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Gen Path Final > Genitourinary Disease and STDs > Flashcards

Genitourinary Disease and STDs Flashcards

1
Q

PENILE DISORDERS:

Malformations
The most common malformations include

A

abnormalities in the location of the distal urethral orifice.

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2
Q

PENILE DISORDERS:

Hypospadias refers to an

A

abnormal opening of the urethra along the ventral aspect of the penis, and occurs in 1/300 live male births. The opening may be restricted and lead to an increased risk of urinary tract infections.

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3
Q

PENILE DISORDERS:

Epispadias refers to the

A

urethral opening on the dorsal aspect of the penis. This abnormality is less common, but also exhibits an increased prevalence of urinary tract infections in addition to predisposition to urinary incontinence.

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4
Q

Premalignant Lesions

Premalignant lesions of the penis appear as

A

white plaque-like thickenings, areas of redness or a mixture.

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5
Q

Premalignant lesions:

Histologically, they may reveal any level of

A

epithelial dysplasia, including carcinoma in situ.

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6
Q

Bowen disease is a synonym for

A

carcinoma in situ of the penis.

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7
Q

Bowen disease is not specific to the

A

penis but may occur on other cutaneous or mucosal surfaces. Its major clinical importance lies in the potential progression to invasive squamous cell carcinoma.

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8
Q

Carcinoma of the Penis

Squamous cell carcinoma of the penis accounts for

A

about 0.4% of cancer in males.

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9
Q

Squamous cell carcinoma and its precursor lesions are the

A

most common penile neoplasms. The lesion is extremely rare among men who are circumcised early in life.

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10
Q

Human papillomavirus (HPV 16/18) may be involved with development of

A

penile cancer, and circumcision may improve hygiene and lessen exposure to oncogenic viruses.

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11
Q

Penile cancer:

This cancer tends to arise in those over

A

40 and may be preceded by Bowen’s disease.

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12
Q

Penile cancer:

Normally, it begins as a

A

crusted plaque or nodule with irregular margins that usually develops a central ulceration.

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13
Q

Penile cancer:

Less frequently, it forms a

A

papillary mass.

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14
Q

Penile cancer:

Treatment is

A

surgical excision. 5-year survival is 66%. Widespread metastasis is rare; however local metastasis to inguinal lymph nodes reduces 5-yr survival to 27%.

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15
Q

DISORDERS OF THE SCROTUM

A
  • Inflammatory processes, fungal infections, dermatoses
  • Rare neoplasms; most squamous cell carcinoma
  • 1st human cancer associated with occupational (environmental) factors (chimney sweeps)
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16
Q

Cryptorchidism refers to

A

failure of testicular descent from the abdomen to the scrotum.

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17
Q

Normally, the testes descend from the body cavity into the pelvis by the

A

third month of gestation and into the scrotum during the last two months of intrauterine life.

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18
Q

Cryptorchidism:

The diagnosis cannot be confirmed until

A

1 year of age because the timing of completion of the descent is variable.

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19
Q

Cryptorchidism is present

in

A

1% of the male population and may be unilateral or bilateral (10%).

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20
Q

Cryptorchidism:

Untreated bilateral cryptorchidism results in

A

sterility.

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21
Q

Cryptorchidism:

In unilateral cases, the contralateral descended testis may undergo

A

atrophy, also leading to sterility.

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22
Q

Cryptorchidism:

Failure of descent also is associated with a

A

3-5 times increased risk of testicular malignancy manifesting as intratubular germ cell neoplasia developing within the atrophic tubules.

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23
Q

Cryptochidism:

Surgical placement of

A

the testes into the scrotum (orchiopexy) before puberty reduces but does not eliminate the risk of cancer and infertility.

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24
Q

Orchitis refers to

A

inflammation of the testes.

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25
Q

Orchitis:

In most cases, the inflammation begins as a

A

primary urinary tract infection with secondary ascending infection of the testes.

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26
Q

Orchitis:

Epididymitis is more

A

common than orchitis.

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27
Q

Epididymitis:

——————- are common signs in affected patients.

A

Swelling and tenderness

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28
Q

Epididymitis

Frequently the origin is a

A

STD (sexually transmitted disease, to be discussed later in this handout) with other common causes including nonspecific orchitis, mumps, and tuberculosis.

