erectile dysfunction etiology and presentation urology

1. ERECTILE DYSFUNCTION-
Etiology, Presentation and
Diagnosis
By-dr sonu kumar plash
Moderator-dr kumar madhavan

2. Definition
ED is defined as “inability to attain
and/or maintain an erection sufficient
for satisfactory sexual intercourse”.

3. Tunica albuginea
Tunical covering of corpora cavernosa: bilayered with multiple sublayers.
Inner layer- circularly oriented.
Intracavernous pillars/struts
Outer layer- longitudinally oriented
Oblique fibers less abundant
Corpus spongiosum: single circular layer of tunica
Emissary veins-run obliquely between the layers.
Tunica absent in glans.

5. Arteries
3 types(droupy classification)
Type 1-paired internal pudendal artery(br of internal iliac
artery)
Type 2- int pudendal + accessory pudendal
artery(branches from obturator or femoral or external iliac
artery,or vesical)
Type 3 –mainly accessory pudendal artery.

6. Penile arterial supply
Paired Int pudendal artery
Cavernosal tumescence by
cavernosal artery
Dorsal artery-glans
engorgement
Bulbourethral artery.

7. veins
Peripheral sinusoids form venules beneath tunica albuginea.
Form Subtunical venous plexus
Exit as emissary veins from inner tunica layer
Emissary veins from the three corpora drains dorsally into deep dorsal veins
(originate near coronal sulcus)(serves as the primary venous drainage of the
glans and distal two-thirds of the corpora)-drains into periprostatic venous
plexus.
Additional venous drainage in circumflex vein laterally and periurethral
ventrally.

8. Physiology/mechanism of erection
Flaccid state-smooth muscles are tonically
contracted-only small amount of arterial flow to
corpora.
Flaccid penis-moderate state of contraction.
Erection-sinusoidal relaxation,arterial dilation,and
venous compression.

10. Sexual stimulation-neurotransmitter release from cavernous nerve terminals.
Smooth muscle relaxation.
Following events-
1)dilation of arteries and arterioles by increased blood flow in diastolic and systolic phases.
2)trapping of incoming blood by expanding sinusoids.
3) compression of subtunical venous plexuses,between peripheral sinusoids and tunica
albuginea-reducing venous outflow.
4)stretching of tunica to capacity occludes emissary veins.

11. 5)increase in po2 to 90 mmhg and intracavernous pressure to 100 mmhg(full erection phase).
6)further pressure increase due to reflex contractions of ischiocavernous (rigid erection phase).

12. Seven phases of erection and detumescence

13. Neurophysiology of erection
Innervation of penis is autonomic and somatic.
Autonomic pathway-cavernous nerves are branches of the pelvic plexus that innervate the
penis.
1)Thoraco-lumbar Sympathetic pathway -T10 TO L2- Superior and inferior hypogastric plexus-
stimulation causes detumescence
2)Sacral Parasympathetic(S2,S3,S4 )-stimulation of pelvic plexus and cavernous nerves-induces
penile erection.
Somatic pathway
Somatosensory-dorsal nerve of penis
Somatomotor-pudendal nerve.

14. Spinal and higher brain centers responsible for 3 types of erection.
1)psychogenic erection
Audiovisual stimuli or fantasy.
Brain impulse modulate spinal erection centres(T11-L2 and S2-S4)
2)Reflexogenic erection
Tactile stimulation of genital organs.
Impulses reach spinal erection centers –activate autonomic nuclei- send
message via cavernous nerves to induce erection.
Preserved in pts with upper spinal cord injury.
3)Nocturnal erection-During REM sleep mostly.

15. Neurotransmitters
Nitric oxide(NO) principal neurotransmitter mediating erection.
Released from NANC(Noradrenergic/Norcholinergic )neurons and endothelium.
NO activates cGMP production which relaxes cavernous smooth muscle.
NO from Nnos IN nitrergic nerves-initiation of erection.
NO from Enos –maintenance of smooth muscle relaxation and erection.

