sexual-arousal-disorders

sexual-arousal-disorders
sex problems

1. Sexual arousal disorders
“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

2. Sexuality and sexual behaviour
Reproduction is a fundamental biological function,
that guarantees the survival of the species.
Due to its evolutionary advantages, most complex
life-forms have evolved methods of sexual
reproduction, which involves the combination of
genetic material from parents of two different
genders.

3. 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.

4. History
First attempt at describing and classifying sexual
disorders began with Richard von Krafft-Ebing
and his Psychopathia Sexualis(1898), which
influenced medical and legal practice for more than 3-
quarters of a century.
Seminal contributions of Havelock Ellis and Albert
Kinsey (sexual behavior in human male and female)

5. Prior to
1950
late
1950s
psychoanalytical concepts guided clinicians
in understanding and treatment of sexual
problems
Sexual symptoms were linked to
unresolved, unconscious conflicts
occurring during specific developmental
periods.
behavioural perspective gained
ascendancy; sexual problems were
understood to be learned (conditioned)
anxiety responses.

6. In
1966
Masters and Johnson.
described the physiology of phases of
sexual functioning, and
later highlighted the deleterious influence
of performance anxiety, the impact of
relationship factors, and the significance
of biological factors on the development
of sexual dysfunctions.
Their work foreshadowed the later
integration of medical and psychological
interventions.

7. The
neo-
Masters
and
Johnson
era
heralded by the publication of
Helen Singer Kaplan's book,
The New Sex Therapy.
Integrated psychoanalytical theory with
Masters & Johnson's cognitive-behavioral
understanding of sexual dysfunction.
Distinguishing between recent and
remote etiological causations, she
recommended behavioral approaches for
the former and reserved traditional
psychodynamic methods for the latter.

8. The
mid-
1980s
current psychobiological era.
This period is distinguished by the
medicalization of treatment approaches,
primarily for male sexual dysfunction.
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.

9. Components of sexuality
Sexual identity: is a pattern of patient’s biological
sexual characteristics
Gender identity: individual sense of maleness/
femaleness, from infinite clues derived from experiences
with family members, peers, teachers & cultural
phenomenon. Established by age of 2 or 3 yrs.
Sexual orientation: describes the object of person’s
sexual impulses. Heterosexual, homosexual, or bisexual.
Sexual behaviour: includes desire, fantasies, pursuit of
partners, auto-erotic activities & activities engaged in to
express & gratify sexual needs.

10. Modelling the human sexual response cycle
Models have been constructed of the normal
sequence of changes during sexual arousal and coitus.
The first models described a simple sequence of
increasing arousal and excitement culminating in
rapid discharge by orgasm, displayed graphically as an
ascent, peak, and then descent.

11. The EPOR model
formulated by Masters and Johnson
four-phase linear, sequential, and incremental model
of the human sexual response cycle
excitation (E) phase (stimuli from somatogenic or
psychogenic sources raise sexual tensions),
plateau (P) phase (sexual tensions intensified),
orgasmic (O) phase (involuntary pleasurable climax),
and finally
resolution (R) phase (dissipation of sexual tensions).

12. 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.
Helen Kaplan, proposed that before the E phase there
should be a ‘desire phase' (D phase).
came from her work with women who professed to have
no desire to be sexually aroused, even by their usual
partners.

13. EPOR replaced by the desire, excitation, 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?

14. (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

15. Phase I: Desire
Psychological phase
Characterised by sexual fantasies & conscious
desire to have sexual activity.
Can be biologically driven or result from a wish to
bond sexually with a particular partner.
Dysfunction: hypoactive sexual desire disorder,
sexual aversion disorder, hypoactive sexual desire
disorder due to general medical condition (man/
woman), substance induced sexual dysfunction
with impaired arousal.

