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“Man survives earthquakes, experiences the horrors of illness, and all of the tortures of the soul. But the most tormenting tragedy of all time is, and will be, the tragedy of the bedroom.” - Tolstoy.
Presented by Dr Pavan Kumar K Chaired by Dr Denzil A Pinto
Sexuality and sexual behaviour
Reproduction is a fundamental biological function,
that guarantees the survival of the species. Due to its evolutionary advantages, most complex lifeforms have evolved methods of sexual reproduction, which involves the combination of genetic material from parents of two different genders.
Sexuality and sexual behaviour
Humans are not sexually static reproductively-driven
mammals. Unlike most animal species, human sexuality is associated with gratification (pleasure), and not just reproduction. Sexual behavior is richly multidetermined. Human sexuality is shaped not only by biology, but by social, cultural, interpersonal, and psychological constraints.
which influenced medical and legal practice for more than 3-quarters of a century.History First attempt at describing and classifying sexual disorders began with Richard von Krafft-Ebing and his Psychopathia Sexualis(1898). Seminal contributions of Havelock Ellis and Albert Kinsey (sexual behavior in human male and female) .
. Prior to psychoanalytical concepts guided clinicians 1950 in understanding and treatment of sexual problems Sexual symptoms were linked to unresolved. behavioural perspective gained late 1950s ascendancy. sexual problems were understood to be learned (conditioned) anxiety responses. unconscious conflicts occurring during specific developmental periods.
. Their work foreshadowed the later integration of medical and psychological interventions. and the significance of biological factors on the development of sexual dysfunctions. the impact of relationship factors. In Masters and Johnson. and later highlighted the deleterious influence of performance anxiety. described the physiology of phases of 1966 sexual functioning.
Integrated psychoanalytical theory with Masters & Johnson's cognitive-behavioral understanding of sexual dysfunction. Distinguishing between recent and remote etiological causations. The neo- heralded by the publication of Masters and Johnson era Helen Singer Kaplan's book. . she recommended behavioral approaches for the former and reserved traditional psychodynamic methods for the latter. The New Sex Therapy.
. The current psychobiological era. primarily for male sexual dysfunction. This period is distinguished by the mid1980s medicalization of treatment approaches. Scientific investigations of cellular chemistry have elucidated the pathophysiology of male sexual arousal problems and have led to the introduction of new oral treatments. such as sildenafil.
homosexual. from infinite clues derived from experiences with family members. Established by age of 2 or 3 yrs. Sexual behaviour: includes desire. peers. pursuit of partners. . Heterosexual. fantasies. teachers & cultural phenomenon.Components of sexuality Sexual identity: is a pattern of patient’s biological sexual characteristics Gender identity: individual sense of maleness/ femaleness. or bisexual. Sexual orientation: describes the object of person’s sexual impulses. auto-erotic activities & activities engaged in to express & gratify sexual needs.
The first models described a simple sequence of increasing arousal and excitement culminating in rapid discharge by orgasm.Modelling the human sexual response cycle Models have been constructed of the normal sequence of changes during sexual arousal and coitus. peak. . displayed graphically as an ascent. and then descent.
and finally resolution (R) phase (dissipation of sexual tensions). and incremental model of the human sexual response cycle excitation (E) phase (stimuli from somatogenic or psychogenic sources raise sexual tensions). sequential.The EPOR model formulated by Masters and Johnson four-phase linear. orgasmic (O) phase (involuntary pleasurable climax). plateau (P) phase (sexual tensions intensified). .
Helen Kaplan. proposed that before the E phase there should be a ‘desire phase' (D phase). . even by their usual partners. came from her work with women who professed to have no desire to be sexually aroused.Modifying the EPOR model into the DEOR model currently accepted model Robinson concluded convincingly that the P phase was simply the final stage of the E phase.
orgasmic. and resolution phase (DEOR) model. Sexual desire that appears to be spontaneous should obviously be placed at the beginning of the model but what of sexual desire created when the person is sexually aroused by another? . EPOR replaced by the desire. excitation.