17. Neurotransmitters.
Flaccidity- norepinephrine, AT2,PGF2a, ET1.
Detumscence:- cessation of NO release, breakdown of CGMP BY PDEs, Sympathetic discharge
during ejaculation.

18. Smooth muscle physiology
Relaxation of cavernous smooth muscle is the key to penile erection.
NO enters smooth muscle cells and stimulates cGMP production.
cGMP activates protein kinase G(PKG).
PKG open potassium and closes calcium channels.
Low cytosolic calcium favors smooth muscle relaxation.
Erectile process.
CGMP degraded by phosphodiesterases(PDE)
Regained smooth muscle tone and detumescence.

19. Epidemiology
•The prevalence of ED increases with advancing
age.
>20 years of age prevalence rate of 10% to 20% worldwide, with the majority of studies
reporting a
rate closer to 20%.
Prevalence
1% to 10% < 40 years,
up to 15% - 40 to 49 years,
up to 30% - 50 to 59 years,
up to 40% - 60 to 69 years,
and 50% to 100% - 70 -90 years

20. Risk factors
Include poor health status/chronic disease states, vascular and metabolic diseases,
conditions of the nervous system, hormonal issues, medication use,
psychiatric/psychological disorders, substance abuse, and certain socio-demographic
factors.

24. Psychogenic
•Mental health issues (e.g., depression, psychosis) are
risk factors for ED. The prevalence of ED in men with a
range of mental health disorders may be as high as
83%.
Two possible mechanisms proposed to explain the inhibition of erection in
psychogenic ED:
(1) direct inhibition of the spinal erection center by the brain as an
exaggeration of the normal suprasacral inhibition.
(2) excessive sympathetic nervous system activation and/or elevated
peripheral catecholamine levels, which may increase penile smooth
muscle tone to prevent
relaxation.

25. Neurogenic
•Any disease, dysfunction,or injury (including surgical)
affecting the brain, spinal cord, or peripheral erectogenic
nerves (i.e., pudendal and cavernous) can induce ED.
•In the Brain- Parkinson disease, stroke, encephalitis,
temporal lobe epilepsy tumors, dementias (including Alzheimer
disease), multiple system atrophy, and traumatic brain injury
(TBI).

26. Neurogenic
•At the Spinal cord level-
•MC spinal cord injury but including spina bifida, disk
herniation, syringomelia, tumor, and multiple sclerosis,
are common causes of ED.
•Reflexogenic erection (in response to tactile
stimulation of the penis) is preserved in approximately
95% of patients with complete upper cord lesions and
approximately 25% of patients with complete lower
cord lesions.

27. Neurogenic
•AT PERIPHERAL NERVE LEVEL-
•Close relationship between cavernous nerves and the pelvic
organs, the incidence of iatrogenic impotence from pelvic surgical
procedures (e.g., radical prostatectomy, abdominoperineal
resection) is high, ranging up to 100% in some series.
•Nerve-sparing approaches have markedly improved erectile
outcomes, majority experience at least a temporary decline in
erectile function after surgery, and few recover completely to
baseline levels.
•Men with ED at baseline and older than 60 are at greater risk.

28. Neurogenic
•Pelvic fracture-ED secondary to either (or both) cavernous
nerve or vascular injury. In men with posterior urethral injury,
early realignment has been associated with better potency
preservation rate relative to delayed anastomosis (ED rate
34% vs. 42%).
•Diabetes may also cause ED via neurogenic or vascular
damage, either of which can impair NO release.
•Finally, age-related declines in penile tactile sensitivity may
contribute to ED by reducing sacral reflexogenic responses.