16. Phase II: Excitement
Brought on by psychological stimulation (fantasy
or presence of love object), physiological
(stroking/ kissing) or combination.
Consists of subjective sense of pleasure &
objective signs of sexual excitement.
Dysfunction: female sexual arousal disorders,
male erectile disorders, male erectile disorder due
to general medical condition, substance induced

17. Phase III: Orgasm
Consists of peaking sexual pleasure, with release of sexual
tension, & rhythmic contraction of perineal muscles &
pelvic reproductive organ.
Lasts for 3-15sec
Dysfunction: female & male orgasmic disorders, premature
ejaculation

18. Phase IV: Resolution
Consists of disgorgement of blood from genitalia, which
brings body back to its resting position.
If orgasm occurs resolution is rapid, if not may take 2-6hrs
& be associated with irritability & discomfort.
Through orgasm it is characterised by sense of well being,
general relaxation, muscular relaxation.
Men have refractory period (mins-hrs), they can’t be
stimulated to further orgasm. This does not exist in
females.
Dysfunction: postcoital dysphoria, postcoital headache.

19. The sexual response cycle

20. organ Excitement phase
mental Several mins-hrs, heightened excitement before orgasm, 30sec-3min
skin Inconsistent Sexual flush, maculopapular rash on abdomen spreads to ant
chest wall, face& neck & include shoulders & forearm
breasts Nipple erection (2/3
rd
), venous congestion & areolar enlargement, size
increases by 1/4
th

clitoris Enlargement in diameter of glans & shaft, just before orgasm shaft retracts
into prepuce
Labia majoraNullipara- elevate & flatten against perineum
Multipara- congestion & edema
Labia
minora
Size increase 2-3 times normal, change to pink, red, deep red before
orgasm
vagina Colour change to dark purple, transudate appears 10-30 sec after arousal,
elongation & ballooning, lower third constricts before orgasm
uterus Ascends into false pelvis, labor like contractions begin in heightened
excitement just before orgasm
others Myotonia
Mucoid secretion from bartholin’s gland during heightened excitement
Cervix swells slightly & is passively elevated with uterus

21. organ Excitement phase
Mental Several mins-hrs, heightened excitement before orgasm
30sec-3min
Skin Just before orgasm, inconsistent Sexual flush, maculopapular rash on
abdomen spreads to ant chest wall, face& neck & include shoulders &
forearm
Penis Erection in 10-30 sec caused by vasocongestion in erectile bodies of
corpus cavernosa of shaft, loss of erection may occur with introduction
of asexual stimulus ( loud noise), with heightened excitement size og
glans & diameter of penile shaft increase further
Scrotum & testesTightening & lifting of scrotal sac & elevation of testes, 50% increase in
size of testes over unstimulated state & flattening against perineum,
signalling impending ejaculation
Cowper’s gland2-3 drops of mucoid fluid that contain viable sperm are secreted
during heightened excitement.
other Breasts- inconsistent nipple erection
Myotonia- semispastic contractions of facisl, abdominal & intercostal
muscles
Tachycardia- upto 175 beats/min
BP- rises to 20-80mm systolic & 10-40 diastolic
Respiration - increased

22. 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

24. Neuroanatomy: Central
Cortical: orbitofrontal (sexual emotions), left
anterior cingulate (hormone control and sexual
arousal)
Subcortical: right caudate (sexual activity)
Limbic: Hippocampus, amygdala, septum, medial
preoptic area, fimbria, anterior thalamic nuclei,
mammillary bodies (Chemical or electrical
stimulation elicited penile erection)

25. Brainstem: nucleus paragigantocellularis, other
serotonergic nuclei
exert inhibitory and excitatory control over spinal sexual
reflexes
projects directly to pelvic efferent neurons in the
lumbosacral spinal cord, apparently causing them to
secrete serotonin, which is known to inhibit orgasms
Spinal cord: receives sensory inputs; reflex centre in
lumbosacral area. sexual arousal and climax are ultimately
organized at the spinal level.

26. Neuroanatomy: Peripheral
Parasympathetic
Pelvic splanchnic
nerves
Roots S2, S3, S4
Reflex impulses
Synergy for erection
Sympathetic
Hypogastric plexus
Psychological
impulses
Ejaculation
Orgasm

27. Neurochemistry
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

28. Neurochemistry
Prostaglandins: penile erection
Nitric oxide: penile erection, ? female genital
response
Vasoactive intestinal polypeptide: arousal in both
men and women

29. Endocrinology
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

30. A more simple classification
Pleasure inhibitors, or sexual dysfunctions – disorders
occurring in the context of a “normal” sexual response
or behaviour.
Pleasure facilitators, or paraphilias – in which
deviations from normal erotic stimuli and activities
are obligatory for sexual arousal and response.