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29
Q

Orchitis:

Orchitis complicates

A

mumps in 20% of infected adult males but rarely in children.

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30
Q

Orchitis:

In severe cases,

A

mumps-associated orchitis can result in sterility.:

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31
Q

Torsion occurs when the

A

spermatic cord (from which the testicle is suspended) twists, resulting in obstruction of venous drainage while leaving the thick-walled more resilient arteries patent.

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32
Q

Rapid, intense vascular engorgement and venous infarction follow unless the

A

torsion is relieved.

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33
Q

Neonatal torsion occurs either

A

in utero or shortly after birth, without know cause.

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34
Q

Adult torsion generally occurs in

A

adolescence secondary to an anatomic defect whereby the testis has increased mobility.

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35
Q

Torsion often occurs without

A

inciting injury and manifests with sudden onset of testicular pain.

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36
Q

Testicular torsion is one of the few

A

urologic emergencies. If the patient undergoes surgical intervention within 6 hours of onset, there are good chances (90 – 100 %) the testis will remain viable.

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37
Q

Tumors of the testis are the most common causes of

A

firm, painless enlargements of the testis.

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38
Q

Approximately 95% of testis tumor cases arise from the

A

germ cells, with almost all malignant. 5 % arise from Sertoli or Leydig cells (sex cord-stromal tumors), and are generally benign.

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39
Q

The peak prevalence of testicular tumors is

A

15-34 years of age, and the number of cases diagnosed is increasing in frequency (6/100K).

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40
Q

As mentioned, a 3-5x increased prevalence of testis tumors is noted in

A

patients with cryptorchidism; but conversely, only 10% of patients with testicular cancer have a history of cryptorchidism.

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41
Q

Although no consistent hereditary genetic abnormality has been found for testis tumors, ———– has been noted in some kindreds.

A

familial clustering

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42
Q

Cancers of the testes typically are divided into

A

seminomas or nonseminomatous germ cell tumors.

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43
Q

Several separate types of ——— are known; but in most instances, these tumors are mixtures of more than one type.

A

nonseminomatous tumors

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44
Q

Two markers have proven to be helpful in diagnosis, staging and follow-up for these cancers:

A

α-fetoprotein and human chorionic gonadotropin (HCG).

These markers are rarely positive in seminomas but frequently beneficial in nonseminomatous tumors.

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45
Q

Seminomas arise from the

A

epithelium of the seminiferous tubules and remain localized for long periods. However, they may spread occurs via lymphatics.

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46
Q

Seminomas respond well to

A

chemotherapy and are extremely radiosensitive. Therefore, they are one of the most curable cancers.

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47
Q

Nonseminomatous tumors (E.g. Embryonal Carcinoma) spread

A

earlier, are less radiosensitive and utilize the hematogenous and lymphatic routes, with the lungs and liver often involved at the time of diagnosis. As Lance Armstrong can attest, treatment of testicular neoplasms is a modern medical success story. Of the 8K cases each year in the US, only about 400 die of their disease. Seminomas are extremely radiosensitive and respond well to chemotherapy. 95 % early-stage seminomas are cured; whereas 90 % of patients with nonseminomatous tumors achieve remission with chemotherapy (most are cured).

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48
Q

The prognosis of nonseminomatous germ-cell tumors has

A

improved dramatically since the introduction of newer chemotherapy regimens. Nevertheless, pure choriocarcinoma (< 1 %) is less chemosensitive and prognosis remains worse.

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49
Q

Prostatitis is clinically apparent

A

inflammation of the prostate which may be acute or chronic. The prostate will be enlarged and tender.

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50
Q

Bacterial prostatitis may be

A

acute or chronic and is caused by the same organisms which commonly produce urinary tract infections (E. coli).

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51
Q

Chronic nonbacterial prostatitis (90-95 % of cases), also known as chronic pelvic pain syndrome, is of

A

unknown etiology and doesn’t respond to antibiotics.

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52
Q

Both acute and chronic prostatitis present with

A

dysuria, urinary frequency, lower back pain and poorly localized suprapubic or pelvic pain.

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53
Q

Antibiotics penetrate the

A

prostate poorly, and the most common cause of recurrent urinary tract infections is the surviving bacteria.