(a) the original EPOR model of Masters and Johnson (b) the DEOR model of Kaplan (c) the proposed modification with desire phase 1 (before initiation of the excitation phase and desire phase 2 during excitation phase) and (d) with added courtship behaviour .
sexual aversion disorder. hypoactive sexual desire disorder due to general medical condition (man/ woman).Phase I: Desire Psychological phase Characterised by sexual fantasies & conscious desire to have sexual activity. substance induced sexual dysfunction with impaired arousal. Dysfunction: hypoactive sexual desire disorder. Can be biologically driven or result from a wish to bond sexually with a particular partner. .
physiological (stroking/ kissing) or combination.Phase II: Excitement Brought on by psychological stimulation (fantasy or presence of love object). Consists of subjective sense of pleasure & objective signs of sexual excitement. Dysfunction: female sexual arousal disorders. substance induced . male erectile disorders. male erectile disorder due to general medical condition.
premature ejaculation . & rhythmic contraction of perineal muscles & pelvic reproductive organ. with release of sexual tension.Phase III: Orgasm Consists of peaking sexual pleasure. Lasts for 3-15sec Dysfunction: female & male orgasmic disorders.
which brings body back to its resting position. Dysfunction: postcoital dysphoria. If orgasm occurs resolution is rapid. general relaxation. postcoital headache. Men have refractory period (mins-hrs). This does not exist in females. they can’t be stimulated to further orgasm. Through orgasm it is characterised by sense of well being. muscular relaxation.Phase IV: Resolution Consists of disgorgement of blood from genitalia. . if not may take 2-6hrs & be associated with irritability & discomfort.
The sexual response cycle .
size increases by 1/4th clitoris Enlargement in diameter of glans & shaft. labor like contractions begin in heightened excitement just before orgasm Myotonia Mucoid secretion from bartholin’s gland during heightened excitement Cervix swells slightly & is passively elevated with uterus . transudate appears 10-30 sec after arousal.congestion & edema Labia minora vagina uterus others Size increase 2-3 times normal. red. just before orgasm shaft retracts into prepuce Labia majora Nullipara. maculopapular rash on abdomen spreads to ant chest wall.organ mental skin breasts Excitement phase Several mins-hrs. change to pink. face& neck & include shoulders & forearm Nipple erection (2/3rd). venous congestion & areolar enlargement. elongation & ballooning. lower third constricts before orgasm Ascends into false pelvis. 30sec-3min Inconsistent Sexual flush.elevate & flatten against perineum Multipara. deep red before orgasm Colour change to dark purple. heightened excitement before orgasm.
signalling impending ejaculation 2-3 drops of mucoid fluid that contain viable sperm are secreted during heightened excitement.inconsistent nipple erection Myotonia.semispastic contractions of facisl.organ Mental Skin Excitement phase Several mins-hrs. heightened excitement before orgasm 30sec-3min Just before orgasm. with heightened excitement size og glans & diameter of penile shaft increase further Tightening & lifting of scrotal sac & elevation of testes.increased Penis Scrotum & testes Cowper’s gland other . abdominal & intercostal muscles Tachycardia. inconsistent Sexual flush. loss of erection may occur with introduction of asexual stimulus ( loud noise).upto 175 beats/min BP. 50% increase in size of testes over unstimulated state & flattening against perineum. face& neck & include shoulders & forearm Erection in 10-30 sec caused by vasocongestion in erectile bodies of corpus cavernosa of shaft. maculopapular rash on abdomen spreads to ant chest wall.rises to 20-80mm systolic & 10-40 diastolic Respiration . Breasts.
Nitric Oxide & Penile/Clitoral Tumescence Sexual stimulation Nitric oxide synthesized in nerve and vascular tissue of penis/clitoris Nitric oxide activates guanylate cyclase GTP cGMP cGMP relaxes smooth muscles of corpus cavernosum and arterioles in penile/clitoral tissue Vasocongestion of penile/clitoral tissues .
septum.Neuroanatomy: Central Cortical: orbitofrontal (sexual emotions). amygdala. medial preoptic area. anterior thalamic nuclei. mammillary bodies (Chemical or electrical stimulation elicited penile erection) . fimbria. left anterior cingulate (hormone control and sexual arousal) Subcortical: right caudate (sexual activity) Limbic: Hippocampus.
which is known to inhibit orgasms Spinal cord: receives sensory inputs. other serotonergic nuclei exert inhibitory and excitatory control over spinal sexual reflexes projects directly to pelvic efferent neurons in the lumbosacral spinal cord. sexual arousal and climax are ultimately organized at the spinal level. reflex centre in lumbosacral area. apparently causing them to secrete serotonin. . Brainstem: nucleus paragigantocellularis.
