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Clinical Medicine 3 > Lecture 12 (GU)-Exam 4 > Flashcards

Lecture 12 (GU)-Exam 4 Flashcards

1
Q

What are the most common causes of male mortality (all ages)

A
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2
Q

Death in men:
* Do they die earlier or later in life than women? Why is that?
* What do men tend to do? (2)
* Age gap leading to death is what?
* Men are less likely to do what?
* men also largely define themselves by what?

A
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3
Q

Regulation of Testosterone & Sperm Production
* What does FSH stimulate?
* What does LH stimulate?
* What is LH close to? What do they contain?

A
  • FSH stimulates Sertoli cells to help spermatogenesis.
  • LH stimulates Leydig cells, which make testosterone. They are 5% of testicular volume.
    * Close proximity to seminiferous tubules so local testosterone levels high
    * They contain sertoli cells that support sperm production
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4
Q

Regulation of Testosterone & Sperm Production
* Testicular insults may show up when?
* What is the normal sperm count?

A
  • Testicular insults may not show up as reduced sperm levels for several months.
  • Normal sperm count 20-200 million sperm/ ml
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5
Q

Regulation of Testosterone & Sperm Production
* Testosterone is aromatized where?
* What changes testosterone to dihydrotestosterone?
* What does ^ this cause?
* Some circulating testosterone is bound what?
* What is finasteride?

A
  • Testosterone is aromatized in fat tissue, liver, etc., to estrogen.
  • 5 alpha-reductases change testosterone to dihydrotestosterone .
  • The latter causes development of male external genitalia, prostate, seminal vesicles, and male hair pattern.
  • Some circulating testosterone is bound to albumin and other proteins
  • Finasteride targets 5 alpha-reductase in BPH treatment

DHTTN – have actual affect on the body

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6
Q

What are the phases of sexual life (plamsa testosterone) in males?

A
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7
Q

Phases of Male Sexual Life
* When does bioavailable testosterone cont. begin to decline?
* What is the total testosterone level in elderly?
* What also declines?

A
  • Beginning at about age 40, mean plasma bioavailable testosterone concentrations decline gradually;
  • Although statistically lower than levels in young men, concentrations of total testosterone usually remain within normal range, even in elderly men. (total includes the bound Testosterone)
  • In older men seminiferous tubule function & sperm production also usually decline.
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8
Q

Phases of Male Sexual Life
* What is often slight elevated?
* What plays a role in development of prostatic hyperplasia & in development of gynecomastia in aging men?

A
  • Plasma LH and FSH levels are often slightly elevated, consistent with a decline in gonadal function.
  • An increase in conversion of androgen to estrogen in peripheral tissues
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9
Q

Phases of Male Sexual Life
* What happens with erection?
* What happens with actual degree of erection?
* What happens with intensity of orgasm?
* What happens with Refractory period?

A
  • Time before an erection is achieved often increases for older men.
  • Actual degree of erection is often less, or full erection is achieved later during a sexual response, in older men.
  • Intensity of orgasm may decrease in older men.
  • Refractory period after orgasm typically increases as men age.
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10
Q

Androgen Deficiency
* What are come causes?
* Leads to the decrease of what?

A

Etiology
* Testicular Failure (Primary Hypogonadism)
* Hypothalamic-pituitary Defects (Secondary Hypogonadism)

Leads to decrease in one or both of the two major functions of the testes: sperm production or testosterone production

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11
Q

Primary or Hypergonadotrophic Hypogonadism
* What is low?
* What is high?
* What is more damaged?

A
  • Testosterone & sperm count low
  • High level of FSH & LH
  • Sperm count is more damaged than testosterone levels.

Pance Pearls: Decrease fucntion of leydig cells (decreased testosterone synthesis), seminiferous tubule dysfunction, alcoholic liver disease

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12
Q

Secondary or Hypogonadotrophic Hypogonadism
* What is low?
* What is low or normal?
* What is proportional?

A
  • Testosterone & sperm count low
  • Low or normal levels of FSH & LH
  • Sperm count level is proportional to testosterone levels

Disorder of the pituitary glnd or the hypothalamus (eg. pituitary adenoma, craniopharyngioma). Affects both spermatogenesis and leydig function

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13
Q

Clinical Findings of Androgen Deficiency
* What are general findings (4)?
* Public hair?
* What are testes and scrotum findings?

A

General
* Loss of libido
* High-pitched voice (if pre-pubertal)
* Smooth skin
* Decreased hair

Pubic hair
* Loss of pubic hair

Testes & scrotum
* Small & soft testes
* Small penis & scrotum
* Loss of erection & ejaculation
* Subfertility

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14
Q
A
  • Adolescents: Failure to undergo or complete puberty (decreased secondary male characteristics)
  • Adults: decreased libido, energy, body hair, muscle mass; osteoporosis, gynecomastia, infertility
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15
Q

Clinical Findings of Androgen Deficiency
* What can happen to skeletal and muscle?

A
  • Eunuchoid (if pre-pubertal or castrated) habitus (gynecomastia, excess growth distally in epiphyses that fuse later because of lack of sex steroid influence)
  • Decreased muscle bulk & power
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16
Q

What is the most common cause of primary hypogonadism?

A

Klinefelter’s Syndrome

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17
Q

Klinefelter’s Syndrome
* Due to the presence of what?
* What is present?
* What levels are low?
* What levels are high?
* Each extra X chromosome reduces what?

A
  • Due to presence of one or more X chromosomes (usually a 47 XXY karyotype)
  • Azoospermia present
  • Testosterone levels low
  • Gonadotropins ↑ (FSH > LH)
  • Each extra X chromosome reduces overall IQ by 15-16 points, with language most affected, particularly expressive skills.
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18
Q

Klinefelter’s Syndrome
* What are the variants?

A

Variants include 48XXYY, 48XXXY, 49XXXXY. These variants tend to have much lower IQ & other congenital abnormalities

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19
Q

Klinefelter’s Syndrome:
* What happens with fertility?
* What is common?
* What decreases?
* What type of pubic hair pattern?
* What happens to the limbs and hips?
* _ disabilities

A
  • Infertility
  • Gynecomastia common(20 x risk of breast cancer)
  • Decreased facial hair
  • Female-type pubic hair pattern
  • Eunuchoid habitus long arms & legs, wide hips
  • Learning disabilities
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20
Q

Klinefelter’s Syndrome
* They have small what?
* Increase risk for what? What screening should be done?