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54
Q

Nodular hyperplasia of the prostate refers to

A

hyperplastic enlargement of the prostate, often associated with urinary symptoms.

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55
Q

Benign prostatic hypertrophy is a time-honored synonym, which is a misnomer and has been replaced with .

A

benign prostatic hyperplasia.

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56
Q

Nodular hyperplasia: The alteration is a common pathosis that begins during the

A

forties (20 % of men) and increases with age; 90% are affected by the eighth decade.

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57
Q

Nodular hyperplasia:

Stromal and glandular proliferation result in

A

enlargement. The central portions of the gland adjacent to the urethra (Inner periurethral zone) are involved most frequently;

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58
Q

Nodular hyperplasia

impingement on the prostatic urethra leads to

A

dysuria (difficulties in starting, maintaining and stopping the stream of urine).

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59
Q

Nodular hyperplasia

Clinical symptoms include

A

hesitancy, urgency, nocturia, and poor urinary stream.

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60
Q

Nodular hyperplasia

Residual urine in the bladder and chronic obstruction increases the risk of

A

urinary tract infection.

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61
Q

Nodular hyperplasia

No more than 10% of men require

A

surgical relief of the obstruction (TURP – Transurethral resection of the prostate) secondary to prostatic hyperplasia.

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62
Q

Nodular hyperplasia:

Medical management with

A

drug therapy may also be considered

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63
Q

Nodular hyperplasia:

Although the cause is unknown, ———— appear to have a central role in its development, since the process does not occur in ————-

A

androgens

males castrated prior to puberty or in those with genetic diseases which block androgens.

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64
Q

Nodular hyperplasia:
It is thought that an increase in local, intraprostatic concentrations of androgens and androgen receptors contribute to the

A

pathogenesis of this condition.

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65
Q

Carcinoma of the prostate is the most common cancer of men over

A

50 years of age, with the peak prevalence between 65-75.

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66
Q

Adenocarcinoma of the prostate accounts for

A

25 % of cancers in this demographic (men over 50), but Many of these cancers are small, asymptomatic, progress slowly and are found incidentally at autopsy or when examining nodular hyperplasia specimens.
The prevalence of this occult form approaches 30% in men between 30-40 years of age and 50% in men over 80.

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67
Q

Carcinoma of the prostate:
Although the cause is unknown and the function of hormones in the pathogenesis of carcinoma of the prostate is not fully understood, significant evidence suggests

A

androgens contribute significantly to the development of this cancer.

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68
Q

Carcinoma of the prostate:

Androgen supplementation should be viewed with

A

caution, and frequent sexual activity has been associated with improved prostate health.

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69
Q

Carcinoma of the prostate:

—— also have been suggested.

A

Hereditary and environmental contributions

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70
Q

Carcinoma of the prostate:

The clinically evident carcinomas invade

A

adjacent structures and metastasize via both the lymphatics and the bloodstream.

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71
Q

Carcinoma of the prostate:

Regional node involvement occurs

A

early.

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72
Q

Carcinoma of the prostate:

Osseous metastasis is the most common form of

A

hematogenous spread and the metastases may be radiolucent but are more commonly radiopaque.

73
Q

Carcinoma of the prostate:

Initial diagnosis from discovery of metastatic foci is not

A

rare.

74
Q

Carcinoma of the prostate:

Both the incipient and clinically evident cancers usually begin in the

A

peripheral zones of the posterior lobe of the prostate; therefore, dysuria is not frequently an early sign.

75
Q

Carcinoma of the prostate:

Prostate specific antigen (PSA) represents a useful marker in the management of

A

prostate cancer, but is elevated in both normal prostate and those affected by cancer, prostatitis, or nodular hyperplasia.

76
Q

Carcinoma of the prostate:

PSA is of limited value when used as an

A

isolated screening test, but its value is enhanced considerably when combined with digital rectal examination, transrectal sonography, and needle biopsy.

77
Q

Carcinoma of the prostate:

In addition to being beneficial in the initial diagnosis, PSA also is important in

A

staging of the neoplasm and judging response to treatment.

78
Q

Localized cancer of the prostate is treated by

A

y surgery and/or radiation.