31. Sexual dysfunctions:
following the response cycle
Disorders of desire
Disorders of arousal (excitement)
Disorders of orgasm
(Though disorders of resolution exist, they have not
been considered in the nosology)

32. Sexual dysfunctions:
outside the cycle
Sexual pain disorders – dyspareunia and vaginismus
Sexual dysfunction, NOS:
Compulsive sexual behaviour (addiction)
Postcoital dysphoria, Postcoital headache
Nymphomania / satyriasis
Distress over sexual orientation
Orgasmic anhedonia
If they are attributable entirely to a general medical
condition, substance use, or adverse effects of
medication, then sexual dysfunction due to a general
medical condition or substance-induced sexual
dysfunction is diagnosed.

33. SEXUAL AROUSAL DISORDERS:
DSM IV TR:
1.Female sexual arousal disorders
2.Male erectile disorder
ICD-10:
Failure of genital response

34. DSM-IV-TR Diagnoses
DSM-IV-TR specifies three criteria for each sexual
dysfunction.
The first criterion describes the psycho-physiologic
impairment; for example, absence of sexual desire,
arousal, or orgasm.
The second requires that the patient have marked
distress or interpersonal difficulty as a result, while
The third asks the clinician to ascertain that some
other Axis I diagnosis, medical illness, medication, or
substances of abuse does not best explain the
problem.

35. DSMIV- TR gives the clinician additional latitude for
deciding when a person who meets the first criterion
qualifies for a disorder.
The doctor is asked to consider the effects of the
individual’s age, experience, ethnicity and cultural
background, the degree of subjective distress,
adequacy of sexual stimulation, and symptom
frequency.

36. MALE ERECTILE DISORDER/ ERECTILE
DYSFUNCTION/ IMPOTENCE.
DSM IV TR:
A.Persistent or recurrent inability to attain, or maintain until
completion of sexual activity, an adequate erection
B.Disturbance causes marked distress or interpersonal
difficulty.
C.Not better accounted for by another axis I disorder not
due to direct physiological affect of drug or general
medical condition.

37. Specify type: Life long type
: Acquired type.
Specify type: Generalized type
: Situational type.
Specify: Due to Psychological factors
: Due to combined factors.

38. ICD-10 F52.2 Failure of Genital
Response
In men, the principal problem is erectile dysfunction.
In women, the principal problem is vaginal dryness or
failure of lubrication.
Includes: Female sexual arousal disorder
: Male erectile disorder
: Psychogenic Impotence.

39. ICD-10:
A.General criteria must be met-
G1- subject is unable to participate in a sexual
relationship as he/she would wish
G2- dysfunction occurs frequently but may be
absent on some occasions.
G3- The dysfunction has been present for at least 6
months.
G4- The dysfunction not entirely attributable to any
of the other mental & behavioural disorders,
physical disorders, drug treatment.

40. B. Erection sufficient for intercourse fails to when it is
attempted. Dysfunction takes one of the following form-
1.Full erection occurs during the early stages of love
making but disappears or declines when intercourse is
attempted (before ejaculation if it occurs)
2.Erection does occur but only at times when intercourse
is not being considered
3.Partial erection, insufficient for intercourse occurs but
not full erection
4.No penile tumescence occurs at all.

41. 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.

42. Pathophysiology
Normal erection – delicate balance
between vasoconstriction & vasorelaxation
of corporal smooth muscle.
If a critical level of relaxation is not
achieved, 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.
ED due to incomplete corporal smooth
muscle relaxation- veno-occlusive
dysfunction.

43. Aetiology
1)Psychological causes:
-Performance anxiety,
-Relationship conflicts/loss of attraction
-Sexual inhibition, Guilt
-Widower’s syndrome.
-Conflicts over sexual preference
-Sexual abuse in childhood
-Depression, Fear of pregnancy or STDs .