A
  • Testes small
  • Increased risk for testicular tumors: patient should have screening with beta-HCG and alpha-fetoprotein levels before age 25
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21
Q

Klinefelter’s Syndrome
* Hypogonadism can be treated with what?
* No increase in what preference?
* What is unlikely to improve?
* Successful fertility has been achieved with what?

A
  • Hypogonadism can be treated with testosterone
  • No increase in homosexual preference compared to peers
  • Hormone replacement unlikely to improve other abnormalities.
  • Successful fertility has been achieved with assisted reproductive technologies in some cases, but there are important genetic implications of these procedures.
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22
Q

Causes of Primary Hypogonadism
* What are the aquired primary testicular failure? (think infections, damage and systemic diseases?

A

Mumps orchitis: more common manifestation when occurs in adulthood than in childhood[median age-29]. Testicular involvement causes painful swelling of the testes followed by atrophy (seminiferous tubules, Leydig cells) OR return to normal function, unilateral-70%.

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23
Q

What are Other Acquired Causes of Primary Testicular Failure

A
  • Malnutrition
  • AIDS
  • Renal failure
  • Liver disease
  • Myotonic dystrophy
  • Paraplegias
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24
Q

What are toxin causes of Primary Testicular Failure

A
  • Alcohol
  • Marijuana
  • Heroin
  • Methadone
  • Lead
  • Antineoplastic & chemotherapeutic agents
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25
Q

Secondary Hypogonadism
* What levels are low?

A

Levels of both testosterone & gonadotropins (FSH/LH) are low
AKA Hypogonadotropic hypogonadism

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26
Q

Causes of Secondary Hypogonadism: Kallmann’s Syndrome
* Impairment of what?
* What are low levels?
* Associated with what?
* What type of loss?
* What type of blindness?
* Common cause of hypogonadism in who?

A
  • Impairment of synthesis & /or release of gonadotropin-releasing hormone(GnRH)
  • Low levels of LH & FSH
  • Associated with anosmia
  • Neurosensory hearing loss
  • Red-green color blindness
  • Common cause of Hypogonadism in females
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27
Q

Prader-Willi Syndrome:
* What is it?
* Stems from what?

A
  • Idiopathic hypogonadotrophic hypogonadism associated with mental retardation, obesity & short stature.
  • Stems from partial paternal chromosome 15 deletion
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28
Q

Pance pearls

Prader-Willi Syndrome
* What are the clinical manifestations in neotates, early childhood and later childhood/adolescence

A
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29
Q

What are other Causes of Secondary Hypogonadism

A
  • Cushing’s Syndrome
  • Congenital adrenal hyperplasia
  • Hemochromatosis
  • Hyperprolactinemia: Pituitary Adenoma & Drugs such as phenothiazines
  • Destruction of pituitary gland by tumors, infection, trauma or metastatic disease
    * Causes disturbances in the production of other pituitary hormones
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30
Q

Hyperprolactinemia
* What can it be caused by? (2)

A
  • Pituitary Adenoma
  • Drugs such as phenothiazines
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31
Q

Clinical Features of Androgen Deficiency
* What are the features before onset of puberty?

A
  • Failure of sexual maturation
  • Eunuchoid proportions: arm span 2 cm greater than height suggests that androgen deficiency occurred before epiphyseal fusion
    * Infantile amount & distribution of body hair
    * Poor development of skeletal muscles
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32
Q

Clinical Features of Androgen Deficiency:
* What are the features after the onset of puberty?

A
  • Diminished libido, sexual function, general strength & energy level
  • Decreased rate of beard growth
  • Gynecomastia & small or soft testes
  • “Male Menopause”: ADAM syndrome (Androgen Deficiency in the Aging Male)
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33
Q

Metabolism of testosterone:
* Where does testosterone come from?
* What is testosterone converted into?

A
  • 25% of Testosterone comes from ovaries/testes, 25% from adrenals, and 50% come from androstenedione produced by both above.
  • Testosterone is either converted into dihydrotestosterone (DHT) by the 5-alpha-reductase enzyme present in hair follicles
  • Or converted into estradiol by the aromatase enzyme present in adipose tissue.
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34
Q

Dx tests:
* What can help to figure out the difference between primary and secondary hypogonadism?

A

Levels of LH & FSH can be used to differentiate between primary (increased LH, FSH) & secondary hypogonadism (decreased gonadotropins); testosterone level should also be drawn to aid in differentiation.

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35
Q

Diagnostic Tests
* Males without true androgen deficiency may have what?

A

may have isolated testosterone levels that are below normal range during day, particularly in afternoon; hence you also need to draw the testosterone level.

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36
Q

Treatment of Androgen Deficiency
* What do you need to replace?
* What does it restore? (3)

A
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37
Q

Treatment of Androgen Deficiency
* What do you do for disorders in which hypogonadism occurred prior to puberty?
* What is the principal goal?
* Testosterone is what?

A
  • Increasing doses of testosterone for disorders in which hypogonadism occurred prior to puberty
  • Restore testosteron level to normal range (300-1000)
  • Testosterone is a controlled substance (schedule III) due to abuse potential
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38
Q

Testosterone:
* What is the parenteral administration?
* What is the principal goal?
* What are the daily application options?

A
  • Parenteral administration of a long-acting testosterone ester(100-200 mg testosterone inundate at 1-to 3- week intervals)
  • Principal goal: restore testosterone level to normal range (300-1000 ng/dL)
  • Daily application of transdermal testosterone patches or gel
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39
Q
A
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40
Q

Side Effects of Androgens
* At physiologic replacement doses, testosterone esters have few what? What should you always discuss though?
* What happens when supraphysiologic doses (Abuse)?

A

At physiologic replacement doses, testosterone esters have few toxic effects in mature men.
* Should always discuss Hypercoagulability with patient

Supraphysiologic doses - abuse
* Gonadotropin secretion inhibited (negative feedback loop effect)
* Testes shrink
* Sperm count falls
* Infertility

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41
Q

Anabolic Steroid Abuse- Male
* What are other sxs?

A
  • Acne
  • Aggressive behavior
  • Fits of rage
  • “Body builder physique”
  • Abnormal LFT’s
  • High levels of LDL & low levels of HDL
  • Small testicles
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42
Q

Side Effects of Androgens
* What are sxs that can happen in older men? (5)

A
  • Polycythemia (hematocrit >52%)->Hypercoagulability (PE)
  • Initiate or worsen symptoms sleep apnea
  • Should be screened for prostate cancer before initiating androgen replacement
  • May lead to edema in patients with underlying heart disease or renal failure
  • May promote growth of & intensify pain from carcinomas of prostate & breast in men

Androgens make cancer grow.

