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Y3R1 - DALR ✋🏻 > Andrology 🧔‍♂️ > Flashcards

Andrology 🧔‍♂️ Flashcards

1
Q

Introduction about the anatomy & Histology of testes

A
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2
Q

Introduction about the anatomy & Histology of epidydimis

A
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3
Q

Introduction about the anatomy & Histology of vas deferens

A
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4
Q

Introduction about the anatomy & Histology of prostate

A
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5
Q

Introduction about the anatomy & Histology of seminal vesicels

A
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6
Q

Introduction about the anatomy & Histology of Cowper (Bulbourethral) glands

A
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7
Q

Introduction about Spermatogenesis

A
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8
Q

Functions of Sertoli cells

A
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9
Q

What is blood testicular barrier formed of?

A
  • Sertoli cells & the basement membrane
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10
Q

What happens if blood testicular barrier is damaged?

A
  • Immunologic infertility
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11
Q

Function of blood Testicular barrier

A
  • prevent developing cells from being recognized as (non-self antigens) by immune system.
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12
Q

Introduction to Leydig cells (Steroidogenesis)

A
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13
Q

Functions of Testosterone

A
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14
Q

Control of testicular function

A
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15
Q

Functions of Epididymis

A
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16
Q

Functions of Vas deferens

A

Sperm transport

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17
Q

What are Accessory sexual glands? And what do they release?

A
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18
Q

Definition of male infertility

A
  • failure to conceive following 1 year of regular unprotected intercourse.
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19
Q

Epidemiology of male infertility

A
  • One of five (20%) married couples demonstrates primary infertility. A male factor is responsible in approximately 1⁄3 to 1⁄2 of these couples.
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20
Q

Pretesticular causes of male infertility

A
  • Hypothalamic causes
  • Pituitary causes
  • Hyperprolactinemia
  • Thyroid disorders
  • Adrenal disorders
  • Increased androgens or estrogens
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21
Q

Definition of male sterility

A

is inability of the male to fertilize the ovum.

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22
Q

Causes of male infertility

A
  • Pretesticular
  • Testicular
  • Post-testicular
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23
Q

Hypothalamic causes of male infertility

A

Kallmann syndrome

  • a genetic ↓ in gonadotropin secretion due to ↓ GnRH. It’s often associated with other congenital anomalies such as anosmia, hare lip & cleft palate
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24
Q

Pituitary causes of male infertility

A
  • Isolated LH or FSH deficiency and Panhypopituitarism
  • May be idiopathic prepubertal OR secondary to neurohpophyseal lesions resulting from: tumors, infarction, iatrogenic damage (by surgery or radiation) & infiltrative or granulomatous processes (such as tuberculosis) involving the hypothalamus or the pituitary gland.
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25
Q

How does hyperprolactenemia cause male infertility?

A

sexual & reproductive dysfunction.

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26
Q

Thyroid disorders effects on male infertility

A

both hypo and hyperthyroidism alter spermatogenesis.

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27
Q

What adrenal disorders affect male infertility?

A

Congenital adrenal hyperplasia, Addison’s disease & Cushing’s syndrome.

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28
Q

Effects of increased androgens & Estrogens on male infertility

A

↓ gonadotropin secretion & ↓ spermatogenesis.

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29
Q

Testicular causes of male infertility

A
  • genetic and chromosomal abnormalities
  • Developmental abnormalities
  • Defective androgen synthesis and action
  • Heat Exposure
  • Radiation
  • Testicular atrophy following trauma or infiction
  • Gonadal toxins
  • hypogonadism associated with systemic diseases
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30
Q

What are genetic and chromosomal abnormalities that may affect male fertility?

A
  • Myotonia dystrophia
  • AZF microdeletion
  • Hermaphroditism
  • Klinefelter’s syndrome (47, XXY karyotype).
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31
Q

What are developmental abnormalities that may affect male infertility?

A
  • Bilateral anorchia
  • Varicocele
  • Sertoli-cell-only syndrome (germinal cell aplasia)
  • Cryptorchidism (undescended testis)
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32
Q

Examples of testicular atrophy following trauma or infection

A

Leprosy and Mumps orchitis

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33
Q

What are systemic diseases that may be associated with hypogonadism?

A
  • chronic renal, respiratory, liver, inflammatory, nutritional diseases as well as acute critical illness and severe burns
  • Non testicular diseases can disrupt different levels of the hypothalamic-pituitary-testicular axis.
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34
Q

Examples of gonadal toxins and chemicals

A

Gonadal toxins such as drugs (e.g., Alkylating agents) and chemicals (e.g., Pesticide)

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35
Q

What does the duration and reversibility of testicular axis disruption depend on?

A
  • severity, chronicity and the patho-physiological mechanisms involved in the underlying disease and its treatment.
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36
Q

Post-Testicular causes of male infertility

A
  • Inadequate sexual performance
  • Ductal obstruction
  • semen factors
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37
Q

Examples of inadequate sexual performance

A
  • erectile and ejaculatory disorders
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38
Q

Types of Ductal obstructions

A
  • Congenital absence of the ductal system, e.g., aplasia of the vasa deferentia.
  • Acquired obstruction following infection (e.g., bilateral gonococcal or tuberculous epididymitis) or vas ligation (voluntary or iatrogenic).
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39
Q

What are semen factors that may affect male fertility?

A

Idiopathic oligoasthenoteratozoospermia the commonest cause of male subfertility.

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40
Q

What causes impaired sperm motility?

A
  • may result from faulty maturation in the epididymis or biochemical abnormalities of seminal plasma due to genital tract infection or idiopathic.
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41
Q

What is Oligoasthenoteratozoospermia (OAT)?

