Antihypertensive drugs and erectile dysfunction,first aid in the workplace questions uk,authenticgames survival 85 - Test Out

The prevalence of erectile dysfunction is higher in treated compared with untreated hypertensive patients, suggesting a detrimental effect of antihypertensive therapy on erectile function. JavaScript is currently disabled, this site works much better if you enable JavaScript in your browser. Our New BMJ website does not support IE6 please upgrade your browser to the latest version or use alternative browsers suggested below. Raised levels of blood pressure result from the complex interplay of environmental and genetic factors. Raised levels of blood pressure result from the complex interplay of environmental and genetic factors leading to the activation or suppression of one or more of a host of physiological systems involved in blood pressure regulation (Figure 1).
The nature of these molecules, and in most cases their single site of action, dictates that when administered to a heterogeneous population, encompassing many hypertensive phenotypes, blood pressure responses will be largely unpredictable and wide ranging (Figure 4). Sexual dysfunction has become an increasingly important and recognized contributor to the side-effect profile in patients treated with antidepressant medications.
Data indicates a 40% to 60% risk of relapse of depression if the medication is stopped in the first few months of treatment.
Assessing the clinical aspects of sexual dysfunction can be difficult based on the patients’ reticence to initiate discussions about the problem. It is also valuable to explain the various categories of sexual side effects in detail before treatment is initiated.
In both men and women, desire disorders manifest themselves as deficient or absent sexual fantasies or a decreased desire to engage in sexual activity.
Hypoactive sexual desire disorder is manifested by persistently or recurrently deficient or absent sexual fantasies and desire for sexual activity with associated marked distress or interpersonal difficulty. Diminished desire that is caused by antidepressants is often difficult to discern from decreased desire as a symptom of depression.14 This again underscores the importance of evaluating sexual functioning prior to the onset of treatment.
Difficulty with arousal often manifests itself as erectile dysfunction in men and decreased vaginal lubrication or engorgement of the genitalia in women. Female sexual arousal disorder is the persistent or recurrent inability to attain or to maintain an adequate lubrication-swelling response of sexual excitement until completion of the sexual activity; this causes marked distress or interpersonal difficulties.
A deficit in the orgasm phase leads to delay or lack of orgasm despite normal desire and arousal phases in both men and women. Sex steroids have direct effects on sexual function in the central nervous system and in peripheral tissues. Among the most popular tricyclic antidepressants (TCAs) are the secondary amines despiramine and nortriptyline, and the tertiary amines amitriptyline and imipramine.
The toxicity of TCAs in overdose led to the development of other medications used to treat depression, ie, selective serotonin reuptake inhibitors (SSRIs), with which suicide by overdose is a major concern. Monoamine oxidase inhibitors (MAOIs) include moclobemide, a reversible, A-subtype selective MAOI, and phenelzine and tranylcypromine, two irreversible, nonselective MAOIs. SSRIs are a commonly used group of antidepressants that includes citalopram, fluoxetine, fluvoxamine, paroxetine, and sertraline. Bupropion is the only drug currently available in the dopamine and norepinephrine reuptake inhibitor class. Mirtazapine is the most commonly used drug in the noradrenergic and specific serotonin receptor antagonists category. Although they differ from each other slightly, nefazodone and trazodone reside in this class. Assessment at the initial evaluation should include a brief sexual history in conjunction with evaluation of the current level of sexual function (Tables 7, 8).47,48 The relationship of any change in sexual functioning with the onset of depressive symptoms should be determined. Common classes of medications known to have sexual side effects include antihypertensive agents, medications affecting hormone levels or function, chemotherapeutic agents, and medications active in the central nervous system. Endocrine measures including free and total testosterone, thyroid function tests, hemoglobin α1C (a measure of chronic blood sugar level reflecting control of diabetes), and prolactin should be con-sidered. The following five main treatment strategies exist for dealing with sexual dysfunction secondary to antidepressant use (Algorithm 1). Reducing the dose of the antidepressant may serve as a second strategy as higher antidepressant doses are associated with a greater sexual dysfunction than lower doses within the therapeutic range.51,52 It is important to decrease the dose carefully to diminish the sexual dysfunction without compromising the antidepressant effect. The fourth solution that may be attempted is the addition of another agent as an antidote for the sexual