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43
Q

Hypogonadism in Females:
* What are common causes of primary hypogonadism?
* What are some common causes of secondary hypogonadism?

A
  • Turner Syndrome are common causes of primary hypogonadism
  • Hyperprolactinemia or Anorexia Nervosa or Kallman Syndrome are common causes of secondary hypogonadism
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44
Q

Hypogonadism in Females
* Hyperprolactinemia can be what?
* Hyperprolactinemia and anorexia can be treated with what?
* What does kallman respond to?

A
  • Hyperprolactinemia can be physiologic (pregnancy or stress) or pathologic (HPA axis disease or pituitary adenomas
  • Hyperprolactinemia and anorexia can be treated with Dopamine agonists such as carbergoline (Dostinex) or bromocriptine (Parlodel)
  • Kallman responds to hormone replacement therapy
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45
Q

Turner Syndrome
* What type of disease is this? Occurs only in who?
* What does it lead to?
* What is a common clinical sign?

A
  • Autosomal Dominant (45X) and only occurs in females
  • Hypergonadotrophic hypogonadism
    * Gonadal Dysgenesis leading to absence of ovarian oocytes and follicles
  • Webbed neck is a common clinical sign
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46
Q

Turner syndrome
* What are the hypogonadism issues?
* What does the physical exam show?
* What does the cardiovascular exam show?

A
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47
Q

Male Infertility
* Not an what?
* Inability to do what?
* Common problem or not?
* Couple is considered to be infertile if there has been no pregnancy after how long?
* Estimated 30% of all fertility is due what?

A
  • NOT an impotence
  • Inability to conceive or to cause pregnancy
  • Common problems in as many as 10% of all marriages
  • Couple is considered to be infertile if there has been no pregnancy after 1 to 1½ years of unprotected sexual intercourse (intercourse occurring no less than 3 times a week)
  • Estimated 30% of all fertility is due to “male” factor
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48
Q

Etiologies of Male Infertility
* Scondary impairment of spermatogenosis by what?
* How does spermatogenic tubule dysfunction cause infertility?
* Immotile what?

A
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49
Q

Etiologies of Male Infertility: ejaculatory obstruction
* What are the congenital and acquired causes?

A

Congenital
* Cystic fibrosis
* In utero DES exposure
* Idiopathic

Acquired
* Previous surgery: inguinal, scrotal, retroperitoneal, bladder neck, vasectomy
* TB
* Leprosy
* GC

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50
Q

Other Etiologies of Male Infertility
* Hx of what?
* Defects of what?
* Disorders of what?
* What type of toxins?
* Abusing what?
* What type of systemic illness?

A
  • History of mumps, testicular injury, VD, exposure to x-rays or any urological surgical procedure
  • Defects of androgen receptor
  • Disorders of sperm transport
  • Radiation, chemotherapeutic agents & environmental toxins
  • Androgen abuse can lead to testicular atrophy & a low sperm count
  • Systemic illness especially chronic hepatic & renal disease
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51
Q

Clinical features: Male infertility
* Evidence of what?
* What can be abnormal? What can be present?
* When seminiferous tubules are damaged prior to puberty, what can happen?
* Postpubertal damage causes what?
* Hx of what?

A
  • Evidence of hypogonadism
  • Testicular size & consistency may be abnormal, Varicocele may be present
  • When seminiferous tubules are damaged prior to puberty, testes are small & firm
  • Postpubertal damage causes testes to be soft
  • History of Varicoceles or cryptorchidism?
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52
Q

Clinical Features: male infert
* What is the key dx test?
* What are the normal findings of sperm count, motility, sperm morpholgy?

A

Key diagnostic test is a semen analysis

Normal Findings
* Sperm count: 20-200 million/ml
* Sperm motility: 60%-80% actively mobile
* Sperm morphology: 70%-90% normal shape

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53
Q

Clinical Features
* Sample should be collected when?
* What is stress pattern?
* What is oligospermia? What motility percentage associated with infertility?
* Testosterone levels should be measured when?

A
  • Sample should be collected after 2-3 days of sexual abstinence
  • “Stress pattern”: > 20% have abnormal appearance & sperm count low. May indicate presence of varicocele or recent febrile illness
  • Sperm counts of < 20 million/ml (oligospermia), with a motility of < 40% are associated with infertility
  • Testosterone levels should be measured if sperm count is low on repeated exam or clinical evidence of hypogonadism
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54
Q

Cryptorchidism
* What is the definition?
* What can be one cause?
* If one testis is undescended-sperm count will be what?
* If both testes are undescended, sperm count will be what?
* Increased risk of what?

A
  • Definition: Incomplete descent of testis from abdominal cavity into scrotum by age of 1 year
  • Etiology unknown but gonadotropin deficiency in utero appears to be one cause.
  • If one testis is undescended-sperm count will be subnormal in 25-33%.
  • If both testes are undescended, sperm count will be severely subnormal & serum testosterone may be reduced.
  • Increased risk of testicular cancer
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55
Q

txt of male infert
* Men with primary hypogonadism may respond to what?
* Men with 2nd hypogonadism require what?
* In vitro fertilization option for who?

A
  • Men with primary hypogonadism may respond to androgen therapy if there is minimal damage to seminiferous tubules
  • Men with 2nd hypogonadism require gonadotropin therapy to achieve fertility
  • In vitro fertilization option for men with mild to moderate defects in sperm quality
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56
Q

Clinical Features in Men with Sexual Dysfunction
* What are the sxs?

A
  • Loss of libido
  • Erectile Dysfunction(Inability to initiate or maintain an erection)
  • Ejaculatory failure – common with cocaine use
  • Premature ejaculation
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57
Q

Clinical Features in Men with Sexual Dysfunction: Evaluation
* What exam do you need to do?
* What do you need to note?
* Check for what?

A
  • General as well as genital Exam
  • Note penile abnormalities, testicular size, & gynecomastia
  • Check for peripheral pulses & bruits
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58
Q

Clinical Features in Men with Sexual Dysfunction: Evaluation
* Neuro exam to assess what?
* What levels?
* What imaging can be done?