A
  • is a condition that includes oligozoospermia (low number of sperm), asthenozoospermia (poor sperm movement), and teratozoospermia (abnormal sperm shape)
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42
Q

Step of evaluation in andrology

A
  • History
  • Examination
  • Investigations
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43
Q

Types of history in andrology

A
  • Personal history
  • Infertility history
  • Sexual history
  • Past history
  • Wife
  • Family history
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44
Q

Personal history

A
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45
Q

Infertility history

A
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46
Q

Sexual history

A
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47
Q

Past history

A
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48
Q

Wife

A
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49
Q

Family history

A
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50
Q

Types of examination in andrology

A
  • General Examination
  • Genital Examination
  • Rectal examination
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51
Q

General examination

A
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52
Q

Genital examination

A
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53
Q

Rectal examination

A
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54
Q

Types of investigations in andrology

A
  • Semen analysis
  • Endocrine evaluation
  • Genetic & chromosomal evaluation
  • Testicular biopsy
  • Surgical exploration of scrotal contents
  • Radiologic evaluation
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55
Q

Types of semen analysis

A
  • Physical examination of semen
  • Microscopic examination of semen
  • Biochemical analysis of semen (markers of obstruction)
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56
Q

Types of physical examination of semen

A
  • volume
  • Color
  • Characteristic order
  • Liquefecation time
  • Viscosity (consistency)
  • pH
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57
Q

What is the normal volume of semen?

A

Normally: 2 – 6 mL.

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58
Q

What is hypospermia?

A

< 1.5 mL.

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59
Q

What is hyperspermia?

A

> 6 mL.

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60
Q

What is Aspermia?

A

absence of semen (no ejaculate).

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61
Q

What is the normal color of semen?

A

grayish white color.

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62
Q

What is the normal equation time of semen? And what does it indicate if it is delayed?

A
  • Normally semen liquefies within 10 – 30 minutes at 37 °C. ⚠
  • If Delayed → Seminal vesicle disease
  • The semen is ejaculated in a liquid form. Seminal vesicle protein is responsible for coagulation & prostatic proteolytic enzymes are responsible for liquefaction. Incomplete liquefaction can cause decreased motility.
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63
Q

What are abnormal colors of semen and what do they indicate?

A

⚠Greenish color: genital tract infection.
⚠ Red or Brown color: haemospermia & drugs.
⚠Yellow color: e.g., jaundice, drugs.

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64
Q

What is the normal viscosity (Consistency) of semen?

A
  • Normally leaves pipette in drops
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65
Q

Abnormalities related to the viscosity of semen

A

⚠ If, after one hour, it forms a thread more than 2 cm long on the pipette, this is referred to as Viscopathy.

  • High viscosity (the sample exits the pipette as a thread) may cause infertility.
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66
Q

What is the normal pH of semen?

A

7.2 - 7.8

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67
Q

What causes abnormal pH of semen?

A
  • pH changes may be caused by acute & chronic inflammation of the prostate, epididymis or seminal vesicles (dysfunction of the accessory glands).

⚠↑ pH > 8 → Infection
⚠↓ pH → Seminal vesicle disease

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68
Q

Aspect of microscopic examination of semen

A
  • Sperm Concentration
  • Motility
  • Sperm morphology
  • Vitality (viability)
  • Sperm Antibodies
  • Cellular components other than sperms
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69
Q

Definition of sperm concentration

A

The number of sperms per milliliter of semen.

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70
Q

How is total sperm count obtained?

A

multiplying sperm concentration
by semen volume.

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71
Q

What is the normal sperm count?

A

≥ 15millions/mL (average 20-200).

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72
Q

What is Azoospermia?

A

Zero (absence of spermatozoa from the ejaculate):

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73
Q

What is Oligozoospermia?

A

< 15 millions/mL

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74
Q

What is Polyzoospermia?

A

> 200 millions/mL

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75
Q

What are categories of sperm motility?

A
  • Progressive motility (PR).
  • Non-progressive motility (NP)
  • Total motility (PR+NP)
  • Immotile sperms
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76
Q

What are reference values for progressive motility & total motility?

A

✅ Progressive motility (PR): ≥ 32%

✅ Total motility (PR+NP): ≥ 40%

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77
Q

What is Asthenozoospermia?

A

Progressive motility (PR) < 32%.

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78
Q

Strict criteria for detection of sperm morphology

A

✅ The change in the evaluation method for sperm morphology by adopting “strict criteria” has lowered the threshold of normal to ≥ 4% morphologically normal sperms.

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79
Q

What is Teratozoospermia?

A
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80
Q

How to differentiate between dead and living sperms?

A
  • We must differentiate between non-motile, living sperms from dead sperms by Eosin Negrosin (vital) stain. Only dead sperms will stain (Pink / Red).
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81
Q

What is the threshold for sperm vitality?

A

≥ 58 %.

➥The test is therefore unnecessary if total sperm motility is ≥ 60 %.

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82
Q

What is Necrozoospermia?

A
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83
Q

What do Anti-sperm IgA and IgG antibodies cause?

A

sperm agglutinations (immune- mediated infertility).

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84
Q

What are tests for sperm antibodies? And what is the normal value?

A
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85
Q

Normal number of Peroxidase-positive leukocytes

A

Normally: Peroxidase-positive leukocytes < 1 million/ml.

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86
Q

What is Pyospermia (leukocytospermia)?

A

peroxidase-positive leukocytes > 1 million/ml

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87
Q

Is it normal to find RBC in semen?

A

Normally absent.

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88
Q

What is Haemospermia? And what causes it?

A

⚠ Haemospermia is the presence of RBCs in the ejaculate.

Can be caused by:
- Congestion
- Prostatovesiculitis
- Bilharziasis of the genital tract.
- Idiopathic
- Malignancy.
- Haemorrhagic diathesis.
- Tuberculosis of the genital tract.

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89
Q

Biochemical analysis of semen (markers of obstruction)

A
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90
Q

What does decrease in the concentration of obstruction markers indicate?

A
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91
Q

What are sperm function tests?

A
  • A number of in-vitro tests have been developed to assess various functional, biochemical & molecular markers of sperm health yielding information on the fertilizing capacity of spermatozoa as well as their ability to support normal embryonic development.
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92
Q

Normal semen parameters according to the last WHO manual (2010)

A
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93
Q

Endocrine evaluation in andrology

A
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94
Q

What are indications for hormonal testing?

A
  • Evidence from the patient’s history suggestive of hormonal abnormalities
  • Particular findings on physical examination.
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95
Q

Evaluation of the hypothalamo-pituitary-gonadal axis

A

(FSH, LH and Testosterone levels).

  • Serum FSH assesses → the state of the seminiferous epithelium
  • Serum LH reflects → the adequacy of Leydig cell function.
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96
Q

When should serum prolactin be obtained?

A

If the patient has:
* signs and symptoms suggestive of pituitary tumour
* sexual dysfunction
* relevant drug history

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97
Q

When should serum Estradiol obtained?