29. Endocrinologic
•Low serum testosterone (T) is a frequent finding in patients
with ED.
•The threshold level of T for normal nocturnal erections has
been reported at about 200 ng/dL , although many men
experience symptoms (including loss of nocturnal erections) at
levels of less than 320 ng/dL.
•Low libido is the most common sexual symptom of low T.
•Importantly, many men with low T levels are asymptomatic.
•The Endocrine Society recommends that T supplementation
be considered only in the context of at least two clearly low
morning serum T levels and symptoms clearly referable to low

30. Endocrinologic
•Any dysfunction of the hypothalamic-pituitary axis can result in low serum
T.
•Hypogonadotropic hypogonadism can be congenital or caused by a
tumor or injury of the hypothalamus or pituitary gland.
•Hypergonadotropic hypogonadism may result from a tumor, injury,
testicular surgery, or severe orchitis.
•High levels of serum prolactin are associated with loss of libido, ED,
galactorrhea, gynecomastia, and infertility.
•Hyperprolactinemia is associated with low serum T, which is thought
to be related to inhibition of gonadotropin-releasing hormone
secretion at the level of the hypothalamus.

31. Endocrinologic
•ED may also be associated with hyperthyroidism and
hypothyroidism.
•Hyperthyroidism is commonly associated with diminished libido
(which may be caused by the increased circulating estrogen
levels) and less often with ED.
•In hypothyroidism, low testosterone secretion and elevated
prolactin levels may contribute to ED.

32. Arteriogenic
•Atherosclerotic or traumatic arterial occlusive disease of the
hypogastric-cavernous-helicine arterial tree can decrease the
perfusion pressure and arterial flow to the sinusoidal spaces.
This has the effect of increasing the time to maximal erection
and decreasing rigidity of the erect penis.
•Usually component of a generalized atherosclerotic
process.
•Common health factors associated with penile arterial
insufficiency include hypertension, hyperlipidemia,
tobacco use, diabetes mellitus, blunt perineal or pelvic
trauma, metabolic syndrome, sedentary lifestyle, obesity,
and pelvic irradiation.

33. Arteriogenic
•Cardiovascular Diseases. ED is highly prevalent in men with coronary,
cerebral, and peripheral vascular disease.
•In one study of men with CAD, ED preceded CAD in 93% of cases at a
mean time interval of 2 years.
•ED- early indicator of systemic endothelial dysfunction and an
indication for cardiac risk stratification.
•ED is common in hyperlipidemia.
•Obesity. High body weight, BMI, and total body fat percentage are
independently associated with greater prevalence of moderate to severe
and complete ED.

34. Arteriogenic
•Hypertension- independent risk factor for ED.
•Older age, longer duration of disease, greater
severity of hypertension, and the use of
antihypertensive medications, some of which
may themselves contribute to ED.

35. Mechanism of Vascular Erectile Dysfunction:
•Enhanced Smooth Muscle Contraction and Vasoconstriction:- Increased
RhoA/Rho-kinase activity leading to increased contractility of the corporeal smooth
muscle has been linked to ED in diabetes ,hypercholesterolemia, hypertension
,hypogonadism , cavernous nerve injury, and aging.
•Endothelin-1 -elevated in men with atherosclerosis, hypertension, and
hypercholesterolemia. Men with organic ED have higher venous and cavernous blood
levels of endothelin-1 as well.
•Angiotensin II may restrict corporal vasodilation by action on the AT1 receptor. AT1
receptor antagonists and angiotensin-converting enzyme (ACE) inhibitors have shown
promise in the treatment of men with ED and hypertension and men with ED and
atherosclerosis, respectively.

36. Mechanism of Vascular Erectile
Dysfunction:
•High adrenergic tone (related to medical or psychological
issues) may lead to insufficient trabecular smooth muscle
relaxation. This has the effect of not only reducing arterial
inflow but also impairing coaptation of the emissary veins by
expanding corporal sinusoids.
•Impaired Endothelium-Dependent Smooth Muscle
Relaxation. Impairment of endothelium-dependent relaxation
in hypertensive animal models has been ascribed to
angiotensin II, thromboxane, superoxide, and direct effects of
increased vascular pressure.