A
  • Neuro exam to assess anal sphincter tone, perineal sensation, & bulbocavernous reflex
  • Serum testosterone & prolactin levels
  • Penile arteriography, electromyography, or penile Doppler US occasionally performed
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59
Q

Erectile Dysfunction (ED)
* What is it?
* Affects how many people?
* Can be what?

A
  • Persistent inability to attain or maintain penile erection sufficient for sexual intercourse
  • Affects 10-25% of middle-aged & elderly men; 10-20 million American men
  • Can be psychogenic but often has an organic component: most commonly vascular disease that decreases blood flow into penis

1992 Consensus Development Conferences recommends use of the term ED rather than “impotence”.

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60
Q

Psychogenic ED
* What are the causes? (8)

A
  • Performance anxiety
  • Depression
  • Relationship conflict
  • Loss of attraction
  • Sexual inhibition
  • Conflicts over sexual preference
  • Sexual abuse in childhood
  • Fear of pregnancy or sexually transmitted disease.
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61
Q

Almost all patients with ED, even when it has a clear-cut organic basis, develop what?

A

develop a psychogenic component as a reaction to ED.

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62
Q

ED:
* What are 3 important questions to ask? What happens if they are yes?

A

Important questions to ask
* “Do you have early morning erection or nighttime emissions?”
* “Do any individuals other than your partner arouse you?”
* “Are you able to masturbate to an erection or climax?”

Positive answer to these questions usually indicates that ED is
psychological/psychogenic in origin

Allowing pt to discuss his problems may serve to vent some of his anxieties

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63
Q

Organic Causes of ED in Men
* What are endocrine causes?
* What are antiandrogens drugs that cause ED?

A

Endocrine causes
* Testicular failure (primary or secondary)
* Hyperprolactinemia

Antiandrogens
* Spironolactone
* Ketoconazole – fungal infection
* H2 blockers (cimetidine)
* Finasteride

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64
Q

Organic Causes of ED in Men
* What are the antihyperstive meds that cause ED?
* What are some other classes of meds? (3)

A

Antihypertensives
* Centrally-acting sympatholytics(clonidine & methyldopa)
* Peripheral acting sympatholytics (guanadrel)
* Beta blockers
* Thiazides

Anticholinergics

Antidepressents -SSRI

Antipsychotics

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65
Q

Organic Causes of ED in Men
* What are some CNS depressents?
* What are some drugs of habituation or addiction?

A
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66
Q

Organic Causes of ED in Men
* What are some penile diseases? (3)
* What are some neurologic diseases (4)

A
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67
Q

Organic Causes of ED in Men
* What are some vascular diseases? (5)

A

A. Aortic occlusion (Leriche syndrome)
B. Atherosclerotic occlusion or stenosis of pudendal &/or cavernosal arteries
C. Venous leak
D. Disease of the sinusoidal spaces
E. Arterial damage from pelvic radiation

68
Q

Male Orgasmic Disorders
* What it is?
* What are the mitigating factors? (2)

A

Definition: Persistent or recurrent delay in or an absence of orgasm after normal sexual arousal

Mitigating factors
* Age
* Adequacy of the stimulation: Focus, intensity, and duration

69
Q

Male Orgasmic Disorders
* What are some etiologies (4)?

A
  • Physical disorders
  • Chemical exposure
  • Use of a substance(e.g., alcohol, opioids, cocaine, antihypertensives, antidepressants, antipsychotics)
  • Depression: common cause of orgasmic difficulty as well as decreased desire and arousal
70
Q

Male Orgasmic Disorders
* Problems with achieving orgasm are usually linked to what?
* What can inhibit arousal and orgasm?
* Arousal can achieve what? But not what?
* Erectile failure (Impotence) may cause what?

A
  • Problems with achieving orgasm are usually linked to difficulty in developing sufficient arousal
  • Emotional state (e.g., anger, anxiety, guilt, boredom) can inhibit arousal & orgasm
  • Arousal may be sufficient to achieve partial or full erection but not to produce orgasm
  • Erectile failure (Impotence) may cause more distress than orgasmic difficulty
71
Q

ED in Diabetes
* Occurs in how many men?
* Pathologic mechanisms are primarily related to what?
* Diabetic macrovascular complications are mainly related to what?

A
  • Occurs in 35 to 75% of men with DM
  • Pathologic mechanisms are primarily related to diabetes-associated vascular & neurologic complications.
  • Diabetic macrovascular complications are mainly related to age, whereas microvascular complications correlate with duration of diabetes & degree of glycemic control
72
Q

Treatment of ED
* If patient hypogonadal?
* Correction of what?
* What are some drugs?

A

Testosterone: If patient hypogonadal & has low testosterone levels

Correction of underlying disorders or discontinuation of responsible medications

Selective cGMP-specific phosphodiesterase type 5 (PDE5) inhibitors
* Sildenafil (Viagra)
* Vardenafil (Levitra)
* Tadalafil (Cialis)

73
Q

When are PDE5 contrindicated?

A

Contraindicated in men receiving any form of nitrate therapy & should be avoided in CHF

74
Q

Treatment of ED
* Sexual stimulation causes the release of what?

A
  • Sexual stimulation causes the release of nitric oxide (NO) by the cavernous nerve into the neuromuscular junction
  • Current med therapy based on inhibition of PDE-5
75
Q
A
76
Q

Other Treatments for ED
* What is MUSE?

A

MUSE (Medicated Urethral System for Erections): small suppository placed into urethra
* Noninvasive

77
Q

Other Treatments for ED
* Vacuum?

A

Vacuum constriction devices (with constricting ring at base of penis)

78
Q

Other Treatments for ED
* What are the injections? What is the other route?
*

A

Injection of alprostadil into corpora cavernosa or urethra (Caverject)
* Comes in suppository too

Injection of papaverine, phentolamine, and prostaglandinE1 (TriMix)

79
Q

Injection of papaverine, phentolamine, and prostaglandinE1 (TriMix)
* What are the SE?
* Only for who?

A
  • SE: Pain & burning. Priapism 4%. Scarring (Peyronie’s disease) 8% after 1 year
  • Only for patients that failed oral meds and other modalities like MUSE
80
Q

Penile Prosthesis
* What it is?
* How does it work?

A
  • Noninflatable semi-rigid rods or cylinders implanted in corpora cavernosa
  • Inflatable devices surgically implanted that can be expanded using pressurized fluid.
  • Tubes connect cylinders to a fluid reservoir implanted in abdomen and subcutaneous pump implanted in scrotum. User inflates cylinders by pressing on small pump.
81
Q

Premature Ejaculation
* What is it?