79
Q

Hormone therapy is utilized for the

A

advanced carcinomas.

80
Q

Carcinoma of prostate:

The prognosis depends upon the

A

anatomic extent and spread of the tumor. The 10 year survival overall is approximately 98 %. Despite all treatments, patients with dissemination have a 10-40% 10-year survival rate.

81
Q

NEOPLASMS OF THE URINARY BLADDER

The most common tumor is

A

urothelial cell carcinoma, which represents 90% of neoplasms of the bladder. This typically occurs in men between the ages of 50 and 80 years and the dominant presenting manifestation is painless hematuria.

82
Q

Urothelial cell carcinoma:

Predisposing factors include

A

cigarette smoking, chronic cystitis, infection with Schistosomiasis, and exposures to various carcinogens.

83
Q

Urothelial cell carcinoma:

The tumor is preceded by a

A

premalignant precursor lesion which often has a papillary growth pattern, but can also be flat.

84
Q

Urothelial cell carcinoma:

Tumor cells generally

A

lack cohesion and are shed into the urine, making cytology a reasonable method for detection.

85
Q

Urothelial cell carcinoma:

The degree of

A

atypia and extent of invasion predict prognosis.

86
Q

Urothelial cell carcinoma

Treatment modalities include

A

transurethral resection, immunotherapy and radical cystectomy.

87
Q

SYPHILIS

Syphilis is a venereal disease that is produced by a

A

spirochete, Treponema pallidum. Greater than 24,000 cases reported in the U.S. in 2015.

88
Q

Syphilis:

There is a strong racial disparity with

A

African Americans affected 30X more often than whites. The peak of incidence is between 20-24 years old, followed by 15-19 years old.

89
Q

Syphilis”

Humans are the

A

only natural host.

90
Q

Syphilis:

Transmission is by

A

direct contact; transplacental transmission readily occurs.

91
Q

Syphilis:

The infection produces

A

The infection produces two types of antibodies: a nonspecific antibody, syphilitic reagin, and a specific antibody, treponemal antibody.

92
Q

Syphilis:

The reagin can be detected by

A

several simple screening serologic tests (VDRL: venereal disease research laboratory, RPR: rapid plasma reagin), but these are not specific for syphilis.

93
Q

Syphilis:

Up to 15% of positive screening tests for syphilis reagin are

A

biologic false-positive results.

94
Q

Syphilis:
The more difficult and expensive specific treponemal antibody tests (FTA: fluorescent treponemal antibody absorption test) should be performed following

A

positive screening tests. The specific treponemal tests remain positive for life, even following successful treatment.

95
Q

The histopathologic hallmark of syphilis is a .

A

lymphoplasmacytic infiltrate associated with obliterative endarteritis, a specific type of vasculitis.

96
Q

Syphilis:

The natural course involves three stages:

A

1) primary, 2) secondary and 3) tertiary.

97
Q

Syphilis:

Primary syphilis is characterized by the

A

painless chancre which arises at the site of entry 9-90 days (mean of 21 days) after exposure.

98
Q

Syphilis: Primary;

Glans penis in the male and the vulva or cervix in females are

A

common sites. Lips, fingers, oropharynx and anus are also possible sites.

99
Q

Syphilis: Primary

The chancre begins as a

A

reddened papule that quickly ulcerates; the organisms may be seen only in special stains or in smears that are examined under a dark field microscope.

100
Q

Syphilis: Primary

Serologic tests begin to become positive after

A

1-2 weeks of infection and are positive in the vast majority by 4-6 weeks.

101
Q

Syphilis: Primary;

Because of the early negativity of the screening tests, dark-field examination of the exudate is

A

extremely important in the diagnosis of early primary syphilis.

102
Q

Syphilis: Primary;

Non-syphilitic spirochetes can be found within the

A

normal oral flora and this makes the dark-field method of limited use for primary oral lesions.

103
Q

Syphilis: Primary;

———- occurs during this stage.

A

Spirochetemia

104
Q

Syphilis: Primary;50% of the females and 30% of the males either

A

never develop or do not detect the chancre. Chancres heal in 4-6 weeks

105
Q

Syphilis: Secondary

In about 25% of untreated patients, healing of the chancre is followed within

A

2 months by secondary syphilis presenting with generalized lymph node enlargement combined with widespread mucocutaneous lesions that are maculopapular, scaly or pustular and even involve the palms and soles.