S3. S4 Reflex impulses Synergy for erection Hypogastric plexus Psychological impulses Ejaculation Orgasm .Neuroanatomy: Peripheral Parasympathetic Sympathetic Pelvic splanchnic nerves Roots S2.
Dopamine: increases libido and sexual activity Acetylcholine: important for erection
Norepinephrine: erection, ejaculation, orgasm
Serotonin: complex role. produced in the upper pons
and midbrain is presumed to have an inhibitory effect on sexual function. Oxytocin: orgasm, reinforce pleasurable activities
Prostaglandins: penile erection Nitric oxide: penile erection, ? female genital
response Vasoactive intestinal polypeptide: arousal in both men and women
Testosterone: libido in both genders In men, stress is inversely correlated with testosterone blood
concentration. Other factors, such as sleep, mood, and lifestyle, influence circulating levels of the hormone. Oxytocin: enhances sexual activity and levels in both sex increase during orgasm Oestrogen: maintains the integrity of the female genital tract GnRH (LHRH): pulsatile release Others: prolactin, thyroid hormones, adrenal steroids
A more simple classification Pleasure inhibitors. or sexual dysfunctions – disorders occurring in the context of a “normal” sexual response or behaviour. or paraphilias – in which deviations from normal erotic stimuli and activities are obligatory for sexual arousal and response. . Pleasure facilitators.
they have not been considered in the nosology) .Sexual dysfunctions: following the response cycle Disorders of desire Disorders of arousal (excitement) Disorders of orgasm (Though disorders of resolution exist.
substance use.Sexual dysfunctions: outside the cycle Sexual pain disorders – dyspareunia and vaginismus Sexual dysfunction. or adverse effects of medication. . Postcoital headache Nymphomania / satyriasis Distress over sexual orientation Orgasmic anhedonia If they are attributable entirely to a general medical condition. then sexual dysfunction due to a general medical condition or substance-induced sexual dysfunction is diagnosed. NOS: Compulsive sexual behaviour (addiction) Postcoital dysphoria.
Male erectile disorder ICD-10: Failure of genital response . Female sexual arousal disorders 2.SEXUAL AROUSAL DISORDERS: DSM IV TR: 1.
arousal. medication. medical illness. absence of sexual desire. or orgasm. or substances of abuse does not best explain the problem. for example. The first criterion describes the psycho-physiologic impairment. The second requires that the patient have marked distress or interpersonal difficulty as a result. .DSM-IV-TR Diagnoses DSM-IV-TR specifies three criteria for each sexual dysfunction. while The third asks the clinician to ascertain that some other Axis I diagnosis.
the degree of subjective distress. The doctor is asked to consider the effects of the individual’s age. and symptom frequency. experience. . adequacy of sexual stimulation.TR gives the clinician additional latitude for deciding when a person who meets the first criterion qualifies for a disorder. DSMIV. ethnicity and cultural background.
Persistent or recurrent inability to attain. Not better accounted for by another axis I disorder not due to direct physiological affect of drug or general medical condition. C. Disturbance causes marked distress or interpersonal difficulty. an adequate erection B. or maintain until completion of sexual activity. DSM IV TR: A.MALE ERECTILE DISORDER/ ERECTILE DYSFUNCTION/ IMPOTENCE. .
. Specify: Due to Psychological factors : Due to combined factors. Specify type: Generalized type : Situational type. Specify type: Life long type : Acquired type.
the principal problem is erectile dysfunction. Includes: Female sexual arousal disorder : Male erectile disorder : Psychogenic Impotence. In women. .2 Failure of Genital Response In men.ICD-10 F52. the principal problem is vaginal dryness or failure of lubrication.