37. Corporal Structural Defects/cavernous(vasculogenic)
•Failure to restrict venous outflow from the penis during erection is
one of the most common causes of vasculogenic ED.
•Veno-occlusive dysfunction may result from degenerative tunica
changes, fibroelastic structural alterations, insufficient trabecular
smooth muscle relaxation, and venous shunts.
•Degenerative changes (e.g., tissue senescence, diabetes) or
traumatic injury to the tunica albuginea (e.g., penile fracture) can
impair the compression of the subtunical and emissary veins.

38. Corporal Structural Defects/Cavernous/vasculogenic
•Endothelium-source of NO and other signaling molecules.
•Disruption of endothelial function- early indicator of
vascular disease.
•Diabetes and hypercholesterolemia alter function of
endothelium-mediated relaxation of the cavernous
muscle and impair erection.

40. Drug induced.
•Medical therapy is commonly associated
with self-reported ED.
ANTIHYPERTENSIVE AGENTS
•Almost all antihypertensive drugs have
ED listed as a potential side effect.

44. Aging,systemic disease and other causes
•There is a progressive decline in sexual function in healthy aging men.
•Greater latency to erection, less turgidity, decreased force and volume of
ejaculation, a longer refractory period, reduced penile sensitivity, and reduced
nocturnal erections are commonly reported with increasing age.
•The cause is incompletely understood- Heightened cavernous muscle
tone,age related decline in serum androgens. impaired endothelial
function, accelerated NO degradation, increased PDE activity, inhibition of
NOS activity by endogenous NOS inhibitors, increased arginase activity,
increased production of RoS, inflammatory reactions, decreased
endothelial progenitor cell number and function, and impaired telomerase
activity or telomere Shortening.

45. Diabetes mellitus
ED- 3 times more common in men with diabetes (28% vs. 9.6%)
-Present at an earlier age.
-Prevalence of ed increases with duration of dm
-14-fold higher risk of coronary artery disease, and cardiac
mortality in men with diabetes.
Mechanism- disruption of penile arterial circulation , reduced androgen
secretion, peripheral neuropathy, impaired endothelium-dependent
relaxation of the corporeal smooth muscle, loss of smooth muscle
structure and activity, endothelial apoptosis, and oxidative stress.

46. Metabolic syndrome
Constellation of glucose intolerance, insulin resistance,
dyslipidemia, and hypertension.
Independent risk factor for ED,prevalence of ED
increases as the number of metabolic syndrome
components increases.
MetS is associated with aging and decreased serum
testosterone levels.
MetS has also been associated with elevated levels of
estrogen, impaired endothelial function and increased systemic
inflammation.

47. Chronic renal failure
Up to 80% of men with end-stage renal disease manifest evidence of
arterial and veno-occlusive ED.
Due to decreased production and/or reduced bioavailability of endogenous NO,
calcification of pudendal arteries, and decreased endothelial reactivity.
Depressive symptoms is also an independent factor predicting sexual dysfunction in male
hemodialysis Patients.
 Significant improvement of sexual function may occur after kidney transplantation.

48. Others
HIV appears to be a direct cause of ED; men with HIV also
experience substantial stress (fear of virus transmission,
changes in body image, HIV-related comorbidities, infection
stigma, obligatory condom use), which may contribute to
psychogenic ED.
Hyperuricemia- Elevated serum uric acid has been linked to worse
erectile function in men.

49. Primary erectile dysfunction
Lifelong inability to initiate and/or maintain erections beginning
with the first sexual encounter or masturbation.
Primary psychological ED is often related to anxiety about sexual performance stemming from
adverse childhood events, traumatic early sexual experience, or misinformation.
Maldevelopment of the penis or its blood/nerve innervation may also lead to primary ED.
Micropenis- defined as symmetrical hypoplasia of the phallus and is often related to urethral
developmental abnormalities such as hypospadias and epispadias or endocrine deficiency. The
erectile tissue in such cases often functions normally; sexual dysfunction usually relates to lack of
penile length or the degree of chordee, rather than to ED.
Vascular abnormalities- hypoplasia of the cavernous arteries or veno-occlusive dysfunction
because of aberrant cavernous venous drainage.
Treatment in most cases is vascular surgery or implantation of a penile
prosthesis.