106
Q

Syphilis: Secondary:

Oral and vaginal areas of localized spongiotic mucositis are called

A

mucous patches.

107
Q

Syphilis: Secondary:

Elevated large broad plaques (condyloma lata) can form

A

in moist skin areas such as the axillae, inner thighs and anogenital area.

108
Q

Syphilis: Secondary:

=————- are not rare and often noted in the oral cavity, pharynx and external genitalia.

A

Mucosal condyloma lata

109
Q

Syphilis: Secondary:

All sites are

A

infectious. The rash can be extremely subtle and may be ignored. All serologic tests are positive.

110
Q

Secondary syphilis:

Virtually all untreated cases of secondary syphilis

A

clear over several weeks, leading to latent syphilis. These patients are asymptomatic, yet all serologic markers are positive. The majority never develop progressive disease. Some have relapses of secondary disease, while others progress to tertiary syphilis.

111
Q

Tertiary syphilis:

Tertiary syphilis arises in

A

30% of untreated patients usually after a latent period of 5-20 years. It may affect any part of the body, but it shows a predilection for the cardiovascular system (80%) and the CNS (10%).

112
Q

Tertiary syphilis:

The aorta may develop

A

scarring, weakening and dilation secondary to obliterative endarteritis.

113
Q

Tertiary syphilis:

Brain atrophy produces

A

dementia.

114
Q

Tertiary syphilis:

Rubbery gray-white areas of total necrosis (gumma) may be seen most frequently in

A

mucocutaneous tissue and bone.

Nasal and palatal bones are not uncommon sites.

115
Q

Tertiary syphilis:

The gumma is due to

A

hypersensitivity to products of the spirochete and to ischemia from obliterative endarteritis.

116
Q

Tertiary syphilis:

Treponemes are difficult to find in

A

tertiary syphilis, and this stage is much less infectious.

117
Q

Tertiary syphilis:

With treatment, gummas will become areas of

A

scar; the cardiovascular and neural damage is irreversible.

118
Q

Tertiary syphilis:

The nonspecific serologic screening tests typically are

A

negative.

119
Q

Tertiary syphilis:

Once exposed to syphilis, the highly sensitive specific treponemal antibody tests are

A

positive for life.

120
Q

Although the treponemes may be transmitted across the placenta at any time during pregnancy, fetal signs of infection typically do not develop until after the

A

fourth month of pregnancy.

121
Q

Treatment within the first four months of pregnancy will generally

A

prevent clinical complications.

122
Q

Although the chance of transmission is greater from newly infected mothers, the fetus may receive the spirochetes if the mother contracted the disease within the last

A

five years.

123
Q

The more active the maternal disease, the

A

better the chance of fetal infection.

124
Q

In the absence of treatment, up to 40% die in utero, typically after the

A

fourth month.

125
Q

Congenital syphilis can be divided into three patterns:

A

stillbirth, infantile and late.

126
Q

Infantile syphilis refers to liveborn infants that at birth or within the first few months of life present with

A

clinical lesions similar to those seen in secondary syphilis.

127
Q

Late congenital syphilis refers to cases of

A

untreated congenital syphilis of more than 2 years duration.
Classic manifestations of this chronic infection include interstitial keratitis of the eyes, saber shins, saddle nose, Hutchinson’s incisors, mulberry molars, eighth nerve deafness, gummas and neurosyphilis.

128
Q

A historically famous pattern of congenital syphilis is called Hutchinson triad and consists of:

A
  1. Interstitial keratitis
  2. Hutchinson’s teeth
  3. Eighth nerve deafness
129
Q

The treatment for syphilis is ———–, with ———– utilized in patients allergic to the primary choice.

A

penicillin

tetracycline

130
Q 
HUMAN PAPILLOMAVIRUS INFECTION 
Human papillomavirus (HPV) is the cause of a number of
A

epithelial proliferations in the genital tract, including condyloma acuminatum, some precancerous lesions and some carcinomas.