The dysfunction not entirely attributable to any of the other mental & behavioural disorders.ICD-10: A. G3.The dysfunction has been present for at least 6 months. physical disorders. General criteria must be met- G1.subject is unable to participate in a sexual relationship as he/she would wish G2. G4. . drug treatment.dysfunction occurs frequently but may be absent on some occasions.
. Erection sufficient for intercourse fails to when it is attempted. Partial erection. No penile tumescence occurs at all. Full erection occurs during the early stages of love making but disappears or declines when intercourse is attempted (before ejaculation if it occurs) 2. Dysfunction takes one of the following form1. insufficient for intercourse occurs but not full erection 4. Erection does occur but only at times when intercourse is not being considered 3.B.
Erectile dysfunction Erectile dysfunction is defined as the consistent inability to achieve and or maintain an erection of the penis sufficient for satisfactory sexual activity. . Epidemiology: 2-4% at 35yrs & 77% at 80yrs ( Kinsey) The chief complaint of men below 35 & 50% of all men treated for sexual disorders is erectile dysfunction.
. there will be incomplete resistance to the outflow of blood from the corpora & a spectrum of penile tumescence will range from flaccidity to near but not complete erection.veno-occlusive dysfunction.Pathophysiology Normal erection – delicate balance between vasoconstriction & vasorelaxation of corporal smooth muscle. ED due to incomplete corporal smooth muscle relaxation. If a critical level of relaxation is not achieved.
-Relationship conflicts/loss of attraction -Sexual inhibition. Guilt -Widower’s syndrome.Aetiology 1)Psychological causes: -Performance anxiety. Fear of pregnancy or STDs . . -Conflicts over sexual preference -Sexual abuse in childhood -Depression.
ii) CAD & CVAs. cardiac failure iv)Dyslipidaemia. 2)Vascular: i)Atherosclerosis: Penis has more vascular smooth muscle than any other organ in the body. v)Peripheral vascular disease. HDL-Cholesterol: inverse relation. ED may be a reflection of vascular disease elsewhere prior to it becoming clinically evident.Atherosclerosis occurs here early. . iii)Hypertension.
Myxedema . Hyperthyroidism. Venous: Cavernous myopathy. . Low GH. Addison's disease DIABETES AND ERECTILE DYSFUNCTION Psychogenic: Anxiety.3)Endocrinological causes: DM. Dysfunction of the pituitary-adrenal-testis axis.Hyperprolactinemia. Acromegaly. Hypogonadism. Neurogenic : Loss of sensory & autonomic nerves. endothelial dysfunction. Arterial: Small vessel disease.
Mumps Genetic disorders .Klinefelter's syndrome Congenital penile vascular and structural abnormalities (Epispadias) .others Renal and urological disorders Peyronie's disease. Hydrocele & varicocele Hepatic disorders Cirrhosis (usually associated with alcohol dependence) Pulmonary disorders . CKD.Respiratory failure Infectious and parasitic diseases Elephantiasis.
Traumatic and neoplastic spinal cord diseases. Temporal lobe epilepsy.Transverse myelitis Parkinson's disease. Tumours. CVA. Encephalitis.Neurogenic etiology Neurological disorders Multiple sclerosis. Disc herniation . Dementia.Tabes dorsalis. General paresis. ALS Peripheral neuropathy.
Gastro-intestinal: Abdomino-perineal resection. Vascular: Aorto-iliac bypass. Proctocolectomy. . pelvic lympahadenectomy. irradiation. Aorto-femoral bypass. Urological : prostatectomy. spinal cord trauma/surgery.Surgery or trauma Neurological: head trauma/surgery. Retroperitoneal lymphnode dissection. Pelvis: trauma.
Alcohol.Recreational drugs i) Nicotine. cocaine. Increases libido . barbiturates) . ii)Cannabis iii)Amphetamines: vasoconstriction of genital tissue. methadone. morphine. prolonged erection (up to 18 hours!) iv)Ecstacy: Erection: impaired in 40% v) other dependence-inducing substances (heroin.Erectile failure.
clonidine. . ii)Anti-hypertensives: CCBs.beta-blockers. methyldopa.act directly at the corporal level or indirectly by decreasing the systemic B. Spironolactone(anti-androgen activity).P. iii)Cardiac: Digoxin(Na-K ATPase blockade). . i)Diuretics: Thiazides.Drugs Accounts for 25% Thiazide diuretics are the most common cause of ED.clofibrate.