50. DIAGNOSTIC EVALUATION
The cornerstone in the evaluation of ED
involves a detailed case history, preferably
taken from patient and partner, physical
examination, and proper laboratory tests.

51. The original National Institutes of Health definition did not
specify a parameter for the duration of symptoms to accept the
diagnosis. Subsequent organizational statements did apply a
3-month interval as a minimal requirement diagnostically,
except for in cases of trauma or surgically induced ED.

53. Sexual history
Objectives of the interview are also to delineate the problem according to such features as
its onset, duration, conditions, severity, and cause.
The conditions of the problem are often determined by reviewing circumstances that
facilitate or hinder erectile function.
Circumstances for achievable erections include stimuli used during sexual encounters, erections
on awakening, and the role of self-stimulation. Circumstances associated with erectile difficulty
include performance anxiety, inability to perform with a designated partner.

54. Medical history
The medical history primarily identifies and evaluates predictors and risk factors associated with
ED. The main objective is to explore the role of possibly related or underlying medical
conditions and to ascertain the existence of comorbidities.

55. Psychosocial history
the presence and interaction of mental health
problems, emotional stressors, and interpersonal
relationship difficulties, past and present, should be
ascertained. Additional questions may be asked
relating to occupational status, financial security, family
life, and social support, which may also influence
sexual function.

56. Physical examination
consists of basic anthropometrics (i.e.,
height, weight, waist circumference),
assessment of body habitus (appearance of
secondary sexual characteristics), and
examination of relevant body parts pertaining
to cardiovascular, neurologic, and genital
systems, with a particular focus on the
external genitalia.

57. Questionnaires and Sexual Function Symptom Scores
The most widely used –International Index of Erectile
Function (IIEF).
The Brief Male Sexual Function Inventory (BMSFI).
The Center for Marital and Sexual Health Sexual Functioning
Questionnaire.
The Changes in Sexual Functioning Questionnaire.
The Erectile Dysfunction Inventory of Treatment Satisfaction
(EDITS).

58. IIEF
Contains 15 items that address and quantify five domains (erectile
function, orgasmic function, sexual desire, intercourse satisfaction, and
overall satisfaction) is the most widely used questionnaire.
Do not distinguish etiological basis of ED.
An abridged five-item version of this instrument, the
IIEF-5, has been useful to clinicians in routine clinical practice.
The instrument classifies ED severity into five categories:
severe (5 to 7), moderate (8 to 11), mild to moderate (12 to 16), mild (17 to
21), and no ED (22 to 25).

59. Laboratory Tests
Recommended laboratory tests for men with sexual problems
typically include serum chemistries, fasting glucose or HbA1c,
complete blood count, lipid profile, and serum total testosterone.
Total testosterone- morning-time blood draw, screens androgenic status,
and, if abnormally low, serum-free (or bioavailable) testosterone and
luteinizing hormone (LH) should be measured.
Prolactin measurement may also be done for hormonal assessment.
Thyroid function tests may be performed at the clinician’s discretion.

60. SPECIALIZED EVALUATION AND TESTING

61. VASCULAR EVALUATION-
Combined Intracavernosal Injection and Stimulation-
First line evaluation of penile blood flow.
Involves the intracavernosal injection of a vasodilatory drug as a
direct pharmacologic stimulus, combined with genital or audiovisual
sexual stimulation, and the erectile response is observed and rated
by an independent assessor.
The test is designed to bypass neurologic and hormonal influences
involved in the erectile response and allows the clinician to evaluate
the vascular status of the penis directly and objectively.