44. 2)Vascular:
i)Atherosclerosis:
Penis has more vascular smooth muscle than any other
organ in the body.Atherosclerosis occurs here early.
ED may be a reflection of vascular disease
elsewhere prior to it becoming clinically evident.
ii) CAD & CVAs, iii)Hypertension, cardiac failure
iv)Dyslipidaemia. HDL-Cholesterol: inverse relation.
v)Peripheral vascular disease,

45. 3)Endocrinological causes:
DM, Dysfunction of the pituitary-adrenal-testis axis,
Hyperthyroidism, Myxedema ,Hyperprolactinemia,
Hypogonadism, Low GH, Acromegaly, Addison's disease
DIABETES AND ERECTILE DYSFUNCTION
Psychogenic: Anxiety.
Neurogenic : Loss of sensory & autonomic nerves.
Arterial: Small vessel disease.
Venous: Cavernous myopathy, endothelial dysfunction.

46. others
Renal and urological disorders
Peyronie's disease, CKD, Hydrocele & varicocele
Hepatic disorders
Cirrhosis (usually associated with alcohol dependence)
Pulmonary disorders - Respiratory failure
Infectious and parasitic diseases
Elephantiasis, Mumps
Genetic disorders - Klinefelter's syndrome
Congenital penile vascular and structural abnormalities
(Epispadias)

47. Neurogenic etiology
Neurological disorders
Multiple sclerosis, Tumours, CVA,
Encephalitis, Dementia,Transverse myelitis
Parkinson's disease, Temporal lobe epilepsy,
Traumatic and neoplastic spinal cord diseases, ALS
Peripheral neuropathy, General paresis,Tabes dorsalis,
Disc herniation

48. Surgery or trauma
Neurological: head trauma/surgery, spinal cord
trauma/surgery, Retroperitoneal lymphnode
dissection.
Vascular: Aorto-iliac bypass, Aorto-femoral bypass.
Gastro-intestinal: Abdomino-perineal resection,
Proctocolectomy.
Pelvis: trauma, irradiation, pelvic lympahadenectomy.
Urological : prostatectomy.

49. Recreational drugs
i) Nicotine, Alcohol.
ii)Cannabis
iii)Amphetamines: vasoconstriction of genital tissue.
 Increases libido ,Erectile failure;
 prolonged erection (up to 18 hours!)
iv)Ecstacy: Erection: impaired in 40%
v) other dependence-inducing substances
(heroin, methadone, morphine, cocaine,
barbiturates)

50. Drugs
Accounts for 25%
Thiazide diuretics are the most common cause of ED.
i)Diuretics: Thiazides, Spironolactone(anti-androgen
activity).
ii)Anti-hypertensives: CCBs,
methyldopa,clonidine,beta-blockers.
- act directly at the corporal level or indirectly by
decreasing the systemic B.P.
iii)Cardiac: Digoxin(Na-K ATPase
blockade),clofibrate.

51. iv)H-2 antagonists: Cimetidine,Ranitidine (anti-
androgen activity).
v)Hormones:
Estrogens,Progesterone,Corticosteroids,
Cyproterone acetate,5-alpha reductase
inhibitors,LHRH agonists.
vi) Cytotoxic drugs: Cyclophosphamide,
Methotrexate.(by causing hypogonadism).
vii)Others:Anticholinergics,Anti-convulsants

52. Psychotropics and sexual
dysfunction
Antipsychotics: lack of libido, ED
Mood stabilizers: rare
Tricyclics: retrograde ejaculation, ED, orgasmic
difficulties
SSRIs: lack of libido, arousal disorders, delayed
ejaculation
Benzodiazepines: not clear
Anticholinergics: failure of vaginal lubrication, ED

53. i) Aging: ED is 4times higher im men in 60s than in
40s.
ii)Arsenic poisoning- alteration in K-gated pump,
plumbism, herbicides
iii)haematological: sickle cell anaemia,leukaemia.
iv)nutritional : malnutrition, zinc deficiency.
v)Bicycling: A study done in 2002 found that the No. of
hours on a bike &/or pressure on the penis from the
saddle of an upright bicycle is directly related to ED.