A

If the patient has: gynecomastia

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98
Q

If the patient is suspected to have multiple end-organ failure, then …

A

Assessment of other endocrine organ functions (adrenal, thyroid, …) is recommended

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99
Q

Methods of Genetic & chromosomal evaluation

A
  • Buccal smear
  • Karyotyping
  • Y-chromosome microdeletion assay
  • PCR
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100
Q

Significance of Buccal smear

A
  • to demonstrate the presence or absence of sex chromatin (Barr body).
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101
Q

Results of Buccal smear

A

✅Normal males: Sex chromatin is absent

⚠Klinefelter’s males: Sex-chromatin positive

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102
Q

What is the normal karyotype?

A

Normal karyotype is 46,XY.

  • Karyotype may identify either numerical or structural chromosomal anomalies.
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103
Q

Y-chromosome microdeletion assay

A

should be performed on all patients with azoospermia.

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104
Q

Significance of PCR in Andrology

A

for detection of specific genes e.g.:

  • AZF (in non-obstructive azoospermia)
  • CFTR (cystic fibrosis genes in obstructive azoospermia due to CBAVD)
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105
Q

Indications of testicular biopsy

A
  • Testicular biopsy is now reserved for therapeutic testicular sperm extraction for ICSI (intracytoplasmic sperm injection).
  • A thorough understanding of the histological appearance of a testis biopsy in normal and diseased patients is crucial.
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106
Q

Biopsy findings

A
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107
Q

Radiologic evaluation In andrology

A
  • Trans-rectal US
  • Scrotal US & Duplex examination
  • Vasography
  • Abdomino-pelvic US
  • CT & MRI
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108
Q

Significance of Trans-rectal US

A
  • Evaluation of SV, ED, prostate
  • Particularly valuable in obstructive amospermia
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109
Q

What is the most important radiological tool in evaluation in andrology?

A

Scrotal US & Duplex examination

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110
Q

Significance of Scrotal US & Duplex examination

A
  • Diagnosis of varicocele, hydrocele, testicular volume
  • Measures early testicular masses
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111
Q

Significance of Vasography

A
  • Absent or obstructed vas and ejaculatory ducts
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112
Q

Significance of Abdomino-pelvic US

A
  • For cases of undescended testis
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113
Q

Significance of CT & MRI in andrology

A
  • Undescended testis
  • Pituitary tumors
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114
Q

What is the most common cause of male infertility?

A

Varicolcele

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115
Q

Examination and evaluation of varicocele

A
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116
Q

If you cannot feel the vas, …..

A
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117
Q

How to determine the level of obstruction in obstructive azoospermia?

A
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118
Q

If there are spermatogenic cells in ejaculate, does this indicate obstruction?

A

no obstruction

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119
Q

Markers of obstruction

A
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120
Q

Brief about treatment in andrology

A
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121
Q

Types of treatment in andrology

A
  • Medical treatment (hormonal and non-hormonal)
  • Surgical treatment
  • Assisted reproductive techniques
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122
Q

Hormonal treatment in andrology

A
  • Gonadotropin releasing hormone (GnRH)
  • Gonadotropins
  • Androgens
  • Antiestrogen therapy
  • Bromocryptine
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123
Q

Uses of Gonadotropin releasing hormone (GnRH)

A

− GnRH stimulates secretion of LH and FSH.

− It can be used in hypogonadotropic hypogonadism.

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124
Q

Uses of Gonadotropins

A
  • Can be used in hypogonadotropic hypogonadism.

a) Human Chorionic Gonadotropin (HCG): Mainly LH activity.

b) Human menopausal gonadotropin (HMG): Both LH & FSH activity, but mainly FSH.

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125
Q

Androgens used in andrology treatments

A

a) Parenteral androgens: e.g., Testosterone propionate.

b) Oral androgens, e.g., Testosterone undecanoate.

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126
Q

Examples of anti-estrogen therapy used in andrology treatments

A

a) Clomiphene citrate.
b) Tamoxifen.
c) Testolactone.
d) Anastrozole

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127
Q

Uses of bromocriptine

A

for treatment of hyperprolactinemia

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128
Q

Non-hormonal Medical treatments in andrology

A
  • antioxidants
  • Kallikrein
  • Nucleotides as ATP
  • Others
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129
Q

Effects of Kallikrein

A
  • stimulates sperm motility
  • enhances sperm transport
  • activates fructolysis.
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130
Q

Effects of ATP on sperm motility

A

↑ sperm motility.

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131
Q

Surgical treatment In andrology

A
  • Repair of penile and urethral disorders
  • Orchiopexy
  • Varicocelectomy
  • Vasovasostomy (correction of vasal occlusion)
  • Epididymovasostomy
  • Artificial spermatocele
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132
Q

Exampls of Repair of penile and urethral disorders

A
  • such as hypospadias, chordee, urethral fistula or stricture.
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133
Q

Indications of Orchiopexy

A
  • early in life to correct cryptorchidism, if trial of gonadotropin fails.
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134
Q

Indications of Varicocelectomy

A
  • in cases of varicocele
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135
Q

Vasovasostomy (correction of vasal occlusion)

A
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136
Q

Indications of Epididymovasostomy

A
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137
Q

Artificial spermatocele

A
  • vasal aplasia, long unbridgeable vasal stenosis, or failure of repeated reconstructive surgery on the seminal pathways.
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138
Q

What are examples of Assisted reproductive techniques?

A
  • Intra Uterine Insemination
  • Semen processing
  • Gamete Intrafallopian Transfer (GIFT)
  • In Vitro Fertilization (IVF)
  • Microfertilization or Microinsemination for severe male factor infertility
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139
Q

Intrauterine insemination

A
  • Artificial Insemination Husband IUI (AIH)
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140
Q

Effect of Semen processing

A

to improve sperm quality (before artificial insemination or in vitro fertilization)

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141
Q

Examples of Microfertilization or Microinsemination for severe male factor infertility

A
  • Subzonal insemination (SUZI) and Intracytoplasmic sperm injection (ICSI)
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142
Q

What determines the method of assisted reproductive techniques used?

A

the quantity and quality of sperm isolated from the semen after processing.

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143
Q

Patients with azoospermia or severely subfertile semen may be treated, with resultant improvement of semen parameters. While the semen parameters may not normalize, they may improve to the point where other treatment options such as IUI are available.