62. Combined Intracavernosal Injection and Stimulation-
Intracavernosal injection of Vasodilator.-Alprostadil 10 to 20
microgram(synthetic PGE1),Bimix 0.3 ml (Papaverine(non specific
PDE-i)+phentolamine(non specific alpha antagonist) Or Trimix 0.3
ml- Alprostadil+ papaverine+ phentolamine.
27-29 gauge needle inserted at lateral base of penis directly into
corpus cavernosum.
Phenylephrine inj (500 microgram/ml) if no detumescence in an
hour.
Normal cis test-rigid erection-means normal erectile
haemodynamics-alternative diagnosis of psychogenic,neurogenic,or
endocrinologic ED may then be considered.

63. Duplex usg
Duplex ultrasound of the penis after pharmacostimulation or CIS
represents second-line evaluation of penile blood flow.
Most reliable and least-invasive diagnostic modality for assessing ED.
Uses high-resolution (7.5 to 12 MHz) real-time ultrasonography and
color-pulsed Doppler, which helps visualize the dorsal and cavernous
arteries selectively.
Flow velocities are measured at baseline before injection and commonly
every 5 minutes afterward up to 20 minutes.

64. Duplex usg
Cavernous arterial insufficiency is suggested when PSV is less
than 25 cm/s; a PSV consistently greater than 35 cm/s defines
normal cavernous arterial inflow.
Veno occlusive dysfunction is suggested when-persistent high psv,High end
diastolic velocity(EDV), Rapid detumescence.
Resistive index(RI)=(PSV-EDV)/PSV; RI< 0.75 asso with veno occlusive
dysfunction(Normal >0.9).

65. Dynamic infusion cavernosometry-cavernosography
3rd line for vascular integrity of penis.
DICC-Evaluation of penile venous outflow system.
-indication-pelvic/perineal trauma-suspected site specific leak,primary/lifelong
ED.
When used, it generally precedes consideration for corrective
penile vascular surgery.
Intracavernosal inj- 2 needles placed –simultaneous saline infusion and
intracavernosal pressure monitoring after intracavernosal pharmacologic
injection.

66. Veno occlusive disease- when failure to increase intracavernosal pressure to
mean SBP or rapid drop in pressure on stopping infusion.
With normal veno-occlusive function, there should be opacification of the
corpora cavernosa with minimal or no visualization of venous structures
or corpus spongiosum.
Cavernosography- to show site of venous leakage.
Dynamic infusion cavernosometry-cavernosography

68. Penile angiography
3rd line.
Reserved for young patient with ED secondary to a traumatic arterial disruption or
with a history of penile compression injury who is being considered for penile
revascularization surgery.
Selective cannulation of the internal pudendal artery and injection of
radiographic contrast.
The intracavernosal injection of a vasodilating agent is optimally used to
induce maximal vasodilation of the penile arterial supply.
The anatomy and radiographic appearance of the iliac, internal
pudendal, and penile arteries are then evaluated and documented.

70. Historical and Investigational Studies of Penile Blood Flow
1. Penile Brachial Pressure Index
2. Penile Plethysmography (Penile Pulse Volume Recording)
3. Radioisotopic Penography
4. Penile Magnetic Resonance Imaging
5. Penile Near Infrared Spectrophotometry
6. Cavernous Smooth Muscle Content

71. Psychophysiologic Evaluation
Not 1st line.
-to assess the erectile response by applying techniques that directly
measure penile tumescence and rigidity.
-Primarily to differentiate psychogenic from organic ED.
-Documentation of a full erection indicates functional integrity of the
neurovascular axis regulating penile erection and thereby raises
suspicion of a psychogenic cause.
-Technical and cost limitations.