dysfunction (Table 9, Algorithm 2, Table 10).53-62 Supplementation of inadequate hormone levels, such as estrogen in women and testosterone in both women and men, may restore the hormonal milieu and enhance neurotransmitter effects on sexual functioning. The final strategy involves completely switching patients from an antidepressant associated with sexual dysfunction to an atypical agent secondary to the lower rates of sexual dysfunction.9 With an abrupt switch, discontinuation symptoms due to withdrawal of the initial antidepressant can be confused with acute adverse events associated with initiation of the second antidepressant. Antidepressant-induced sexual dysfunction is a significant barrier to the effective treatment of depression. E-newsletter Opt-inSent no more than 2–3 times each month, our E-Newsletter brings you recent findings and commentary from the psychiatric literature. This chapter aims to summarize the effects of the various antihypertensive drug categories on erectile function, highlight the differences between drug categories, and discuss the effects of switching antihypertensive drug class on erectile function. Patients were subdivided into five year age bands up to 85 (patients aged ?85 were analysed as one group) and prescribing trends across the population were assessed by estimating the proportion of patients prescribed with antihypertensive drug or statin drug, or both, in each group.Results Of the 41?250 records screened in this study, 36?679 (89%) patients did not have a history of cardiovascular disease and therefore could be considered for primary preventive treatment.
The complexity of blood pressure control mechanisms has major implications for individual responsiveness to antihypertensive drugs.
The major haemodynamic finding associated with higher levels of blood pressure is a rise in peripheral vascular resistance. If, in a particular case, blood pressure levels are largely determined by activation of the RAAS, for example in renal artery stenosis, marked falls in blood pressure with impairment of renal function may follow the administration of an ACE-Inhibitor.3 On the other hand, in the elderly and in those of African origins, where the activity of the RAAS is generally suppressed, blood pressure reductions4,5 with an ACE-Inhibitor may be small. The condition may take several forms and must be differentiated from a prior or unrelated condition.
Thus, it is extremely important for the clinician to be proactive in evaluating sexual functioning, including discussing patients’ premorbid and current sexual function before starting drug therapy.
This empowers patients with the knowledge to raise the issue with the clinician in the future. The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition,13 classifies two disorders during this phase of the sexual response cycle—hypoactive sexual desire disorder and sexual aversion disorder. Complaints of diminished genital sensation or decreased intensity of arousal may also be reported, requiring increased stimulation to achieve adequate arousal. Male erectile disorder is manifested by the persistent or recurrent inability to attain, or to maintain an erection to completion of the sexual activity plus distress or interpersonal conflict. This phase of the sexual response cycle appears to be quite susceptible to the effects of antidepressants,14 and changes in this phase are rarely associated with depression.15 Thus, orgasmic dysfunction is much more easily attributed to pharmacotherapy than impairment occurring in other phases of the response cycle.
Dyspareunia is recurrent or persistent genital pain associated with sexual intercourse that is not due to a general medical condition and it is associated with marked distress or interpersonal difficulty.
This was the impetus to develop and use the SSRIs where suicide by overdose is much less of an issue.

Venlafaxine inhibits the reuptake of serotonin, norepinephrine, and, to a lesser extent, dopamine, and its pharmacology is dependent on the dose prescribed.
It acts by inhibiting presynaptic α2 receptors, which then disinhibit serotonin and norepinephrine transmission.
Both inhibit the 5-HT2 receptor.?This is the opposite effect that SSRIs have on the 5-HT2 receptor,?resulting in less antidepressant-induced sexual dysfunction than SSRIs (Tables 3, 4, and 5). A complete history of medical and psychiatric diagnoses should be obtained, with documentation of current medications, alcohol or tobacco use, and abuse of illicit substances.
Identification of any demographic or psychosocial risk factors for sexual dysfunction may help guide treatment. In women, additional measures might include sex hormone-binding globulin, estradiol, follicle-stimulating hormone, and luteinizing hormone as indicated. Unfortunately, dose reduction often leads to the re-emergence of depressive symptoms secondary to utilization of a subtherapeutic dose. Any effects can be anticipated and monitored by adding the second antidepressant to the first, then slowly discontinuing the first antidepressant after stabilization of the replacement antidepressant. It is important to obtain a thorough sexual history from the patient to rule out other causes of sexual impairment.