131
Q

HUMAN PAPILLOMAVIRUS INFECTION

Condyloma acuminatum is usually associated with

A

HPV types 6 or 11 and typically arises on moist mucocutaneous surfaces. They present as benign papillary nodules, and frequently appear in clusters.

132
Q

HUMAN PAPILLOMAVIRUS INFECTION Other types of HPV (16, 18, 31, 33, 45, 52, and 58) are found more frequently in

A

epithelial neoplasia, including cervical and oropharyngeal cancer.

133
Q

HUMAN PAPILLOMAVIRUS INFECTION

Condylomata sometime occur

A

singly but more often in multiple sites. The penis and around the anus are the common sites in men, while the vulva is the most frequent site in females. Occasional lesions are seen intraorally and it is not uncommon to develop synchronous lesions.

134
Q

HUMAN PAPILLOMAVIRUS INFECTION

Genital HPV can be transmitted to

A

neonates during vaginal delivery and may result in life-threatening papillomas of the upper respiratory tract.

135
Q

HUMAN PAPILLOMAVIRUS INFECTION
Neonate upper respiratory papillomas:
These lesions are treated with

A

surgery, laser ablation, cryotherapy, or topical imiquimod.

136
Q

Malignant transformation of ——— can occur but is uncommon.

A

condyloma acuminatum

137
Q

GONORRHEA:

Gonorrhea is a frequent sexually transmitted disease caused by

A

Neisseria gonorrhoeae, a gram-negative diplococcus.

138
Q

GONORRHEA
An estimated ——— cases occur annually in the U.S., and this is complicated by the emergence of strains which are resistant to multiple antibiotics.

A

800K cases

139
Q

GONORRHEA Humans are the ———-, and spread requires direct contact with the mucosa of an infected person.

A

only natural reservoir

140
Q

GONORRHEA

Sites of entry include the

A

urethra, oropharynx, eyes and the anorectum.

141
Q

GONORRHEA

The diplococcus evokes a

A

neutrophilic inflammatory reaction which produces copious amounts of pus.

142
Q

GONORRHEA

two to seven days after exposure, symptomatic males exhibit

A

dysuria, urinary frequency and mucopurulent exudation from the urethra; the main symptoms in females are dysuria, lower pelvic pain and vaginal discharge.

143
Q

GONORRHEA:

—–of the females and —- of the males are asymptomatic.

A

80%

40%

These asymptomatic individuals are the major reservoir of infection.

144
Q

GONORRHEA:

If untreated, it spreads up the genital tract and may produce

A

sterility in both sexes.

145
Q

GONORRHEA

In males, ascending infection results in

A

acute prostatitis, epididymitis or orchitis.

146
Q

GONORRHEA

Ascending infection involving the uterus, fallopian tubes, and ovaries results in

A

acute salpingitis.

147
Q

GONORRHEA

Following the acute infection, granulation tissue and fibrosis results in

A

permanent deformities, giving rise to pelvic inflammatory disease.

148
Q

GONORRHEA

Mothers may produce

A

blindness in infants from gonococcal contamination at birth - gonococcal ophthalmia neonatorum; this is presently rare because of a prophylactic antibiotic placed in the eyes of all newborns.

149
Q

GONORRHEA:

Culture of the organism from discharges has been the

A

primary diagnostic test.

150
Q

GONORRHEA

Treatment for gonorrhea in the past was

A

penicillin, but resistance has become a problem.

151
Q

NONGONOCOCCAL URETHRITIS AND CERVICITIS

Nongonococcal urethritis and cervicitis are the most common forms of

A

sexually transmitted disease which must be reported to CDC.

152
Q

NONGONOCOCCAL URETHRITIS AND CERVICITIS

This infection mimics ——- in males and is mostly —– in females, although occasionally it does produce cervicitis and/or urethritis.

A

gonococcal urethritis

asymptomatic

153
Q

NONGONOCOCCAL URETHRITIS AND CERVICITIS

Most cases appear related to

A

Chlamydia trachomatis, but a number of other organisms also have been implicated as a possible cause in some cases.

154
Q

NONGONOCOCCAL URETHRITIS AND CERVICITIS

The infection is usually

A

milder with fewer complications than gonorrhea but does produce suppuration within the infected area.