A
  • Orgasm & ejaculation with minimal sexual stimulation
  • Persistently or recurrently occurs before, during, or shortly after penetration & before person desires
82
Q

Premature Ejaculation
* Due to what combinations of psychological & physiologic factors (3)

A
  • Usually related to anxiety or a learned behavior
  • May be partner related
  • Most men can delay orgasm during masturbation for much longer than they can during coitus

3-5min is the avg time

83
Q

Premature Ejaculation
* What is the txt?

A

Amenable to behavioral therapy (sex therapy)

Treatment with medications such as selective serotonin reuptake inhibitors (SSRIs)-Prozac, Zoloft, Celexa & Paxil
* Drug is taken either daily or 1 to 2 h before a sexual encounter

84
Q

Retrograde Ejaculation
* What it is?
* Consider this when?

A

Ejaculation into bladder
* Results when internal urethral sphincter does not close

Consider this when persistently see semen on UA

85
Q

Gynecomastia
* What is it?
* What is it due to?

A
  • Breast enlargement (gynecomastia) is most consistent feature of feminizing states in men
  • Gynecomastia is due to an increase in both glandular & adipose tissue
86
Q

What are the three peaks of gynecomastia?

A
  • Neonatal (due to mother’s estrogen)
  • Puberty: 13-14, uncommon after 17 (usually lasts 6m-2years)
  • Older men
87
Q

Increased Male Plasma Estrogen Levels
* When can you have increase levels? (3)

A

Elevations in estrogen production & estrogen plasma levels
* Increase in plasma precursors (liver or adrenal disease) especially in cirrhosis
* Increased extraglandular aromatization (obesity)
* Increased production by testes (testicular tumors, androgen resistance, gonadotropin stimulation).

88
Q

Increased Male Plasma Estrogen Levels
* Most of estradiol and all of estrone produced in normal men is formed by what?
* What is a normal valve in males?
* What is the normal estrone level?

A

Most of estradiol and all of estrone produced in normal men is formed by extraglandular aromatization of circulating androgens.
* Estradiol usually is <180 pmol/L (50 pg/mL) in normal men
* Estrone level is somewhat higher but usually is <300 pmol/L (80 pg/mL).

89
Q

Gynecomastia
* What are some drug causes? (9)

A
  • Calcium channel blockers
  • Digitalis
  • Estrogens
  • Griseofulvin
  • INH
  • Methyldopa
  • Phenytoin
  • Spironolactone
  • Testosterone
90
Q

Gynecomastia
* What are some other causes? (5)

A
  • Cirrhosis
  • Chronic renal failure
  • Hypogonadism
  • Hyperthyroidism
  • Idiopathic
91
Q

Pre-Pubertal Gynecomastia
* What are the sxs?
* When does it appear and go away?
* When does it occur?

A
  • It is usually painful & may be unilateral or bilateral.
  • Gradually appears & gradually disappears within 1 year of onset.
  • Pubertal changes that occur during Tanner stages 2&3 include growth spurt, growth of testes & penis, spermarche, acne, axillary perspiration, & appearance of pubic hair.
92
Q

What is Phimosis & Paraphimosis?

A
  • Phimosis: orifice of prepuce so small that foreskin cannot be retracted from glans
  • Paraphimosis: Tight foreskin, once retracted, may become edematous, so that it cannot resume its normal position over glans

Pic from smarty pants

93
Q

Phimosis
* Scarred down what?
* What is the tx?

A

Distal Scarred down foreskin (after trauma, inflammation or infection) which cannot be retracted over head of penis

Tx:
* Proper hygiene and streching excises of foreskin (pance pearl)
* Topical corticosteroid (betamethasone) if able to urinate
* Circumcision if unable

94
Q

Balanitis
* What is it?
* What are negative?

A
  • Inflammation of the glans occurs only in uncircumcised individuals and is often associated with phimosis
  • Dark field and serologic tests are negative
95
Q

Dr. V overview

Balanitis
* MCC organism?
* MC populations (3)
* What is the txt?

A
96
Q

Balanoposthitis
* What is this?
* What is the MC organisms?
* What is the txt?

A
  • Inflammation of the opposing surfaces of the glans penis (balanitis) & prepuce (posthitis) & occurs most commonly in uncircumcised diabetic males.
  • Usually caused by Candida albicans and group B beta-hemolytic Streptococcus.
  • Treatment: based on cause
97
Q

Priapism
* What is it?
* Probably involve waht?
* Appears to result from what?

A
  • Prolonged painful penile erection, unaccompanied by sexual desire or excitation
  • Mechanisms are poorly understood but probably involve complex vascular & neurologic abnormalities
  • Appears to result from a blockage of venous drainage from penis, while arteries remain patent
98
Q

Etiologies of Priapism
* What are some causes? (6)

A
  • Prolonged sexual activity
  • Hemoglobinopathies such as Sickle cell disease or trait (MCC)
  • Leukemia or other blood dyscrasias
  • Pelvic hematoma or neoplasm
  • Genital infection & inflammation, especially if complicated by a bladder calculus
  • Spinal cord injuries, tumor or neurosyphillis

Pearl: Trazodone (medication that can cause it)

99
Q

Priapism Management
* What injection?
* What should be extracted?
* In those with Sickle cell and recurrent priapism, consider what?

A

Phenylephrine injection (FIRST LINE and under 4 hours)
* 100–500 μg/ml injected intracavernously every 5 minutes
* Generally should reach out to specialist if 2-3 doses have not worked.

Blood extraction with syringe and/or scalpel (over 4 hours)

In those with Sickle cell and recurrent priapism, consider hydroxyurea to reduce vaso-occlusive complications

100
Q

Pance pearl:
* how do you dx it?

A
  • Clinical
  • Cavernosal blood gas: high flow results similar to ABG and normal glucose but low flow shows hypoglycemia, hypoxemia, hypercarbia and acidemia
101
Q

Peyronie’s Disease
* What is it?
* It is generally what?
* Affects how many people?

A
  • Disease of unknown cause it is characterized by a fibrous band in corpus cavernosum
  • It is generally unilateral & results in deviation of penis during erection
  • Affects 1% of population, age 40-70
102
Q

Peyronie’s Disease
* What is the clinical presentation?

A
  • Lump in penis
  • Pain, especially during erection
  • Bending or deformity of erect organ
  • Difficulty in vaginal penetration
103
Q

Peyronie Disease
* Depending on extent of fibrous band, condition may make what painful?
* What can you give? (medication)
* Occasionally need to do what?