A

..

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144
Q

Parts of posterior urethra

A
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145
Q

Basic anatomy of anterior urethra

A
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146
Q

Basic anatomy of Male urethra

A
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147
Q

Compare between Bulbous urethra & penile urethra

A
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148
Q

Widest part of the urethra

A
  • the Bulbous Urethra
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149
Q

Narrowest part of the urethra

A
  • the External Urinary Meatus
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150
Q

Lining of Fossa navicularis

A

a fusiform dilatation lined by
stratified squamous epithelium

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151
Q

What does the external urinary meatus open into?

A

The external urinary meatus opens into the Fossa Navicularis

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152
Q

What is the rest of the Anterior Urethra and the ducts of Littre’s & Cowper’s glands lined by?

A
  • The rest of the Anterior Urethra and the ducts of Littre’s & Cowper’s glands are lined by columnar epithelium.
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153
Q

Def of Lacuna of morgagni

A
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154
Q

Littr’s glands

A
  • secrete mucus and their ducts open into the roof and sides of penile urethra. They are particularly numerous in the fossa navicularis.
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155
Q

Cowper (bulbourethral glands)

A
  • lie on either side of the membranous urethra, but their long ducts open into the floor of the bulbous urethra.
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156
Q

Tyson’s glands

A
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157
Q

Paraurethral ducts

A
  • are small blind channels in the substance of the glans penis that open near or within the lips of the external urinary meatus.
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158
Q

Basic anatomy of female urethra

A
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159
Q

Lining of female urethra

A
  • The part adjacent to the bladder is lined by transitional epithelium,
  • The length is lined by stratified squamous epithelium with islets of columnar epithelium in the proximal part.
  • Many small mucous glands open into the urethra and their ducts are lined by columnar epithelium.
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160
Q

Skene’s glands

A
  • are situated on either side of the lower end of the urethra.
  • Their ducts which open beside or just inside the urethral orifice are lined by columnar epithelium.
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161
Q

Length of female urethra

A

4cm long

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162
Q

Bartholin’s glands

A
  • lie in the posterior third of each labium majus (at 4 and 8 o’clock) and their ducts open on the inner surface of each labium minus just external to the hymenal ring.
  • The ducts are lined by columnar epithelium.
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163
Q

Histology of Anal Canal and Rectum

A
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164
Q

Histology of Conjunctiva

A
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165
Q

Histology of Pharynx

A
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166
Q

Main presentations of STDs

A
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167
Q

What are physiological urethral discharges?

A
  • Prostatorrhoea
  • Urethrorrhoea (Prosemen)
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168
Q

What is Prostatorrhoea?

A
  • An escape of prostatovesicular fluid from the external urinary meatus independent of orgasm.
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169
Q

What causes Prostatorrhoea?

A
  • Its escape is noticed when the patient strains at stools or at urination.
  • It is an excess of secretion expressed by the pressure of hard stools on the prostate & the vesicles.
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170
Q

Characters of Prostatorrhoea

A
  • It is clear, sticky, whitish discharge.
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171
Q

Does Prostatorrhoea Contain pus?

A
  • Normally it doesn’t contain pus cells unless there is inflammation.
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172
Q

What is Urethrorrhoea (Prosemen)?

(Urethral secretions during sexual excitement)

A
  • An escape of normal urethral secretion from the external urinary meatus without coitus being indulged in.
  • It is an excess of secretion from the accessory sexual glands in the urethra like Cowper’s or Littre’s
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173
Q

What causes Urethrorrhoea?

A
  • Its occurrence in some quantity at times of sexual excitement & before ejaculation is a normal event as it helps to alkalinize the urethra to receive the aftercoming semen.
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174
Q

Caracters of Urethrorrhoea

A
  • It is clear viscid fluid mucus, free of pus cells
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175
Q

What is Urethrorrhoea Mistaken for?

A
  • frequently mistaken for gonorrhoea by the laity.
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176
Q

Where is Urethrorrhoea Common?

A

common in young unmarried men.

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177
Q

Pathological urethral discharges

A
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178
Q

Other uncommon causes of urethral discharge

A
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179
Q

Definition of Gonorrhea

A
  • An acute infectious disease of the genitourinary mucous membrane caused by Neisseria gonorrhoeae.
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180
Q

Transmission of Gonorrhea

A
  • It is almost exclusively transmitted by sexual intercourse and may also cause local or metastatic complications.

(More in females due to late diagnosis)

1) Sexual
2) Non-sexual
3) Perinatal transmission (mother to infant)

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181
Q

Host of Neisseriae gonorrhoea

A

It is a fragile organism with only man as a host.

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182
Q

Morphology & Characters of Neisseriae gonorrhoea

A
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183
Q

Culture requirments of Neisseriae gonorrhoea

A

O2: Aerobe or Facultative Anaerobe

CO2: 5%

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184
Q

Culture media for Neisseriae gonorrhoea

A
  • It can be cultivated on enriched media in the presence of moisture & 5% CO2.

Culture media:
- Ordinary Media
- Transport Media
- Growth Media
- Growth-Transport Media

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185
Q

Does Neisseriae gonorrhoea Grow on ordinry media?

A
  • Does NOT grow
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186
Q

Transport media for Neisseriae gonorrhoea

A
  • Non-nutritional, semisolid media that maintain a state of reduction during transport, e.g. Stuart’s medium.
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187
Q

Growth media for Neisseriae gonorrhoea

A

Non-selective media
e.g. McLeod’s chocolate agar.

Selective media
- that eliminate the growth of common contaminants by addition of antimicrobial agents, e.g. Thayer-Martin medium.

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188
Q

Growth-transport media for Neisseriae gonorrhoea

A
  • That provides both nutritional and transport requirements

a) Nonselective as modified Thayer-Martin medium.
b) Selective as Biological environment chamber.

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189
Q

Colonial morphology of Neisseriae gonorrhoea

A
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190
Q

Confirmation of positive culture Of N. Gonorrhea

A
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191
Q

Fermentation reactions of N. Gonorrhea

A
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192
Q

Pathogenesis of N. Gonorrhea

A
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193
Q

What does the gonococcus require to gain access to the body?

A
  • The gonococcus requires a mucosal surface to gain access to the body
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194
Q

What does the gonococcus Have predilecation for?

A

columnar epithelium

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195
Q

What happens after the gonococcus gains access to the body?