Experimental data suggests that significant between-class and in-class differences exist regarding the effects of antihypertensive agents on erectile function. The underlying haemodynamic disorder in the majority of cases is a rise in peripheral vascular resistance.
This observation led to the discovery and development of increasingly sophisticated and targeted vasodilators, although many of the earlier antihypertensive drugs, by virtue of their actions blocking the sympathetic nervous system, had a vasodilator component to their mode of action. A detailed sexual history will provide the clinician with the information necessary to recognize other potential causes of sexual dysfunction, including comorbid medical or psychiatric conditions, other medications, or drugs of abuse.10 Other medications include, but are not limited to, antihypertensive medications, histamine H2 blockers, and hormonal contraception. Various tools, such as the Arizona Sexual Experiences Scale11 or the Changes in Sexual Functioning Questionnaire-Clinical version,12 may aid the physician in objectively assessing the patient’s sexual functioning at different points along the course of treatment. Loss of the subjective sense of excitement, losing interest, or becoming distracted once sexual activity has begun, may contribute to arousal phase problems. Vaginismus is recurrent or persistent involuntary spasm of the musculature of the outer third of the vagina that interferes with sexual intercourse and causes marked distress or interpersonal difficulty. Numerous serotonin receptors have been identified, and serotonin acting at the 5-HT2A and 5-HT2C receptors is thought to have direct inhibitory effects on sexual activity,19,20 particularly orgasm, in both males and females. They have a well-known side-effect profile, which was founded based on their actions at a number of receptors.
Although they have largely been replaced by other antidepressants for the treatment of depression, TCAs continue to be used as a treatment modality for chronic pain and sleep disorders, and in treatment-resistant patients.
At low doses, venlafaxine behaves similarly to the SSRIs, while at medium-range doses it inhibits norepinephrine uptake23,39 as well.
Dysfunction secondary to antidepressants may occur in any of the phases of the sexual response cycle and may be caused by many classes of antidepressant medications despite their varied mechanisms of action. A critical review of selective serotonin reuptake inhibitor inhibitor-related sexual dysfunction: incidence, possible etiology and implications for management. Antidepressant-associated sexual dysfunction: a potentially avoidable therapeutic challenge. The Changes in Sexual Functioning Questionnaire (CSFQ): development, reliability and validity. Sexual dysfunction associated with the treatment of depression: a placebo-controlled comparison of bupropion sustained-release and sertraline treatment. Neurochemical profile of moclobemide, a short-acting and reversible inhibitor of monoamine oxidase type A.
Selective serotonin reuptake inhibitor discontinuation syndrome: A randomized clinical trial.
Basic pharmacology of antidepressants, part one: Antidepressants have seven distinct mechanisms of action.
The safety and tolerability of venlafaxine hydrochloride: Analysis of the clinical trials database.
Emergence of adverse events following discontinuation of treatment with extended-release venlafaxine. SSRI-induced sexual dysfunction: fluoxetine, paroxetine, sertraline and fluvoxamine in a prospective, multicenter and descriptive clinical study of 344 patients. A randomized, double-blind, placebo-controlled trial of buspirone in combination with an SSRI in patients with treatment-refractory depression.
Sildenafil for iatrogenic serotonergic antidepressant medication-induced sexual dysfunction in 4 patients.
Pramipexole augmentation in the treatment of unipolar and bipolar depression: a retrospective chart review. Adjunctive dopamine agonists in treatment-resistant bipolar II depression: an open case series. Psychotropic medications and their effects on sexual function: diagnosis, biology, and treatment approaches. Observational and small randomized studies, large clinical trials, and meta-analyses point towards the same direction. The first non-specific vasodilator, hydralazine, was followed by vasodilatation which involved blockade of calcium channels on vascular smooth muscle cells [the calcium channel blockers (CCBs)], blockade of post-synaptic alpha-adrenoceptors on peripheral sympathetic neurones (the alpha blockers) and, finally, vasodilatation achieved by blockade of the renin–angiotensin–aldosterone system (RAAS) [angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), direct renin inhibitors (DRIs)] (Figure 3).
