It is often associated with overactivity of the detrusor urinae muscle, a pattern of bladder muscle contraction observed during urodynamics. It is also possible that the increased contractile nature originates from within the urothelium and lamina propria, and abnormal contractions in this tissue could stimulate dysfunction in the detrusor or whole bladder. Catheter-related irritation
If bladder spasms occur or there is no urine in the drainage bag when a catheter is in place, the catheter may be blocked by blood, thick sediment, or a kink in the catheter or drainage tubing. Sometimes spasms are caused by the catheter irritating the bladder, prostate or penis. Such spasms can be controlled with medication such as butylscopolamine, although most people eventually adjust to the irritation and the spasms go away. Diagnosis
Diagnosis of OAB is made primarily on the persons signs and symptoms and by ruling out other possible causes such as an infection. Urodynamics, a bladder scope, and ultrasound are generally not needed. Additionally, urine culture may be done to rule out infection. The frequency/volume chart may be maintained and cystourethroscopy may be done to exclude tumor and kidney stones. If there is an underlying metabolic or pathologic condition that explains the symptoms, the symptoms may be considered part of that disease and not OAB.Psychometrically robust self-completion questionnaires are generally recognized as a valid way of measuring a persons signs and symptoms, but there does not exist a single ideal questionnaire.
Ultimately, when large coronary arteries undergo vasospasm, this can lead to either complete or transient occlusion of blood flow within the artery. As a result, ischemia to the tissues served by the artery can occur. Symptoms due to ischemia can follow.Some of the factors that have been proposed to contribute to coronary vasospasm include the following:
Endothelial dysfunction
Certain vasodilatory agents exert their effects by working via the endothelium, the cells that make up the lining of blood vessels. Specifically, these agents work by enhancing the production of nitric oxide from endothelial nitric oxide synthase. Normally, nitric oxide then works to promote vasodilation in a blood vessel through its own mechanisms such as inhibiting the release of agents that cause vasoconstriction. Endothelial dysfunction wherein there is a deficiency in the production of nitric oxide has been found to be associated with coronary vasospasm in some but not all cases. Vasodilatory agents with mechanisms dependent on a functional endothelial nitric oxide synthase can cause vasoconstriction instead in the setting of endothelial dysfunction, leading to coronary vasospasm. Chronic inflammation
Various markers of low-grade chronic inflammation have been found in cases of coronary vasospasm. In addition to this, one of the risk factors for coronary vasospasm is smoking. Chronic inflammation due to smoking has been shown to be damaging to endothelial cell function. Oxidative Stress
Oxygen free radicals contribute to the pathogenesis of coronary vasospasm through their damaging effects on vascular endothelial cells and degrading nitric oxide, an important vasodilatory agent.