A
  • Subsequently the infection can spread to the other structures lined with columnar epithelium such as Littre’s glands, Cowper’s glands, Prostate, Seminal vesicles & Epididymis in the male, and Skene’s glands & Fallopian tubes in the female.
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196
Q

What happens in untreated cases of N.Gonorrhoea?

A

resolve by fibrosis

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197
Q

Other ways of infection by gonococcus

A
  • The organism is able to infect the vulva and vagina of prepubertal girls, and the eye in both adults and neonates. In either sex it may gain entry to the blood stream with resultant disseminated disease
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198
Q

What happens if N.gonnorohea gains access to blood?

A

Dissemenated Diseases

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199
Q

Summary of the Pathogenesis of gonorrhea

A
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200
Q

Clinical manifestations Of N.gonorrhoea

A
  • Genital gonococcal infections in men & women
  • Extragenital gonococcal infections in men & women
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201
Q

Extragenital gonococcal infections in men & womeN

A
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202
Q

Genital Infection in Men

A

Urethritis: Inflammation of urethra

Epididymitis: Inflammation of the epididymis

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203
Q

What is the most common clinical manifestation of gonorrhoea in men?

A
  • urethritis
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204
Q

Incidence of local complications of Gonorrhoea In men

A

local complications of gonorrhoea are rare.

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205
Q

Mode of infection by Gonococcal Urethritis in men

A
  • Sexual intercourse is the principal mode of infection in adults
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206
Q

IP of Gonococcal Urethritis in men

A

2-5 days (from last sexual intercourse).

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207
Q

Symptoms & signs of Gonococcal Urethritis in men

A
  • Dysuria
  • Urethral discharge: profuse (abundant), yellowish & usually purulent (contains pus).
  • Constitutional symptoms, e.g: fever, headache, malaise may occasionally develop.
  • The urinary meatus may appear red & oedematous.
  • Slight tender enlargement of inguinal lymph nodes occurs in some cases.
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208
Q

Investegations to diagnose Gonococcal Urethritis in men

A
  • Smear examination
  • Culture
  • Non-culture tests (DNA-based tests)
  • Two-glass test
  • Three-glass test
  • Serological tests
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209
Q

Smear Examination

Gonococcal Urethritis in men

A
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210
Q

Culture

Gonococcal Urethritis in men

A
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211
Q

What is the gold standard for diagnosis of Gonococcal Urethritis in men?

A

Culture

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212
Q

What are Non-Culture tests (DNA-Based tests) used in diagnosis of Gonococcal Urethritis in men?

A
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213
Q

Two-Glass test

Gonococcal Urethritis in men

A
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214
Q

Three-Glass test

Gonococcal Urethritis in men

A
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215
Q

DDx of Gonococcal Urethritis in men

A
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216
Q

Serological tests

Gonococcal Urethritis in men

A
  • These tests depend on detection of antibody against gonococci in the patient serum.

⚠ However, they do not show a high degree of specificity or sensitivity & cannot differentiate between past and present gonococcal infection.

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217
Q

Compare between Gonococcal Urethritis in men & Non-Gonococcal Urethritis in men

A
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218
Q

What are local Complications of anterior urethritis?

A
  • Complications tend to occur when symptoms and signs have been ignored and treatment delayed.

Local Complications:

  • Balanoposthitis
  • Tysonitis
  • Paraurethritis
  • Littritis
  • Peri-urethral abscess
  • Urethral stricture
  • Cowperitis and Cowper’s gland abscess
  • Posterior urethritis
  • Cystitis (trigonitis)
  • Prostatitis and prostatic abscess
  • Seminal vesiculitis
  • Epididymitis
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219
Q

What is Balanoposthitis? and what may develop afterwards?

A
  • inflammation of preputial sac & glans penis may occur in uncircumcised patient, severe phimosis then develops.
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220
Q

Predisposing factors for local Complications of anterior urethritis

A
  • alcoholism, physical exertion, trauma (instrumentation), vigorous prostatic massage, irrigation, and sexual indulgence.
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221
Q

what is Tysonitis? and what may follow it? and what predisposes for it?

A
  • A tender swelling with a bead of pus next to the frenum
  • Abscess may develop.
  • May occur when the prepuce is long and hygiene is poor.
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222
Q

what causes Peri-urethral abscess?

A
  • spread of the infection into the submucous tissue of the urethra results in a boggy, painful swelling on the undersurface of the penis
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223
Q

what is Paraurethritis?

A

paraurethral ducts present beads of pus at their openings on pressure.

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224
Q

what is Littritis?

A

threads appear in the first glass in the two-glass urine test.

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225
Q

Manifestations & Compliactions of Peri-urethral abscess

A
  • The abscess may open into the urethra or the surface of the penile shaft or the scrotum.
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226
Q

what causes Urethral stricture?

A
  • a chronic sequel of peri-urethral inflammation which causes fibrous stricture
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227
Q

Symptoms of Urethral stricture

A
  • The patient may complain of morning gleet, difficulty in passing urine and a narrow stream, subsequently retention of urine may occur.
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228
Q

where is Cowperitis and Cowper’s gland abscess best felt?

A
  • Best felt between the thumb on the perineum and a forefinger in the rectum.
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229
Q

what is Cowperitis and Cowper’s gland abscess?

A
  • A painful swelling palpable on either side of the median raphe of the perineum
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230
Q

Posterior urethritis as a complication of anterior urethritis

A
  • if the infection is untreated, the posterior urethra may become involved in about 10-14 days.
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231
Q

Symptoms of Posterior urethritis

A
  • There is increasing dysuria, urgency, frequency and terminal haematuria. Both glasses of urine in the two-glass urine test are hazy in appearance.
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232
Q

Cystitis (trigonitis)

A
  • when the bladder is infected, the trigon is most often involved
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233
Q

Symptoms, Signs & Complications of Prostatitis and prostatic abscess

A
  • Acute prostatitis causes an exacerbation of the symptoms of urethritis together with perineal pain and suprapubic discomfort, fever and malaise.
  • On rectal examination the gland is found to be swollen and tender.
  • When prostatic abscess develops, the symptoms of acute prostatitis become even worse. The abscess may rupture into the urethra or rectum; or point to the perineum and a sinus or a fistula may form.
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234
Q

what is Seminal vesiculitis usually associated with?