There exist a number of options for relief of sexual dysfunction associated with the use of antidepressants. Both are defined as pain with sexual intercourse and do not take into account pain with other sexual activity.
Once remission of the major depressive episode has been achieved, continued sexual dysfunction may represent effects of other illnesses or substances, psychosocial factors, a residual symptom of depression, or a side effect of the antidepressant.
If sexual dysfunction appears to be a problem related to a patient’s treatment, several strategies are available to manage antidepressant-induced sexual dysfunction, thus enhancing medication adherence and quality of life. Poster presented at: the 154th annual meeting of the American Psychiatric Association, New Orleans, LA, May 2001. Diuretics and beta-blockers seem to exert detrimental effects on erectile dysfunction, ACE inhibitors and calcium antagonists seem to exert neutral effects, while ARBs and nebivolol seem to be associated with beneficial effects on erectile function.
Prolonged differences in blood pressure: prospective observational studies corrected for the regression dilution bias. There were no consistent differences in prescribing trends by sex.Conclusions Previously described undertreatment of women in secondary prevention of cardiovascular disease was not observed for primary prevention. These average values disguise the extremely wide ranging responses in individuals across a fall of 20–30 mmHg systolic at one extreme, to no effect at all, or even a small rise in blood pressure at the other.

These disparities in statin prescription existed despite a higher proportion of women being above the recommended target cholesterol concentration.The situation for primary prevention is less clear. The second factor determining individual responses to monotherapy is the extent to which initial falls in pressure are opposed by reflex responses in counter regulatory mechanisms that are activated following the blood pressure reduction. To our knowledge, no previous studies have assessed the impact of age and sex on prescribing patterns in a primary preventive population.
What then is the next step if blood pressure is not a goal after the patient has been treated with monotherapy for a few weeks? We assessed the impact of age and sex on prescription of antihypertensive drugs and statins for primary prevention of cardiovascular disease in a typical primary care population.MethodsWe carried out a cross sectional retrospective study of primary care medical records. We obtained anonymised data from the electronic health records of all patients aged 40 and above registered at 19 general practices across the West Midlands.
The practices were purposefully selected to represent different practice sizes and different levels of socioeconomic deprivation by using the indices of multiple deprivation score of the practice area. Relevant data were extracted with MIQUEST software.Data queries were run from 17 October 2008 to 6 October 2009. Extracted information included demographic data, cardiovascular disease risk factors, and records of prescribed drugs.
The presence of data for blood pressure or cholesterol concentration, or both, in the five years before the query date was defined as a non-zero value recorded in a value field linked to a relevant Read code for blood pressure or total cholesterol concentration.
Table 1 shows the proportion of patients with recorded cardiovascular disease risk factors?.
We extracted data concerning prescription of drugs to lower blood pressure and cholesterol concentration in the 90 days before the query date.Table 1 ?Characteristics of total population (by age group in years) potentially eligible for primary prevention treatment. A history of cardiovascular disease was defined as any patient with a Read code for cardiovascular disease in their medical records. We assumed that, because of quality standards in the UK whereby general practitioners are paid based on accurate recording of information such as this,4 these data would be sufficiently accurate to identify the true secondary prevention population.All patients without a history of cardiovascular disease were considered potentially eligible for primary prevention drugs.
Those aged 85 and over were analysed in a single group because five year age bands above this age contained too few patients for reliable analyses between groups.We used descriptive statistics to identify the proportion of patients with measured information on cardiovascular disease risk factors such as blood pressure, total cholesterol concentration, smoking status, and prescription for an antihypertensive drug or statin. We performed logistic regression analyses to examine associations between age group, sex, and prescription (statin and antihypertensive). Odds ratios were estimated to determine the change in likelihood of prescription of drug treatment per five year increase in age (with prescription rates in the first age group (aged 40-44) used as the reference category).
All data are presented as means and standard deviation, odds ratios with 95% confidence interval, and percentages of the total primary prevention population (unless otherwise stated).ResultsOf the 90?516 patients registered at participating practices, 41?250 matched our inclusion criteria (patients aged ?40). Of these, 4571 (11%) had a record of existing cardiovascular disease, leaving 36?679 patients potentially eligible for primary preventive treatment. Recording of both blood pressure and cholesterol concentration improved with age, albeit from a much lower baseline for cholesterol.