155
Q

NONGONOCOCCAL URETHRITIS AND CERVICITIS

Males develop

A

urethritis which may spread into the epididymes;

156
Q

NONGONOCOCCAL URETHRITIS AND CERVICITIS

females develop

A

urethritis and/or cervicitis which may spread into the oviducts and even produce pelvic inflammatory disease.

157
Q

NONGONOCOCCAL URETHRITIS AND CERVICITIS

Infants born of infected mothers may develop

A

conjunctivitis or neonatal pneumonia.

158
Q

NONGONOCOCCAL URETHRITIS AND CERVICITIS

The infection often is recognized by its

A

persistence following penicillin treatment for gonorrhea (“postgonococcal urethritis”).

159
Q

NONGONOCOCCAL URETHRITIS AND CERVICITIS

Positive identification of C. trachomatis by culture is not

A

available routinely.

160
Q

NONGONOCOCCAL URETHRITIS AND CERVICITIS

The diagnosis is made by

A

exclusion of gonorrhea by smear and culture and possibly with detection of bacteria by molecular techniques.

161
Q

NONGONOCOCCAL URETHRITIS AND CERVICITIS

Best approach is to treat all patients with

A

gonorrhea-like symptoms with a regimen which is effective against both gonorrhea and chlamydia.

162
Q

NONGONOCOCCAL URETHRITIS AND CERVICITIS

=——— is the treatment of choice.

A

Ceftriaxone combined with doxycycline

163
Q

NONGONOCOCCAL URETHRITIS AND CERVICITIS

Reactive arthritis (Reiter Syndrome) is a significant manifestation of

A

chlamydial infection. This is an immune-mediated process that develops in response to genitourinary or gastrointestinal infections and predominates in patients who are HLA-B27 positive.

164
Q

reactive arthritis:

It typically presents as a combination of

A

urethritis/cervicitis, arthritis, conjunctivitis, and mucocutaneous lesions.

165
Q

GENITAL HERPES SIMPLEX:

Genital herpes simplex (herpes genitalis) is a common STD that affects an estimated 50 million individuals in the U.S. and occurs from infection by herpes simplex virus. Most are caused by

A

HSV Type II, with a small percentage related to Type I.

166
Q

GENITAL HERPES SIMPLEX

Spread is possible when the virus comes in contact with a

A

mucosal surface or broken skin.

167
Q

GENITAL HERPES SIMPLEX

HSV actively shed during periods of

A

clinically visible lesions.

168
Q

GENITAL HERPES SIMPLEX

The clinical manifestations vary considerably, depending on whether the infection is

A

primary or recurrent.

169
Q

GENITAL HERPES SIMPLEX

Primary infections may be

A

asymptomatic; the remainder develop painful focal lesions with dysuria, fever, lymphadenopathy, headache and malaise.

170
Q

GENITAL HERPES SIMPLEX

The glans penis or surrounding areas in men and the cervix in women are the

A

usual sites. Involvement of the vagina, vulva and labia may also be seen.

171
Q

GENITAL HERPES SIMPLEX

The lesions are small vesicles that quickly

A

ulcerate;

172
Q

GENITAL HERPES SIMPLEX

the diagnosis is made via a

A

smear or biopsy which will reveal the cytopathologic effects of the virus in epithelial cells (ballooning degeneration of epithelial cells with large, multinucleate “Tzanck cells”).

173
Q

GENITAL HERPES SIMPLEX

Without treatment, the clinical manifestations of primary herpes may last

A

3-6 weeks.

174
Q

GENITAL HERPES SIMPLEX

Recurrent herpes presents with

A

periodic vesiculo-erosive lesions that heal in 7-10 days.

175
Q

GENITAL HERPES SIMPLEX

More than 80% of the patients with HSV Type II genital herpes have

A

one or more recurrences yearly for several years.

176
Q

GENITAL HERPES SIMPLEX

Herpes is a significant clinical problem since it can spread to others and may produce

A

infections in newborns that often are fatal (neonatal herpes).

177
Q

GENITAL HERPES SIMPLEX

Such infection of the newborn occurs in about

A

half of infants delivered vaginally of mothers suffering from either primary or recurrent genital infection.

178
Q

GENITAL HERPES SIMPLEX

Approximately 60% of affected infants

A

die of the infection.

Gen Path Final (18 decks)

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