A
  • This is usually associated with prostatitis
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235
Q

Manifestations of Seminal vesiculitis

A

Manifested by haemospermia, frequent erections and ejaculations. The inflammed seminal vesicles may be felt per rectum as tender sausage-like structures above the prostate.

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236
Q

what is the most common local complication of anterior urethritis in men?

A

Epididymitis

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237
Q

Manifetations of Epididymitis

A
  • The condition is usually unilateral and presents as a painful, hot, red swelling.
  • If both epididymides are involved, sterility will result.
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238
Q

Gonorrhea in women

A
  • In contrast to gonorrhea in men, gonococcal infection in women is often asymptomatic, but of far greater consequence because of the potential for serious complications (e.g., PID) from the infection.
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239
Q

IP of Urogenital gonorrhea

A
  • usually longer than 2 weeks.
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240
Q

Primary site of Urogenital gonorrhea

A
  • Endocervical canal & the Urethra.
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241
Q

CP of Urogenital gonorrhea

A
  • The condition is symptomless in almost 50% of cases. In some, symptoms may be related to the co-existing trichomoniasis or candidiasis.
  • The other 50% complains of symptoms of urethritis and/or cervicitis.
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242
Q

Symptoms of Gonorrheal acute urethritis in women

A
  • Dysuria.
  • Frequency will indicate the presence of trigonitis or cystitis
  • In severe cases, there is terminal hematuria.
  • On examination (in lithotomy position) the external urinary meatus maybe reddened with edematous lips. On massaging the urethra with the index finger in the vagina (milking of the urethra), yellow purulent discharge can be expressed from the urethral orifice.
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243
Q

Examination of Acute gonococcal urethritis in women

A
244
Q

Symptoms of Gonocval Cervicitis

A
245
Q

Examination in Gonococcal Cervicitis

A
  • On examination: a mucopurulent or purulent discharge is seen coming from the external os which appear congested.
  • There may be signs of acute cervical erosions.
246
Q

Local Complications of Gonnococal Cervicitis

A
  • Skenitis
  • Bartholinitis
247
Q

Diagnosis of Gonnococal Cervicitis

A
248
Q

Manifestations of Skenitis

A
  • Beads of pus seen or expressed from the Skene’s ducts, Paraurethral cyst or abscess of Skene’s glands rarely occur as a result of blockage of their ducts.
249
Q

Manifestations of Bartholinitis

A
  • Bartholin’s glands may be infected unilaterally or bilaterally, causing pain & swelling of the vulva with discomfort and difficulty in sitting & walking.
250
Q

what happens if Bartholin duct is blocked?

A
  • abscess of the gland develops and eventually this may rupture through the skin or mucous membrane.
251
Q

Symptoms & Signs of Chronic Bartholinitis or Bartholin’s cyst

A
  • On examination, there will be swelling of the vulva on the affected side.
  • The abscess can be felt between the fingers with the thumb on the outer surface of the labium majus and the index finger in the vagina.
252
Q

TTT of bartholin abcess

A
  • Treated by drainage. However, simple incision and drainage can often lead to recurrence, so marsupialization is usually done for recurrent Bartholin’s cysts or abscesses.
253
Q

Pelvic infection as a local complication of gonococci

A
  • Extension of gonococci to the pelvis may result in salpingitis, pyosalpinx or parametritis.
  • Lower abdominal pain, pyrexia and general malaise are common manifestations that often occur during or within a week after menstruation.
254
Q

what is PID?

A
  • is a collective term for the involvement of the fallopian tubes, ovaries and adjacent peritoneum. It is a serious condition with agonizing sequelae such as chronic pelvic pain, dyspareunia (pain on intercourse), ectopic (tubal) pregnancy and infertility.
  • A Clinical syndrome associated with ascending spread of microorganisms from the vagina or cervix to the endometrium, fallopian tubes, ovaries, and contiguous structures.
255
Q

Comparison between Gonorrhea in Males and in Females

A
256
Q

Extragenital Gonoccocal Infections In Men & Women

A
  • Gonococcal Proctitis (Anorectal gonorrhea)
  • Oropharyngeal Gonorrhoea
  • Gonococcal Conjunctivitis
  • Disseminated Gonococcal Infection (DGI)
  • Gonococcal Perihepatitis (Fitz-Hugh-Curtis Syndrome)
257
Q

Gonococcal Proctitis (Anorectal gonorrhea)

A
  • The rectal mucosa may be infected by the gonococcus in either sex.
258
Q

Gonococcal Proctitis (Anorectal gonorrhea) in women

A
259
Q

Symptoms of Gonococcal Proctitis (Anorectal gonorrhea)

A
  • The patient may have no symptoms. When present, they may include anal pain or irritation, a change in bowel habits, tenesmus, and mucoid, purulent, or blood-stained anal discharge
260
Q

Proctoscopy in Gonococcal Proctitis (Anorectal gonorrhea) shows ….

A
261
Q

Diagnosis of Gonococcal Proctitis (Anorectal gonorrhea)

A

Rectal mucosa smear for Gram’s stain and culture may help in diagnosis.

262
Q

MOI by Oropharyngeal Gonorrhoea

A

orogenital contact.

263
Q

Manifestations of Oropharyngeal Gonorrhoea

A
264
Q

Epidemeology of Gonococcal Conjunctivitis

A
  • It is rare in adults
265
Q

MOI by Gonococcal Conjunctivitis

A
  • Occurs from direct contamination of the eye with infectious discharge by fingers or towels.
266
Q

Symptoms of Gonococcal Conjunctivitis

A
267
Q

Epidemeology of Disseminated Gonococcal Infection (DGI)

A

Blood-borne dissemination of gonococci occurs mainly in women

268
Q

After How long does Disseminated Gonococcal Infection (DGI) occur after mucosal infection?

A

7 - 30 days after mucosal infection, About 1-2% of mucosal infections → (DGI)

269
Q

Manifestations of Disseminated Gonococcal Infection (DGI)

A
  • Mild (benign gonococcaemia) presenting as a triad of fever, arthritis, & dermatitis.
  • The rarer but more serious manifestations include endocarditis, myocarditis, pericarditis, meningitis, osteomyelitis, and hepatitis.
270
Q

what Increases the risk of Disseminated Gonococcal Infection (DGI)?