As expected, blood pressure increased with age but while antihypertensive treatment also increased, many older people did not receive blood pressure lowering drugs and most people of all ages were not prescribed statins.
Adverse reactions to bendrofluazide and propranolol for the treatment of mild hypertension. As the population ages, both statins and antihypertensive drugs offer the prospect of further reducing mortality and cardiovascular disease events, but only if they are prescribed.10 31Strengths and weaknesses of the studyIn this large study we used routine data from practices across the West Midlands and included all registered patients over the age of 40. In addition, we captured accurate data on all prescribed drugs over the preceding 90 days rather than having to rely on self reported accounts from participating patients, as was the case in the Health Survey for England.33We included all patients in this analysis, regardless of their calculated cardiovascular risk. Given that age is the most significant factor in cardiovascular risk scores,22 30 if we had done the analysis taking account of risk, the association of older age with non-use of preventive drugs would have been more marked.
This ambiguity exists not because of conflicting trial results, but because trials have not been conducted in this population.39 There is no evidence to suggest that prescribing statins in elderly patients causes any increased side effects or adverse effects.
Given the underlying risk associated with age30 42 and that the protective effects of primary prevention drugs can be realised within just one year,43 a case can be made for offering primary prevention to a larger proportion of people aged 80 and over than are currently receive it.In contrast with previous research on secondary prevention15 16 we found minimal clinically significant differences in prescription rates between men and women.
This is perhaps surprising given that at any age men are at greater risk of a cardiovascular disease event than women.30 42Implications for policy, research, and clinical practiceIt is difficult to interpret whether the low use of preventive treatments (particularly statins) in older people reflects appropriate or inappropriate care.
The non-use of these drugs might reflect a considered decision that has taken into account factors associated with age that might deter doctors from prescribing such as multiple comorbidity, polypharmacy, and cognitive decline as well as the patient’s choice. There is only limited evidence of effectiveness, for statins at least, in people over the age of 80. Nevertheless, there is a striking contrast between use of statins and use of antihypertensive drugs in older people, which does point to possible underuse of statins.
To better understand the clinical implications of our findings, more research is needed to determine why general practitioners refrain from prescribing primary preventive treatment in elderly people, the attitudes of older people towards preventive drugs, and the costs and benefits of prescribing in this age group. The number of people aged 80 and over is projected to rise rapidly,44 and greater use of these drugs might reduce disability and prolong healthy life expectancy in this age group.Ultimately, evidence is needed to inform new guidelines that offer more precise recommendations on primary prevention for older people. Future research should test whether innovative treatment strategies, such as use of a polypill, could reverse these age inequalities in treatment of absolute risk of cardiovascular disease.
JPS and SS are funded by the National Institute for Health Research Birmingham and Black Country Collaboration for Leadership in Applied Health Research and Care. They were responsible for the overall conduct of the study and ensured the relevant contracts, insurance and approvals were in place prior to the start of the study.
Prevention of cardiovascular disease: guidelines for assessment and management of cardiovascular risk. Lipid modification: Cardiovascular risk assessment and the modification of blood lipids for the primary and secondary prevention of cardiovascular disease. EGUI05501, 2009.?Colhoun HM, Betteridge DJ, Durrington PN, Hitman GA, Neil HAW, Livingstone SJ, et al. Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS): multicentre randomised placebo-controlled trial. Prevention of cardiovascular events with an antihypertensive regimen of amlodipine adding perindopril as required versus atenolol adding bendroflumethiazide as required, in the Anglo-Scandinavian Cardiac Outcomes Trial-Blood Pressure Lowering Arm (ASCOT-BPLA): a multicentre randomised controlled trial. Effects of intensive blood-pressure lowering and low-dose aspirin in patients with hypertension: principal results of the hypertension optimal treatment (HOT) randomised trial. Primary prevention of cardiovascular disease with pravastatin in Japan (MEGA Study): a prospective randomised controlled trial. Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial-Lipid Lowering Arm (ASCOT-LLA): a multicentre randomised controlled trial.

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