A
  • Depending on extent of fibrous band, condition may make erection painful & intromission impossible
  • Oral pentoxifylline-increases blood flow to the affected microcirculation (if curve over 30 degrees or associated with sexual dysfunction and within 3 months of onset)
  • Occasionally surgery is required to remove fibrous band
104
Q

Penile Fracture with Urethral Injury
* Give an example of a patient situation?
* What does the exam reveal?
* What is the txt?

A
  • A 29-year-old man complained of sudden-onset groin pain during intercourse when he heard an audible “crack.“
  • Examination revealed a large deformity & angulation of midshaft of his penis with meatal blood.
  • Is a true emergency:Tunica Albugenia has to be sewn back together
105
Q

Hematospermia
* What is it?
* Most patients have what?

A
  • Bloody Semen
  • Most patients have recurrent hematospermia, although some experience it just once
106
Q

Hematospermia
* What are the causes?

A
  • Usually idiopathic
  • Seminal vesiculopathy due to unidentified infection or vascular congestion
  • May be associated with prolonged sexual abstinence or frequent or interrupted coitus
  • Bleeding disorder
107
Q

Seminal Vesiculitis
* What is it?
* May cause what?
* difficult to do what?
* How do you dx?

A
  • Inflammation of seminal vesicles
  • May cause painless, bloody ejaculate
  • Difficult to diagnose by culture technique
  • Transrectal US allows aspiration, which confirms seminal vesicles as source of blood in ejaculate
108
Q

Hematospermia
* What is the workup?
* What is the txt?

A

Workup
* Disorder usually benign & rarely associated with malignancy or serious infection
* Patients should be evaluated for prostatic infection or urethral strictures

Treatment
* Empiric unless a cause is found
* Some urologists advocate 5-7 day trial of tetracycline 250 mg qid followed by gentile prostatic message

109
Q

Urethritis in Men
* What is present?
* What does the urine culture show?
* Prominent male symptom in what?

A
110
Q

Penile Discharge
* What is it?
* Bloody is assocaited with what?
* Purulent?

A
  • Continuous or intermittent flow of fluid from urethra
  • Bloody: associated with ulcerations, neoplasms, and/or urethritis
  • Purulent discharges - thick & yellowish-green are associated with GC urethritis or chronic prostatitis

Must ask about exposure to STI’s, sexual partners & whether partners have any known illnesses

111
Q

Gonococcal Urethritis
* What is the hx?
* What are the sxs?

A
112
Q

Gonococcal Urethritis
* MCC of what?
* What does purulent urethral discharge produce?
* What are the PE findings?

A
  • Most common cause of urethritis worldwide
  • Purulent urethral discharge produces severe dysuria.
  • PE Findings:Yellow-green discharge; spontaneous or copious amounts with stripping of penis
113
Q

Gonococcal Urethritis: Dx
* Collect specimens when?
* What do the culture/stain show?

A
  • Collect specimens at least 1 hour, preferably 4 hours after last voiding
  • Gram stain, culture-R: intracellular gram-negative diplococci of Neisseria gonorrhoeae on urethral smear.
114
Q

Gonococcal Urethritis
* What is the txt?
* What else should you cover for??

A
115
Q

Nongonococcal Urethritis
* Caused by what?

A

Typically caused by Chlamydia trachomatis or Mycoplasma genitalium

116
Q

Nongonococcal Urethritis
* What are the sxs?

A
  • Unprotected sexual activity
  • Longer incubation period 1-5 weeks
  • Meatal itching or irritation
  • Scant mucoid-like discharge > 1 week , if present before first voiding of the day; may be present only with urethral massage
  • Symptoms vary and range in severity for urgency, frequency,& dysuria
117
Q

Chlamydia Urethritis
* What type of discharge?
* Chlamydia trachomatis causes various what?
* Common cause of what?

A
  • Thin mucoid discharge may be absent or minimal while penile milking or stripping
  • Chlamydia trachomatis causes various sexually transmitted diseases, transmitted by oral, vaginal or anal sex.
  • Common cause of Infertility in females
118
Q

Nongonococcal Urethritis
* What are the dx studies?

A

Diagnostic Studies
* Gram stain; culture
* DNA probe for Chlamydia
* Urine screen for DNA; Chlamydia particles
* DNA/NAAT amplification test can detect genetic material in secretions within 24 hours.

119
Q

Nongonococcal Urethritis
* What is the txt?

A

Azithromycin, Doxycycline, Erythromycin, Ofloxacin

120
Q

Reiter’s Syndrome – Reactive Arthritis
* What is there a history of?
* What are teh physical findings?

A

History
* Joint and tendon involvement
* Urethritis (Chlamydia)
* Can occur from Salmonella, Shigella, Campylobacter GI infection

Physical findings
* Joint and tendon involvement
* Decreased range of motion
* Skin and mucous lesions
* Conjunctivitis

121
Q

Reiter’s Syndrome – Reactive Arthritis
* What are the dx studies?

A
  • Blood, synovial fluid for NAAT;
  • HLA-B 27 antigen
  • X-Rays
122
Q

Lymphogranuloma Venereum(LGV)
* What it is caused by?
* Can start how?
* Dx with what?
* What can be present?
* Increase risk in US with what population?

A
  • Chlamydiae Trachomatis
  • Occurs rarely in US
  • Can start with small genital ulcer which resolves before lymphadenopathy (usually painless, so confused with syphilis)
  • Diagnose with compliment fixations titers > 1 :64
  • Buboes
  • Increase in US with MSM proctitis
123
Q

LGV Buboes
* Lymphadenopathy is usually what?
* Groups of swollen nodes are termed what? May be confused with what?

A
  • Lymphadenopathy is usually unilateral, with a matted, fluctuant appearance, and frequently goes on to become suppurative.
  • Groups of swollen nodes are termed “buboes“& may be confused with syphilitic buboes or adenopathy associated with chancroid or genital herpes.
124
Q

LGV Treatment
* What is the txt?
* What is the txt for preg?
* What is an another txt?

A

Standard treatment regimens for Chlamydia trachomatis with exception that treatment must be continued for at least three weeks.
* Doxycycline 100 mg p.o. BID x 3 weeks
* Pregnant patients may be treated with erythromycin 500 mg p.o. QID x 3 weeks
* Another alternative is sulfisoxazole 500 mg p.o. QID 8 3 weeks

  • Patients with rectal LGV may require more prolonged courses of treatment. Compliance with a three-week course of therapy is often a problem in this patient population, making careful follow-up mandatory.
125
Q

LGV Treatment
* What is contraindicated?