A
  • Terminal (C5-C9) complement deficiencies
271
Q

Mortality Rate in Disseminated Gonococcal Infection (DGI)

A
  • Mortality is very rare, even with disseminated infection
272
Q

Skin Lesions in Gonococcal dermatitis

A
  • skin lesions are generally found on the extremities as small macules, papules, pustules or vesicles that may be haemorrhagic or necrotic.
273
Q

Resolution of Gonococcal dermatitis

A
  • Spontaneous resolution and relapses may occur
274
Q

DDx of Gonococcal dermatitis

A
  • meningococcal septicemia, pyoderma, and drug rash.
275
Q

Characters of Gonococcal Arthritis

A
  • Is always monoarticular
  • If polyarticular, it is additive (when another joint is affected, the previous affected joint remains affected).
276
Q

Dx of DGI

A
277
Q

Epidemeology of Gonococcal Perihepatitis (Fitz-Hugh-Curtis Syndrome)

A
  • The condition occurs mainly in women
278
Q

what is Gonococcal Perihepatitis (Fitz-Hugh-Curtis Syndrome) associated with?

A
  • There are usually associated symptoms of salpingitis, or the pelvic infection may have been asymptomatic.
279
Q

How does the infection reach the subphrenic area in Gonococcal Perihepatitis (Fitz-Hugh-Curtis Syndrome)?

A

The infection is believed to reach the subphrenic space by spread from the fallopian tube along the peritonium and paracolic gutters.

280
Q

Symptoms of Gonococcal Perihepatitis (Fitz-Hugh-Curtis Syndrome)

A
281
Q

Signs in Gonococcal Perihepatitis (Fitz-Hugh-Curtis Syndrome)

A
282
Q

Intro to TTT of Gonorrhoea

A
283
Q

General Measures in TTT of Gonorrhoea

A
284
Q

Treatment of Uncomplicated (urethral discharge only) genital infections in males & females

A
285
Q

TTT of Uncomplicated Gonococcal Infections of the Cervix, Urethra, pharynx and Rectum

A
286
Q

Treatment of Pharyngeal Gonorrhea

A

Ceftriaxone 250 mg IM single dose. This is the only option (spectinomycin not effective in this setting).

287
Q

Treatment of adult gonococcal conjunctivitis

A
  • Ceftriaxone 1 gm IM single dose.
  • Spectinomycin, 2 gm IM once.
288
Q

What causes most PIDs?

A

N. gonorrhoeae, C. trachomatis, or Gram-negative bacilli.

289
Q

TTT of Gonorhhoeal PID

A
290
Q

TTT of Gonorrheal DGI

A
291
Q

Follow Up in TTT of Gonorrhoea

A
292
Q

Transmission of Gonorrhoea in Prgenancy & Its results

A
  • Gonorrhoea Can be transmitted from the mother’s genital tract to the newborn during birth, and can cause:
    1. Gonococcal ophthalmia neonatorum.
    2. Systemic neonatal infection

It can also cause endometritis and pelvic sepsis in the mother.

293
Q

TTT of Gonorrhoea in Pregnancy

A
  • The Cephalosporins and Spectinomycin (2g IM once) are safe.
  • Azithromycin is safe and can be prescribed for chlamydia.
294
Q

Gonorrhoea in infants & Children

A
295
Q

What predisposes for Gonococcal Vulvovaginitis in prepubertal girls?

A

In prepubertal girls the vaginal mucosa is thin, immature and has alkaline pH. Thus, it is susceptible to gonococcal infection.

296
Q

MOI by Gonococcal Vulvovaginitis

A
297
Q

CP of Gonococcal Vulvovaginitis

A

(Urethritis, vulvovaginitis, proctitis)

1- Dysuria, vulvovaginal itching or soreness and difficulty in walking

2- The underwear may be stained & the purulent discharge is often obvious

3- The vulva & vagina are swollen, red and discharging mucopurulent discharge

298
Q

Dx of Gonococcal Vulvovaginitis

A
  • Swabs for Gram stain and Culture.
  • Other members of the household should be investigated.
299
Q

Other Causes of Gonococcal Vulvovaginitis

A
300
Q

TTT of Gonococcal Vulvovaginitis

A
301
Q

MOI by Gonococcal Ophthalmia Neonatorum

A
  • Infection of the babys’ eyes during parturition through the infected cervix.
302
Q

CP of Gonococcal Ophthalmia Neonatorum

A
303
Q

O

IP of Gonococcal Ophthalmia Neonatorum

A

2 - 5 days.

304
Q

TTT of Gonococcal Ophthalmia Neonatorum

A
305
Q

what is th commonest sexually transmitted disease in western countries?

A

NGU

306
Q

Prophylaxis in Gonococcal Ophthalmia Neonatorum

A
307
Q

Def of NGU

A

Sexually or nonsexually transmitted urethral inflammation which is NOT due to Neisseria gonorrhoea”

308
Q

what does NGU Include?

A
  • Patients with postgonococcal urethritis in which the gonococcus disappears but symptoms of urethritis remain are included in this category (NGU).
309
Q

What Causes NGU?

A
  • The syndrome results from a dual infection with N. gonorrhoea and other agents that cause NGU and the later are unmasked when the gonorrhoea is treated with drugs that are not effective for NGU.
310
Q

Etiology of NGU

A
  • Sexually transmitted urethritis
  • Non-Sexually acquired urethritis:
  • Non-specific urethritis
311
Q

Non-Sexually transmitted urethritis as a cause of NGU

A
312
Q

Sexually transmitted urethritis as a cause of NGU

A
313
Q

Non-specific urethritis as a cause of NGU

A
314
Q

CP of NGU

A
315
Q

Course of NGU

A
316
Q

Complications of NGU

A
317
Q

Dx of NGU

A
318
Q

TTT of NGU

A
319
Q

Follow up in NGU

A
320
Q

All persons found to have certain STDs should be tested for ……

A

Other STDs; Including:

  • Chlamydia
  • Syphilis
  • Gonorrhoea
  • Hepatitis-B
  • HIV

➥ For both patient and partner

321
Q

??

A

Onside

322
Q

Examples of Viral STDs

A
323
Q

wha causes increase in cases of Genital Herpes by HSV type 1?

A
  • increased practice of orogenital contact
324
Q

Etiology of Genital Herpes

A
325
Q

Transmission of Genital Herpes

A
326
Q

IP of Genital Herpes

A

2 - 7 days.