Cyproterone acetate.LHRH agonists.Progesterone.Corticosteroids.5-alpha reductase inhibitors.Anti-convulsants . vi) Cytotoxic drugs: Cyclophosphamide. Methotrexate. vii)Others:Anticholinergics.Ranitidine (anti- androgen activity). iv)H-2 antagonists: Cimetidine.(by causing hypogonadism). v)Hormones: Estrogens.
ED . orgasmic difficulties SSRIs: lack of libido.Psychotropics and sexual dysfunction Antipsychotics: lack of libido. delayed ejaculation Benzodiazepines: not clear Anticholinergics: failure of vaginal lubrication. arousal disorders. ED. ED Mood stabilizers: rare Tricyclics: retrograde ejaculation.
zinc deficiency. plumbism.leukaemia.alteration in K-gated pump. of hours on a bike &/or pressure on the penis from the saddle of an upright bicycle is directly related to ED. . iv)nutritional : malnutrition.i) Aging: ED is 4times higher im men in 60s than in 40s. v)Bicycling: A study done in 2002 found that the No. ii)Arsenic poisoning. herbicides iii)haematological: sickle cell anaemia.
3)Psychological assessment.Clinical evaluation 1)History 2)Physical exmination. 4)Tests .
It also allows the physician to establish a rapport with the couple. and the clinician must be sensitive to the patient's comfort level. and psychosocial history. Taking the history provides an opportunity for the physician to initiate patient and partner education about ED and its treatments and to facilitate communication. medical.History The first step in the management.sexual. A sensitive topic. which assists in treatment .
Derogatis Sexual Function Inventory. Rush Sexual Inventory. SHIM -Sexual Health Inventory for Men. questionnaires: IIEF –International Index of Erectile Function. Brief Sexual Function Questionnaire. . Changes in Sexual Functioning Questionnaire. Arizona Sexual Experience Scale.
partner’s sexual function & others psychological factors. substance use should be documented.or mastubatory-related erections. Organic causes – characterized by an insidious & consistent change in rigidity or inability to sustain morning. penile curvature. Also enquire about: penile sensation. trauma. coital. altered libido. prior prostate surgery. any history of pelvic surgery. . or radiation to the prostate. Obtain information about current medications.
serious cardiovascular pathology. or hypertension. vascular. evidence of possible prostate cancer.Physical examination A physical examination is necessary for every patient. and neurologic systems. such as penile plaques. . thyroid dysfunction. The physical examination may corroborate history findings and reveal unsuspected physical findings. prostate infections. small testes. with particular emphasis on the genitourinary.end-stage kidney disease. All peripheral pulses should be measured.
but not while attempting intercourse with his wife. long-lasting erections during the night or early mornings. Underlying relationship problems are the cause and they must be addressed. The man is able to produce rigid.Psychological assessment The main diagnostic feature of psychogenic ED vs selective ED. with certain partners. in response to magazines or videos. .
Tests 1)Nocturnal Penile Tumecsence(NPT) Useful in distinguishing psychogenic ED from Organic. Patient is asked to wear it on 2-3 successive nights. Erections occur during REM sleep. Sleep can be monitored by polysomnography . A band is placed around the penis.
strapped to the patient’s thigh& 2 loops placed around the base &tip of the penis just behind the corona. Logging unit. . capable of continuously monitoring penile circumference & rigidity. Shotrcomings: lack of information regarding partial rigidity.monitoring device.of erections & duration of erections. There are 2 methods: i)Snap-Gauge band:Velcro band fitted around the penis. ii) Rigi scan:Home. No.
2)Vascular studies: i)Intra –cavernous vaso-active drug injection: A positive test – rigid erectile response(unable to bend) . Color doppler can also be used.that appears within 10mins after the intracavernous injection(of 20mcg of PGE1 or papaverine)& lasts for 30mins. .functional origin. A positive response indicates. Limited use ii) Duplex ultrasound of penile arteries: Measurements are compared between flaccid & pharmacological erect penis.
iv)Penile angiogram v)Digital subtraction angiography vi)Magnetic Resonance Angiography . iii) Arteriography & Dynamic Cavernosometry or Cavernosography(DICC): Used to detect failure of veno-occlusive mechanism. Cavernosography using radiographic contrast enables the detection of potential leakage into all penile venous drainage systems.