54. Clinical evaluation
1)History
2)Physical exmination.
3)Psychological assessment.
4)Tests

55. History
The first step in the management- sexual, medical,
and psychosocial history.
A sensitive topic, and the clinician must be sensitive
to the patient's comfort level.
Taking the history provides an opportunity for the
physician to initiate patient and partner education
about ED and its treatments and to facilitate
communication.
 It also allows the physician to establish a rapport with
the couple, which assists in treatment

56. questionnaires:
IIEF –International Index of Erectile Function.
SHIM -Sexual Health Inventory for Men.
Arizona Sexual Experience Scale,
Brief Sexual Function Questionnaire,
Changes in Sexual Functioning Questionnaire,
Derogatis Sexual Function Inventory,
Rush Sexual Inventory.

57. Organic causes – characterized by an insidious &
consistent change in rigidity or inability to sustain
morning, coital,or mastubatory-related erections.
Also enquire about: penile sensation, penile curvature,
altered libido, partner’s sexual function & others
psychological factors.
Obtain information about current medications, any
history of pelvic surgery, trauma, prior prostate
surgery, or radiation to the prostate.
 substance use should be documented.

58. Physical examination
A physical examination is necessary for every patient,
with particular emphasis on the genitourinary,
vascular, and neurologic systems.
The physical examination may corroborate history
findings and reveal unsuspected physical findings,
such as penile plaques, small testes, evidence of
possible prostate cancer, prostate infections, or
hypertension, thyroid dysfunction,serious
cardiovascular pathology,end-stage kidney disease.
All peripheral pulses should be measured.

59. Psychological assessment
The main diagnostic feature of psychogenic ED vs
selective ED.
The man is able to produce rigid,
long-lasting erections during the night or
early mornings,
with certain partners,
in response to magazines or videos,
but not while attempting
intercourse with his wife.
Underlying relationship problems are the cause and
they must be addressed.

60. Tests
1)Nocturnal Penile Tumecsence(NPT)
Useful in distinguishing psychogenic ED from
Organic.
Erections occur during REM sleep.
A band is placed around the penis.
Patient is asked to wear it on 2-3
successive nights.
Sleep can be monitored by polysomnography

61.  There are 2 methods:
i)Snap-Gauge band:Velcro band fitted around the penis.
Shotrcomings: lack of information regarding partial
rigidity, No.of erections & duration of erections.
ii) Rigi scan:Home- monitoring device,
capable of continuously monitoring penile
circumference & rigidity.
Logging unit- strapped to the
patient’s thigh& 2 loops placed around the base &tip of
the penis just behind the corona.

62. 2)Vascular studies:
i)Intra –cavernous vaso-active drug injection:
A positive test – rigid erectile response(unable to
bend) ,that appears within 10mins after the
intracavernous injection(of 20mcg of PGE1 or
papaverine)& lasts for 30mins.
A positive response indicates- functional origin.
Limited use
ii) Duplex ultrasound of penile arteries:
Measurements are compared between flaccid &
pharmacological erect penis.
Color doppler can also be used.

63. 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.
 iv)Penile angiogram
 v)Digital subtraction angiography
 vi)Magnetic Resonance Angiography

64. 3)Neurological studies:
i)Bulbo-cavernous reflex latency:
The physician squeezes the glans of the
penis,which immediately causes the anus to
contract, if the nerve function is normal.
The latency between sqeeze & contraction is
measured by observing the anal spincter or feeling
it with a gloved finger inserted past the anus.
ii) Nerve conduction Studies

65. 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.

66. 4)Endocrinological studies:
Testosterone,prolactin,FSH,LH,GH.
5)Other tests:
Fasting glucose & lipid profile,
PSA,psychodiagnostic tests.

67. PLISSIT: a simple model for
routine practice (Annon)
P – permission
LI – limited information
SS – specific suggestion
IT – intensive therapy

68. PLISSIT: a simple model for
routine practice

70. Treatment
1)Psychotherapy
2) Non-pharmacological methods
3)Vacuum devices
4)Pharmacotherapy: topical, injectales, oral.
5) Surgery.

