drugs and the Kidney: Update 1

Last Updated on Sunday, 27 February 2011 18:45

DRUGS AND THE KIDNEY: WHAT’S NEW TODAY?

Drugs & kidney interaction:drugs_2

Excretion of drugs: 

Kidney is a route of removal in healthy state. 

In disease of kidneys drugs accumulate in the kidneys. 

Doses of drugs must be adjusted in renal failure. 

Drugs produce renal injury: 

Avoid in certain situation. 

Apply strategies to protect when unavoidable. 

37% of all acute renal failure (ARF) seen in major tertiary referral hospital is Drug induced or Drug aggravated

Drugs reported to cause alteration of renal function:

-Antineoplastic and/or immunocompressive agents like Cis-platinum, Methotrexate, Interferon, Cyclosporin

Radio-opaque contrast agents like Diatrizoate meglumine, Diatrizoate sodium, Iodipamide.

Analgesics like Salicyclates, Aminopyrine, Phenylbutazone, Indomethacin, Ibuprofen, Naproxen, Fenoprufen, Tolimetin, Phenacetin.

Diuretics like Mannitol, Thiazides, Frusemide.

Anaesthetic agents like Chloroform, ethyl chloride, Halothane, Fluroxene, Cyclopropane.

Anti-hypertensive like Hydralazine, Propanolol, Nifedepine, Captopril.

Sulphonamides

Penicillins

Tetracycline

Doxycycline

Diazepam

Neomycin

Streptomycin

Gentamicin

Allopurinol

Acyclovir

Prevention:

Early detection 

Doctor education 

Patient education 

Role of FDA / Others 

High Risk Doctors:

Orthopedic surgeons 

Surgeons 

Dental surgeons 

Radiologists / Angiographers 

Ayurvedic / Homeopathic 

Indigenous medicine 

Doctor Education:

Knowledge of Pharmacokinetics 

Recognition of high risk situations / increased vigilance 

Product insert / PDR 

Continuing medical education programs 

Prescription review in hospitals 

Fear of legal actions 

Renal Susceptibility to Drug Toxicity: 

High renal blood flow

Renal tubule cells – high metabolism

Renal enzymes blocked by -8H groups

High concentration of drugs in medulla (counter current renal multiplier)

High concentration of urine in tubules

Urinary PH changes render drugs insoluble

Largest surface area of vascular endothelium

Tubular transport ionic mechanisms

Large tubular epithelial surface.

Clinical Syndromes of Drug Induced Renal disease:

- Pre – renal azotemia                           - Sterile pyuria

- Acute renal failure                              - Fanconi syndrome

- Hypertension                                     - Renal tubular acidosis

- Acute nephritis                                  - Renal salt wasting

- Nephrotic syndrome                            - Isolated proteinuria

- Chronic renal failure                            - Hyperkalemia

Hypercalcemia induced ARF

Drugs Producing Acute Renal Failure:

Nephrotoxic nephropathy - Aminoglycosides

Dose dependent toxicity - Cephalosporins,tetracyclines,amphotericin, Colistin,radiocontrast agents

Allergic nephritis - Methicillin,rifampicin,penicillin,cephalosporin, sulfa ; NSAID`s ; allopurinol,diuretics

Drugs causing hemolysis - esp. in G6PD deficiency

Drugs causing hypercalcemia – Vit.D intoxication

Poisons - Lead, mercury, cadmium,bismuth, gold

Agents masquarading as drugs - Glycols, carbontetrachloride, tetrachloroethylene

Radio Contrast Renal Failure: 

Risk Factors 

Pre existing renal insufficiency 

Diabetes mellitus 

Multiple myeloma 

Dehydration 

History of ARF due to dye in past 

Large contrast load 

Congestive Heart failure 

Advanced age 

Vascular disease 

Proteinuria  

Hyperuricemia  

Liver disease 

PREDISPOSING FACTORS: 

Pre existing CKD 

Diabetes 

Low EF/ dehydration 

Concomitant undiagnosed RAS 

Other nephrotoxic drugs 

Age 

Liver disease 

Higher doses of contrast 

Ionic contrast 


 

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