3)Neurological studies: i)Bulbo-cavernous reflex latency: The physician squeezes the glans of the penis. The latency between sqeeze & contraction is measured by observing the anal spincter or feeling it with a gloved finger inserted past the anus. if the nerve function is normal. ii) Nerve conduction Studies .which immediately causes the anus to contract.
iii)Penile Biothesiometry: A small electro-magnetic test probe is placed on the right & left of the shaft and on the glans. . A decreased perception of vibration may indicate nerve damage in the pelvic area. which can lead to impotence.
prolactin. .psychodiagnostic tests.FSH. 4)Endocrinological studies: Testosterone.GH.LH. PSA. 5)Other tests: Fasting glucose & lipid profile.
PLISSIT: a simple model for routine practice (Annon) P – permission LI – limited information SS – specific suggestion IT – intensive therapy .
PLISSIT: a simple model for routine practice .
. injectales. oral. 5) Surgery.Treatment 1)Psychotherapy 2) Non-pharmacological methods 3)Vacuum devices 4)Pharmacotherapy: topical.
insight oriented psychotherapy) .Management: psychotherapies Dual sex therapy developed by Masters & Johnson (Sensate Focus) Behavioural therapy (assumes sexual dysfunction as learned maladaptive behaviour) Hypnotherapy Group therapy Psychodynamic therapy Integrated therapy (sex therapy integrated with supportive. psychodynamic.
Nonpharmacologic Treatment Options Lifestyle changes: • Reduce fat and cholesterol in diet • Decrease or limit alcohol consumption • Eliminate tobacco use and substance abuse • Weight loss if appropriate • Regular exercise .
which results in an increase in corporeal blood flow & erection. The time taken to achieve erection -2-30mins. . These devices exert a negative pressure on the penis.Vacuum devices: Can be used by almost all patients with ED.
3) Other intracavernosal & transdermal drugs 4) Oral therapies .Pharmacotherapy 1) Prostaglandin delivery systems: intra-cavernosal : intraurethral 2) Transdermal delivery.
Administration: i)reconstitution of the powder of the drug.the injection site should be alternated between the cavernosa . ii)The skin over the penis should be pulled taut & the needle & syringe are held at right angles to the penis iii)The drug should be injected directly into one corpus cavernsum.Intra cavernosal PGE1 Caverject: injectable form of Alprostadil. .avoiding visible veins.
multiple myeloma.Side-effects: Pain. Priapism. sicle cell anemia.g. Other drugs: i)Moxisylte. E. Containdications: Known hypersensitivity to the drug. . ii)Vasoactive intestinal polypeptide. Prolonged use. leukemia. Patients with conditions that predispose to priapism.selective alpha-1 blocker.corporal fibrosis.
Intra urethral PGE1 Alprostadil administered using MUSE(Medicated Urethral System for Erection) It is rapidly absorbed from the urethral mucosa. .. Usual onset of action:20mins & erections last for 30-60min.
Others: Testosterone patches. . 1-2 patches containing 2. back thighs or upper arms.5-5mg of testosterone applied daily to the abdomen. Administration of vaso-active substances(PGE1) across the skin to the penis.Transdermal delivery Minimizes systemic exposure & tissue traumatization.
PDE5 Inhibitors Mechanism of Action: • PDE inhibitor and increases the cGMP that promotes and sustains smooth muscle relaxation Indications: • Psychogenic ED • Mild vasculogenic ED • Neurogenic ED • Side effects from medication(s) patient is already taking .
Mechanism of Action of PDE5 Inhibitors . SM .
myalgia. flushing and nasal congestion Nitrates FEBRUARY 2003 30min 36hrs Headache. bluish vision and nasal congestion CONTRAINDI CATION Nitrates . dyspepsia.DRUG RELEASED IN ONSET OF ACTION SILDENAFIL MARCH 1998 30 min VARDENAF TADALAFIL IL APRIL 2003 25-45min 6hrs Headache. Backache. Angina. DURATION OF 5hrs ACTION SIDE.nasal congestion Nitrates. Hypertension.EFFECTS Headache . flushing.