A

Incision and Drainage of the buboes
* Contraindicated as it does not shorten course of disease & may in fact promote development of chronic cutaneous fistulas

126
Q

Herpes Simplex
* HSV-2 usually transmitted how?
* Incubation?
* Rapidly develop into what?
* What is the txt?

A
  • HSV-2 usually transmitted venereally.
  • Incubation 2-21 days.
  • Rapidly develop into vesicles & later ulcers covered with grayish exudate.
  • Treatment: acyclovir, famciclovir, valacyclovir
127
Q

Syphilis (Treponema pallidum) stages
* What is the primary and secondary phases?

A
  • Primary: Painless sore (chancre) may go undetected. Infectious. Eventually heals as infection progresses
  • Secondary: Rash appears (usually palms of hands & soles of feet). May be accompanied by flu-like symptoms. Condyloma lata: moist flat confluent patches
128
Q

Syphilis (Treponema pallidum) stages
* What is the latent stage?
* What is the tertiary phase?

A

Latent: Infected persons may not show any symptoms while bacteria multiples

Tertiary:
* From 3 to 40 years later. Heart failure, aortic regurgitation and aneurysm, paralysis, blindness, liver damage, mental disturbance & death
* Gummas are nodular lesions with granulomatous inflammation

129
Q

Primary Syphilis
* What does ir produce?

A
  • Primary syphilis produces a painless ulcer (chancre) within 10 days to 3 months after exposure, but usually within 2-6 weeks
  • Ulcer heals (unlike in chancroid or cancer)
130
Q

Secondary Syphilis
* What typically erupts?
* Active bacteria are presents what?
* Rash is very what?

A
  • Typical eruption of red flat lesions over whole body but especially palms of hands & soles of feet.
  • Active bacteria are presents in sores and can be transmitted from broken skin of infected person
  • Rash is Very contagious
131
Q

Syphilis Treatement
* What is the txt for primary, early latent, secondary, tertiary and late latent?
* Recent push for what?

A

Benzathine penicillin G IM
* Primary and early latent: 2.4 million units
* Secondary: 2.4 million units
* Tertiary and late latent: 7.2 million units total, 2.4 million units/ week x 3
* Recent push for Amoxicillin instead of PCN G, with or without Probenecid, in HIV coinfection

132
Q

Syphilis Treatement
* What type of reaction can occur?
* Penicillin allergic patients need what?
* Treat partners when?
* What is the txt for HIV patients?

A
  • Jarisch-Herxheimer Reaction: fever, headache, myalgias occur within 24 hours of treatment (Sepsis like)
  • Penicillin allergic patients need desensitization
  • Treat partners within 90 days of exposure even if seronegative
  • In HIV patients - amoxicillin 3g daily with probenecid 750mg for 2 weeks
133
Q

Chancroid
* Caused by what?
* What is the sxs?
* Lymph glands in groin may do what?

A
  • Caused by a small gram-negative bacterium Haemophilus ducreyi. Incidence in U.S. has declined.
  • Soft chancre, accompanied by painful lymphadenopathy.
  • Lymph glands in groin may swell, creating a pus-filled bulge (bubo) enlarge until they burst through skin.
134
Q

Chancroid
* What are the sores like?
* What can be seen on gram stain?

A
  • Painful, irregularly shaped sores with “ragged edges” that can vary from 1-2 mm to 1-2 cm. Unlike chancre of syphilis, chancroid ulcer edge is soft, changes shape when squeezed
  • “Railroad tracks” can be seen on gram stain
135
Q

Treatment of Chancroid
* What do you give?

A
  • Azithromycin 1 G x 1
  • Ceftriaxone 500 mg IM x 1
  • Ciprofloxacin 500 MG PO BID x 3 days (contraindicated in pregnant or lactating females)
  • Erythromycin 500 mg TID x 7 days

Pance pearl said: Azithromycin 1 G x 1 and Ceftriaxone 500 mg IM x 1 as first line

136
Q

Molluscum Contagiosum
* What is it caused by?
* What are the sxs?
* occurs where?
* What is the txt?

A
  • STD caused by a poxvirus
  • Lesions are pearly white, often umbilicated, smooth & dome shaped with discrete margins
  • Occur most commonly on glans penis
  • No treatment usually required (self-limited)
137
Q

Pearly Penile Papules
* Are what?
* Also known as what?
* What are the sxs?
* Tend to fade with what?
* What can be done electively?

A
  • Are benign, not related to HPV
  • Also known ashirsutoid papillomas
  • Small, skin-colored bumps that form around the head of the penis
  • Tend to fade with advancing age
  • Cosmetic cryosurgery or laser therapy can be done electively
138
Q

Candida Infection in Men
* usually not what?
* What does it produce?

A
  • Yeast infection is not usually transmitted sexually.
  • Produces a rash and balanitis (red patches & blisters). It is also a cause of intertrigo: painful inflamed skin in skin folds of obese patients.
139
Q

Condyloma Acuminatum
* Caused by what?
* What is the sxs?

A
  • Caused by Human Papillomavirus and spread by sexual contact. Involve scrotum, penis, anus.
  • Cauliflower-like painless growths.
140
Q

Condyloma Acuminatum
* What are the txt? (6)

A
  • 0.5% podofilox solution
  • Burning with trichloracetic acid
  • Blistering agent (20% podophyllin solution);
  • 5% 5-fluorouracil cream
  • Aldara (Imiquimod) cream (immune response modifier also used for AK 7 BCC
  • Condylox (podofilox)
141
Q

Carcinoma of Penis
* Generally what?
* Tends to occur in who?
* Often appears as what?
* Where?
* A lot have what?

A
  • Generally squamous
  • Tends to occur in uncircumcised men who practice poor hygiene
  • Often appears as a painless ulceration that, unlike a syphilitic chancre, fails to heal
  • Majority arise on glans
  • 30-60% have inguinal LAD
142
Q
A
143
Q

Carcinoma of Penis
* how are the lesions by the time help is sought?
* Typically managed how?