71. 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, insight oriented
psychotherapy)

72. 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

73. Vacuum devices:
Can be used by almost all patients with ED.
These devices exert a negative pressure on the
penis, which results in an increase in corporeal
blood flow & erection.
The time taken to achieve erection -2-30mins.

74. Pharmacotherapy
1) Prostaglandin delivery systems: intra-cavernosal
: intraurethral
2) Transdermal delivery.
3) Other intracavernosal & transdermal drugs
4) Oral therapies

75. Intra cavernosal PGE1
Caverject: injectable form of Alprostadil.
Administration:
i)reconstitution of the powder of the drug.
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,avoiding visible veins;the
injection site should be alternated between
the cavernosa .

76. Side-effects:
Pain, Prolonged use- corporal fibrosis.
Priapism.
Containdications:
Known hypersensitivity to the drug.
Patients with conditions that predispose to priapism.
E.g; sicle cell anemia, multiple myeloma, leukemia.
Other drugs: i)Moxisylte- selective alpha-1 blocker.
ii)Vasoactive intestinal polypeptide.

77. 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..

78. Transdermal delivery
Minimizes systemic exposure & tissue traumatization.
Administration of vaso-active substances(PGE1)
across the skin to the penis.
Others:
Testosterone patches.
1-2 patches containing 2.5-5mg of testosterone applied
daily to the abdomen, back thighs or upper arms.

79. 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

80. Mechanism of Action of
PDE5 Inhibitors
..
SM

81. DRUG SILDENAFIL VARDENAF
IL
TADALAFIL
RELEASED IN MARCH 1998 APRIL 2003FEBRUARY
2003
ONSET OF
ACTION
30 min 25-45min 30min
DURATION OF
ACTION
5hrs 6hrs 36hrs
SIDE- EFFECTSHeadache ,
flushing, bluish
vision and nasal
congestion
Headache,
flushing and
nasal
congestion
Headache,
myalgia,
dyspepsia.
Backache,nasal
congestion
CONTRAINDI
CATION
Nitrates Nitrates Nitrates,
Angina,
Hypertension,
Hypotension.

82. Medication
(Yohimbine, Yocon, Erex, Yohimex)
•Alpha 2 andrenoreceptor antagonist
•Dose: 5.4 mg TID
•Results: ~20% (same as placebo)
•Side effects: increase blood pressure, tachycardia,
anxiety

83. Medication
Trazodone(Desyrel)
•Anti-depressant associated with priapism
•Mechanism of action not fully understood
•Not FDA approved for ED
•Side effects: drowsiness, dry mouth, sedation,
priapism

84. Medication
Apomorphine (Spontane)
•Dopaminergic mechanism with hypothalamic activity
•Sublingual administration
•64% to 67% response rate with ED
•Side effects: nausea, sweating, hypotension, yawning
•Awaiting FDA approval

85. Medication
Phentolamine (Vasomax)
•Alpha-blocker
•Relaxes smooth muscle tissue
•40% efficacy in mild organic ED
•Side effects: nasal congestion, tachycardia, dizziness,
hypotension
•Awaiting FDA approval

86. Surgery
1)Venous leakage:
2 approaches are adopted:
i) ligation of all veins draining to the penis i.e deep
dorsal,cavernosal & crural veins.
ii)ligation & division of the deep dorsal vein.
2)Arterial revascularization.
3)Peyronie’s disease: The Horton – Devine procedure.
: The Nesbit procedure.

87. 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

88. 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.

89. An innovative drug-delivery system –
nanoparticles encapsulating NO or prescription
drugs – shows promise for topical treatment of ED,
-Science Daily (Sep. 20, 2009)
A study done by Dr.Yoram Vadi in Nov 2009,
showed that 75% of men suffering from ED, treated
with shock-wave therapy showed a return of
erectile functioning.(release of VEGF- stimulates
the growth of new blood vessels in the genital
area).