Erex. tachycardia. Yohimex) • Alpha 2 andrenoreceptor antagonist • Dose: 5. anxiety .4 mg TID • Results: ~20% (same as placebo) • Side effects: increase blood pressure.Medication (Yohimbine. Yocon.
sedation. dry mouth.Medication Trazodone(Desyrel) • Anti-depressant associated with priapism • Mechanism of action not fully understood • Not FDA approved for ED • Side effects: drowsiness. priapism .
Medication Apomorphine (Spontane) • Dopaminergic mechanism with hypothalamic activity • Sublingual administration • 64% to 67% response rate with ED • Side effects: nausea. yawning • Awaiting FDA approval . hypotension. sweating.
hypotension • Awaiting FDA approval . dizziness. tachycardia.Medication Phentolamine (Vasomax) • Alpha-blocker • Relaxes smooth muscle tissue • 40% efficacy in mild organic ED • Side effects: nasal congestion.
cavernosal & crural veins. . 2)Arterial revascularization.Surgery 1)Venous leakage: 2 approaches are adopted: i) ligation of all veins draining to the penis i.e deep dorsal. 3)Peyronie’s disease: The Horton – Devine procedure. : The Nesbit procedure. ii)ligation & division of the deep dorsal vein.
PENILE PROTHESIS 2 types: i)Semi-rigid rods Consists of 2 rod-like cylinders that are implanted into the corpora cavernosa Types: Malleable & Mechanical rods ii) Inflatable Cylinders. Unitary. Two-piece. Three piece .
Penile prosthesis Penile prosthesis has highest satisfaction ~93% Infection rate: ~2% virgin & 4% diabetic Malfunction rate ~10% at 10years Surgical Procedure – Requires Anesthesia – Takes approximately 90 min. .
An innovative drug-delivery system – nanoparticles encapsulating NO or prescription drugs – shows promise for topical treatment of ED.Yoram Vadi in Nov 2009. 2009) A study done by Dr. showed that 75% of men suffering from ED. treated with shock-wave therapy showed a return of erectile functioning.(release of VEGF. 20. .stimulates the growth of new blood vessels in the genital area). -Science Daily (Sep.
cyproheptadine. amantadine. nefazodone Psychological interventions Sildenafil Others – dopamine agonists. bupropion.Treatment of antidepressantinduced sexual disorders Drug holidays Switching – mirtazapine. buspirone .
generalised/ situational. B. due to psychological factors or combined factors. Specify: lifelong/ acquired type. an adequate lubrication swelling response. Disturbance causes marked distress or interpersonal difficulty. or maintain until completion of sexual activity. Persistent or recurrent inability to attain. C.FEMALE SEXUAL AROUSAL DISORDERS: DSM IV TR: A. Not better accounted for by another axis I disorder not due to direct physiological affect of drug or general medical condition. .
. G4. physical disorders.subject is unable to participate in a sexual relationship as he would wish G2.dysfunction occurs frequently but may be absent on some occasions.The dysfunction not entirely attributable to any of the other mental & behavioural disorders.ICD-10: A. drug treatment. General criteria must be metG1.The dysfunction has been present for at least 6 months. G3.
Situational: lubrication occurs only in some situations (with one partner not another. Lubrication may occur initially but fails to persist for long enough to allow comfortable penile entry. experienced as failure of vaginal lubrication. together with inadequate tumescence of the labia. during masturbation. . Dysfunction takes place one of the following forms: 1. when vaginal intercourse is being contemplated. There is failure of genital response.B. 3. General: lubrication fails in all relevant circumstances 2.
Studies shown 14-16% women having chronic lubrication difficulties & 23% with intermittent problems. May be associated with dyspareunia or lack of desire. Postmenopausal.44% Less research on physiological components of dysfunction in women than men . Women with excitement phase dysfunction often have orgasmic problems as well.