A
  • Lesions are often extensive by time help is sought, either because of fear or because lesion is unnoticed under foreskin
  • Typically managed by Moh’s or penectomy
144
Q

Etiologies of Scrotal Enlargement: SXS of PAINLESS
* _ or _ tumor
* Hernia:
* Variocelce:
* Speratocele:
* Hydrocele:
* Epididymal cyst:

A
  • Testicular or epididymal Tumor
  • Hernia: soft fullness, often intermittent, revealed during Valsalva maneuver
  • Varicocele: feels like bunch of worms; collapses when patient lies down, worse with Valsalva
  • Spermatocele: scrotal mass that contains sperm that is greater than 2 cm
  • Hydrocele: tense, fluid-filled mass; transilluminate
  • Epididymal cyst: smooth, lobulated mass on epididymis, separate from testicle
145
Q

Etiologies of Scrotal Enlargement: SXS of PAIN
* Epididymitis/Orchitis:
* Torsion of spermatic cord
* _ Hernia

A
  • Epididymitis/Orchitis: Acute inflammation of epididymis or testis
  • and Epididymal hypertension
  • Torsion of spermatic cord: Acute onset, swollen, tender mass, younger age (10yo-20yo)
  • Strangulated hernia
146
Q

Scrotal Enlargement
* What are important questions to ask? (7)

A
  • “When did you first notice the enlargement?”
  • “Is it painful?”
  • Have you sustained any injury to your groin?”
  • “Does the enlargement change in size?”
  • “Have you ever had it before?”
  • “Have you ever had a hernia?”
  • “Have you had any problems with fertility?”
147
Q
A
148
Q

Groin Mass or Swelling
* What is the MCC?
* Adenopathy from what?
* When it is carcinoma?

A
  • Hernia (most common cause)
  • Adenopathy from any infection of external genitalia
  • Carcinoma of the testis if scrotal skin is involved
149
Q

Groin Mass or Swelling
* What are important questions to ask? (4)

A
  • “When did you first notice it?”
  • “Is the mass painful?”
  • “Does it change in size with different positions?”
  • Have you had any venereal disease”
150
Q

Hydrocele
* What is it?
* What is shown on PE?
* Testicle is contained within

A
  • Abnormal collection of clear fluid in parietal and visceral layers of the tunica vaginalis which directly surrounds the testis and the spermatic cord
  • It transilluminates and the examining fingers can get above the mass within the scrotum
  • Testicle is contained within the cystic mass preventing actual palpation of testis itself
151
Q

What is communicating and noncommunicating hydrocele?

A
  • Com: peritoneal/abdominal fluid enters the scrotum via a patent processus vaginalis that failed to close
  • Noncom: Derived from fluid from the mesothelial lining of the tunica vaginalis (no connection to the peritoneum)
152
Q

What does this show?

A

Picture on left shows hydrocele with collection of fluid in space around testis. The fluid allows passage of light (transillumination) seen in picture on the right.

153
Q

Pearl

how do you dx hydrocele

A

Testicular US is uded to r/o associated testicular tumor, other masses or inflammatory scrotal conditions

154
Q

Treatment of hydrocele?

A
  • Most hydroceles do not require intervention. Treatment is only indicated in patients who are symptomatic with pain or a pressure sensation or when the scrotal skin integrity is compromised from chronic irritation. For asymptomatic patients with hydroceles, there is no need for routine follow-up.
  • The most common surgical procedure is excision of the hydrocele sac. Simple aspiration is generally unsuccessful because of the rapid reaccumulation of fluid but may be effective if combined with instillation of a sclerosing agent (tetracycline, alcohol) into the sac
155
Q

Varicocele
* What it is?
* Where are the varicosities?
* What does palpation feel like?
* Usually waht?

A
  • Enlargement of the spermatic cord due to dilatation of the pampiniform plexus
  • These varicosities are usually on the left side
  • Impression on palpation has been likened to that of feeling a bag of worms
  • Usually gravity dependent and only visible while the pt is standing or straining

Occur in 25-40% of men with unexplained infertility

156
Q

Large Varicocele on Inspection
* Varicosities are usually where? What does it cause?
*

A

These varicosities are usually on L side Impression on palpation has been likened to that of feeling a bag of worms
* Increased blood flow, raises testicular temperature & thereby Causes damage to seminiferous tubules (infertility)

157
Q

Large Varicocele on Inspection
* Usually what?
* Pt is asked to do what?
* What confirms the diagnosis
* What is the txt?

A
  • Usually gravity dependent & only visible while pt is standing or straining
  • Pt is asked to turn his head and cough while spermatic cords are held
  • A sudden pulsation confirms the diagnosis (pance pearls said you can use US as first test)
  • Treatment: Ligation
158
Q

Spermatocele
* What is it?

A

Pea-sized nontender mass that contains spermatozoa usually attached to the upper pole of epididymis

159
Q

Testicular Torsion
* What is it?
* Usually results of what?
* More common in who?

A
  • Twisting of spermatic cord upon itself that results in obstruction of blood vessels supplying testis & epididymis.
  • Usually result of anomalous suspension of testes within scrotum (Bell Clapper testes).
  • More common in children, but accounts for 20% of acute scrotal pathology in post-pubertal males
160
Q

Testicular Torsion
* What are the common causes of an acute scrotal pain?
* What is difficult on PE?

A
  • Testicular torsion & acute epididymitis or epididymo-orchitis are most common causes of an acute scrotal pain.
  • Differentiating between the entities that cause acute scrotal pain is often difficult on PE
161
Q

What is the blue dot sign?

A
  • Cause by torsion resulting in ischemia of epididymis
  • Present early in torsion

Ischemia of epididymis or testicle. Can also be testicular appendage.

162
Q

Pulsed and Color Doppler Exam-Right Testicular Torsion
* What will it show?
* What is normal?
* What reflex is absent?

A
  • Diminished flow in right testicle (arrow) & increased flow in scrotal wall.
  • Left testicle & epididymis are normal.
  • Cremasteric reflex is absent
163
Q

Testicular Torsion
* How do you tell the different from epididymitis or orchitis?
* What signs ?

A
  • Differentiating Acute Torsion vs. Epididymitis
  • Decreased or absent blood flow within the testicle on doppler examination indicates acute torsion
  • Increased blood flow indicates epididymitis or orchitis
  • Prehn’s (negative in testicular torsion) and Cremasteric (negative in testicular torsion) signs are both insensitive and nondiagnostic
164
Q

How do you do testicular detorsion?

A
165
Q

Testicular Torsion
* What happens in delayed treatment?

A

Delayed treatment results in a much lower salvage rate.

Clinical Medicine 3 (27 decks)

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