90. Treatment of antidepressant-
induced sexual disorders
Drug holidays
Switching – mirtazapine, bupropion, nefazodone
Psychological interventions
Sildenafil
Others – dopamine agonists, cyproheptadine,
amantadine, buspirone

91. FEMALE SEXUAL AROUSAL DISORDERS:
DSM IV TR:
A.Persistent or recurrent inability to attain, or
maintain until completion of sexual activity,
an adequate lubrication swelling response.
B.Disturbance causes marked distress or
interpersonal difficulty.
C.Not better accounted for by another axis I
disorder not due to direct physiological affect
of drug or general medical condition.
Specify: lifelong/ acquired type, generalised/
situational, due to psychological factors or
combined factors.

92. ICD-10:
A.General criteria must be met-
G1- subject is unable to participate in a sexual
relationship as he would wish
G2- dysfunction occurs frequently but may be
absent on some occasions.
G3- The dysfunction has been present for at
least 6 months.
G4- The dysfunction not entirely attributable to
any of the other mental & behavioural
disorders, physical disorders, drug treatment.

93. B. There is failure of genital response, experienced as
failure of vaginal lubrication, together with
inadequate tumescence of the labia. Dysfunction
takes place one of the following forms:
1.General: lubrication fails in all relevant
circumstances
2.Lubrication may occur initially but fails to persist
for long enough to allow comfortable penile entry.
3.Situational: lubrication occurs only in some
situations (with one partner not another, during
masturbation, when vaginal intercourse is being
contemplated.

94. Women with excitement phase dysfunction often have
orgasmic problems as well.
May be associated with dyspareunia or lack of desire.
Studies shown 14-16% women having chronic lubrication
difficulties & 23% with intermittent problems.
Postmenopausal- 44%
Less research on physiological components of dysfunction
in women than men

95. Masters & johnson found normally responsive women to
desire sex premenstrually.
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.

96. Causes of female sexual arousal
disorder
Classified as:
1)Psychological domain.
2)Physical domain.
Psychological factors:
i)Impact of events during childhood
and adolescence.
- studies have shown some probative links
between chidhood sexual abuse &
sexual dysfunction in later life.

97. ii) Individual factors:
Stress & fatigability.
Over-exposure to pornography &
style media which is thought to lead to poor body
image, self- consciousness and lowered self esteem.
- Psychiatric disorders
like depression, anxiety, OCD, PTSD.
iii)Relationship factors:

98. Physical factors: 30-80% of the cases.
Circulatory & neurological disorders are the most
likely causes of sexual dysfunction.
i)Circulatory: HTN, CAD.
Damage to blood vessels decreases blood flow
damage to nerves in pelvic area diminishes arousal.
ii)General medical condition: Diabetes, Anaemia.
iii)Hormonal:
Low level of sex hormones , due to aging(menopause)
Thyroid dysfunction, disorders of adrenal gland etc.

99. iv)Recreational drugs: alcohol,smoking.
v)Medications:
Anti-depressants, Anti-psychotics, Sedatives,
Anti-hypertensives, OCPs &
Other hormone containing pills.
vi)Post baby coolness:
Extreme loss of lidido after childbirth.

100. 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, which results in dryness.

101. Persistent sexual arousal syndrome
in women
Infrequent,
distressing and perplexing not only because of its
mysterious onset, but also because of the feelings of
shame and discomfort that accompany the phenomenon.
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.

102. Interventions
1)PsychologicalTreatment
Education about anatomy,
Physiology and expectations.
couples therapy.
Masters & Johnson-sensate focus.
progressive levels of touching,
starting with non-sexual, sexual
and sexual intercourse.
CBT: uses thought records to capture the cognitions
that accompany emotions.

103. 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

104. 4)Hormonal:
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.

105. 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.

106. 6)Others:
i)Topical vasodilators: PGE1- increases genital arousal.
ii)Dopamine agonists – increases sexual interest, orgasm &
improves patient-partner sexual satisfaction.
7) Alternative medicine:
Natural estrogens such as soya products.
Belladona ,ginkgo biloba etc.
Prognosis:
Generally once a woman seeks the appropriate help they
are quite likely to find a way to resolve their problem.

107. 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.
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.

108. Thank u
Men look for youthfulness and physical attractiveness, smooth
complexion, optimum stature, and good physique, and they value
virginity and chastity. Partner variety is highly desired.
Women, look for high-quality mates with abundant resources and
emotional and financial status and security.