72. Nocturnal penile tumescence and rigidity (NPTR)
testing
-Assessment of physiologic erectile ability.
Uses nocturnal monitoring devices that measure the number of episodes,tumescence
(circumference change by strain gauges), maximal penile rigidity, and duration of nocturnal
erections.
Documentation of REM sleep is important.
The conventional approach is to perform monitoring in conjunction with EEG, electro-
oculography, and electromyography (EMG), with nasal airflow and oxygen saturation to document
rapid eye movement (REM) sleep and the presence or absence of hypoxia (sleep apnea).
Performed for 2-3 night.
RigiScan is an automated, portable device used for NPTR, which combines the monitoring of
radial rigidity, tumescence, number, and duration of erectile events. The device employs two loops,
one placed at the base of the penis and the other placed at the coronal sulcus (respectively, base
and tip recording sites), and these loops record penile tumescence (circumference) and radial
rigidity with timed, standardized constrictions of the loops.

73. Rigiscan

74. NPTR
A baseline initialization is performed with the patient in the
office, and then it is calibrated for home use. At home,
registrations of penile rigidity are done every 3 minutes and
increased to every 30 seconds when the base loop detects a
circumference increase of greater than 10 mm.
Recommended criteria for normal NPTR include four to
five normal erectile episodes per night,mean duration >30
mins,increase in circumference > 2 cm at tip and > 3 cm at
base,maximal rigidity > 70% at tip and base.

75. Rigiscan

76. Audiovisual and vibratory stimulation
Erotic stimulation by explicit videotape material with monitoring
has been used as a reliable as well as a time- and cost-effective
alternative to NPTR for differentiating between organic and
psychogenic ED presentations.
It is also considered more physiologic, consistent with erectile
behavior when awake.

77. Psychological evaluation
These aspects should not be underestimated.
ED associated with anxiety,depression,low self esteem,negative outlook
on life,emotional stress,fear of failure,performance anxiety,loss of
attraction for the sexual partner,adjustment to chronic illness or surgery
and relationship conflicts.

78. Neurologic evaluation
Reserved usually for research protocols and medicolegal investigations.

79. Hormonal evaluation
Serum testosterone
Serum gonadotrophin
Serum prolactin
Mri imaging of pituitary
Serum thyroid function tests

80. Serum testosterone
Low testosterone in 2%-33% men with ed
Aging-primary cause of declining androgens
Circulates in three fractions-
Free (0.5% to 3%)
SHBG bound (30%)
Albumin and other serum protein bound(67%)
Bioavailable testosterone= free + albumin bound

81. Best indicator of androgen status is calculated bioavailable testosterone(free testosterone and
albumin bound testosterone).
For Screening purposes-total testosterone
Total testosterone reference range -:280-1000 ng/dl
7 am to 11 am
Low normal or low- repeat for confirmation

82. Serum gonadotropins
Before second total testosterone- LH,FSH, and Prolactin.
Helps to Localize the source of hypogonadism.
Primary hypogonadism(testicular failure):low testosterone, increased LH AND FSH.
Secondary hypogonadism(central cause): normal or low LH and FSH with low testosterone.

83. Serum prolactin
Hyperprolactinemia causes hypogonadism by suppression of GnRH from the hypothalamus
which impairs the pulsatile LH secretion required for testosterone production by the gonads.
Also interferes with conversion of testosterone to DHT
Hyperprolictinemia Suspected when low testosterone with low or inappropriately normal LH
Hyperprolactinemia causes : antipsychotics,TCA,Opiates
,prolactinoma,hypothyroidism,hypothalamic lesions,renal insufficiency,cirrhosis,chest wall
lesions.

84. MRI pituitary indications
Severe central (hypogonadotropic) hypogonadism: testosterone <150 ng/dl
Suspicion of pituitary disease (pan hypopituitarism, persistent hyperprolactinemia, tumor mass
effect symptoms.

85. Serum thyroid function tests.
Hyperthyroidism causes ED by increasing aromatization of testosterone into estrogen (which
raises levels of SHBG) or by increasing adrenergic tone(which causes smooth muscle contractile
effects or exerts psychobehavioral effects).
Hypothyroidism- low testosterone secretion,elevated prolactin contribute to ED.

86. THANKYOU