. Another set of dysfunctional women found felt the greatest sexual excitement at the time of ovulation Evidence indicates dysfunctional women are less aware of physiological responses in their bodies. like vasocongestion during arousal. Masters & johnson found normally responsive women to desire sex premenstrually.
studies have shown some probative links between chidhood sexual abuse & sexual dysfunction in later life. . Psychological factors: i)Impact of events during childhood and adolescence. 2)Physical domain. .Causes of female sexual arousal disorder Classified as: 1)Psychological domain.
iii)Relationship factors: .ii) Individual factors: Stress & fatigability. OCD. self. .consciousness and lowered self esteem. Over-exposure to pornography & style media which is thought to lead to poor body image. anxiety. PTSD.Psychiatric disorders like depression.
Damage to blood vessels decreases blood flow damage to nerves in pelvic area diminishes arousal. Physical factors: 30-80% of the cases. due to aging(menopause) Thyroid dysfunction. . i)Circulatory: HTN. disorders of adrenal gland etc. ii)General medical condition: Diabetes. Circulatory & neurological disorders are the most likely causes of sexual dysfunction. Anaemia. CAD. iii)Hormonal: Low level of sex hormones .
Sedatives. v)Medications: Anti-depressants. Anti-hypertensives.smoking. vi)Post baby coolness: Extreme loss of lidido after childbirth.iv)Recreational drugs: alcohol. Anti-psychotics. OCPs & Other hormone containing pills. .
. which results in dryness. Role of Male Circumsicion The `valve' mechanism of foreskin of uncircumcised penis is thought to retain the natural lubrication provided by the female because the bunched up foreskin acts to block the lubrication escaping from the vagina.
distressing and perplexing not only because of its mysterious onset.Persistent sexual arousal syndrome in women Infrequent. . persistent feelings of vaginal congestion and other physical signs of sexual arousal in the absence of any awareness of sexual desire provoking or accompanying this arousal or persisting for hours after attaining orgasm. but also because of the feelings of shame and discomfort that accompany the phenomenon.
starting with non-sexual. CBT: uses thought records to capture the cognitions that accompany emotions. couples therapy. Physiology and expectations. sexual and sexual intercourse. Masters & Johnson-sensate focus. progressive levels of touching. .Interventions 1)PsychologicalTreatment Education about anatomy.
2)Lubricants: Helps in vaginal dryness & the resulting dyspareunia. 3)Pharmacotherapy: i)Sildenafil: Dose: 50-100mg/day. Found to be superior to placebo in effects of arousal. ii)The Non- SSRI: Bupropion Especially in those with SSRI induced dysfunction. Dose: 300-400mg/day
Providing exogenous source of hormones ameliorate
vasomotor symptoms in menopausal women. Women with vaginal atrophy & donot wish to take systemic therapy – topical estrogen creams. Transdermal delivery: Natural progestin containing creams combined with estrogen. Tibolone: Synthetic steroid sex hormone.Superior to HRT.
5)Clitoris Vacuum therapy: A small ,handheld device ,connected by a tubing to a
small ,soft plastic cup, that is placed over the clitoris. When gentle vacuum is created , blood flow to the genitalia causes genital engorgement, increased vaginal lubrication & enhanced ability to achieve orgasm. May be used prior to having intercourse or 3-4times a week to rehabilitate sexual responses.
Prognosis: Generally once a woman seeks the appropriate help they are quite likely to find a way to resolve their problem.ginkgo biloba etc. Belladona . 7) Alternative medicine: Natural estrogens such as soya products. ii)Dopamine agonists – increases sexual interest.increases genital arousal. orgasm & improves patient-partner sexual satisfaction. . 6)Others: i)Topical vasodilators: PGE1.
Hence early detection & treatment should be our goal as successive episodes are reinforcing and cause anticipatory anxiety perpetuating the problem. Arousal disorders are usually not diagnosed or treated in women as they rarely seek treatment.CONCLUSION: Sexual arousal disorders are quite common & very distressing both in men & women but appears to be high in men causing distress to both partners & causing interpersonal problems. .
. and good physique. and they value virginity and chastity. Women. look for high-quality mates with abundant resources and emotional and financial status and security.Thank u Men look for youthfulness and physical attractiveness. Partner variety is highly desired. smooth complexion. optimum stature.
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