327
Q

Clinical Features of Genital Herpes

A
  • The genital infection may be asymptomatic or present with varying degrees of severity.
  1. primary attack
  2. Recurrent attacks
328
Q

CP of Primary attack of Genital Herpes

A
329
Q

CP of Recurrent attacks of Genital Herpes

A
330
Q

Complications of Genital Herpes

A
331
Q

DDx of Genital Herpes

A
332
Q

Diagnosis of Genital Herpes

A
333
Q

TTT of Genital Herpes

A
334
Q

Def of Condyloma Accuminata

A
  • Papillomatous growth found in the urogenital, perineal & perianal regions caused by infection with the Human papillomavirus (HPV).
335
Q

What Causes Condyloma Accuminata?

A

HPV

336
Q

HPV

  • Family
  • Genome
  • Genotypes
  • Transmission
  • Oncogenic Potential
A
337
Q

Clinical findings of Condyloma Accuminata

A
338
Q

Complications of Condyloma Accuminata

A
339
Q

Diagnosis of Condyloma Accuminata

A
340
Q

DDx of Condyloma Accuminata

A
341
Q

Managment of Condyloma Accuminata

A
342
Q

Prevention of Condyloma Accuminata

A
  • Prophylactic vaccines for genital HPV are currently under development.
343
Q

Def of AIDS

A
344
Q

What causes AIDS?

A
345
Q

Modes of transmission of HIV

A
346
Q

HIV

  • Family
  • Envelope
  • Genome
  • Types
  • Special Contents
  • Characters
  • Susceptibility
A
347
Q

what are body fluids with highst concentration of HIV?

A
  • Blood, semen, vaginal fluids, and breast milk are the body fluids known to have the highest concentrations of HIV.
348
Q

IP of HIV

A

3 - 10 years

349
Q

Pathogenesis of HIV

A
350
Q

Stages of HIV

A

Stage 1: Acute viral infection, seroconversion

Stage 2: Early disease, completely asymptomatic

Stage 3: Intermediate phase, overt disease

Stage 4: AIDS

351
Q

Stage 2 of HIV

A
352
Q

Stage 1 of HIV

A
353
Q

Stage 3 of HIV

A
354
Q

Stage 4 of HIV

A

(severe opportunistic infections & uncommon malignancy)

355
Q

Clinical Presentations of HIV

A
  • HIV infection can have myriad manifestations ranging from subclinical laboratory abnormalities to the opportunistic infections and malignancies that define the acquired immunodeficiency syndrome (AIDS).
  • The term AIDS has been used to describe the more severe manifestations of this disorder, particularly opportunistic infections and unusual tumors associated with immunodeficiency. The other major clinical presentations of HIV infection include PGL (persistent generalized lymphadenopathy) and ARC (AIDS-related complex).
  • It is not known which patients will progress from the asymptomatic seropositive state to the symptomatic phase of ARC or AIDS.
356
Q

Asymptomatic carrier state of HIV

A
357
Q

Persistent generalized lymphadenopathy (PGL) stage

A
358
Q

AIDS-related complex (ARC)

A
359
Q

Criteria for diagnosis of ARC

A
360
Q

Prognosis of ARC

A
  • In some cases, these features may disappear spontaneously. In others ARC may be an intermediate stage between the initial infection and AIDS, or a chronic manifestation of HIV infection.
361
Q

What are the Syndromes that maybe associated with HIV infection?

A
362
Q

Criteria For AIDS

A
363
Q

Aquired immunodeficiency syndrome AIDS

A
  • Severe opportunistic infections and uncommon malignancies occur on a background of profound immunosuppression (CD4 cell count below 200 cells/mm3) and the mortality is high.
  • The patients present in many ways
364
Q

Types of Manifestations of AIDS

A
  • Cutaneous manifestations of AIDS
  • Major noncutaneous clinical manifestations of AIDS
365
Q

Cutaneous manifestations of AIDS

A
  • The cutaneous manifestations may be divided into 3 large categories: infections, neoplastic and
    others.
  • Pre-existing diseases, such as psoriasis, may worsen in HIV-infected individuals and may present in atypical, exaggerated forms because of the underlying immunosuppression.
366
Q

Infectious diseases

Cutaneous manifestations of AIDS

A
367
Q

Neoplastic Diseases

Cutaneous manifestations of AIDS

A
368
Q

Characters of Kaposi’s sarcoma

A
  • A multicentric tumor arising from local hyperplasia of vascular endothelium.
  • It occurs as deep red to blue macular, plaque and nodular lesions on the skin, oral mucosa and internal organs.
369
Q

Other cutaneous manifestations

Cutaneous manifestations of AIDS

A
370
Q

Major noncutaneous clinical manifestations of AIDS

A

The clinical manifestations of AIDS are protean and affect virtually every organ in the body. The clinical manifestations depend upon the particular secondary disease.

A) Protozoal and helminthic infections
B) Fungal infections
C) Bacterial infections
D) Viral infections
E) Cancer

371
Q

Protozoal & Helminthic infections

Major noncutaneous clinical manifestations of AIDS

A
372
Q

Fungal Infections

Major noncutaneous clinical manifestations of AIDS

A
373
Q

Bacterial Infections

Major noncutaneous clinical manifestations of AIDS

A
374
Q

Viral Infections

Major noncutaneous clinical manifestations of AIDS

A
375
Q

Cancer

Major noncutaneous clinical manifestations of AIDS

A
376
Q

History of diseases in HIV

A
377
Q

Physical Examination in HIV

A
378
Q

Lab findings in HIV

A
379
Q

Imaging studies in HIV

A
  • Chest radiograph
  • Head CT scan
380
Q

when is chest radiograph required in HIV?

A
  • Cough or dyspnea
  • Fever without a source
  • Night sweats, fever, or weight loss
381
Q

How does Pneumocystic carini pneumonia appear in Chest radiograph?

A
  • Diffuse bilateral interstitial infiltrates
  • Spontaneous pneumothorax
382
Q

How does Tuberculosis appear in Chest radiograph?

A
  • Upper lobe infiltrates or cavitation
  • Hilar adenopathy
  • Pleural effusions
  • Miliary TB pattern
383
Q

When is head CT scan indicated in HIV?

A
  • Indicated for complaints of headache or focal neurologic deficit.
384
Q

Examples of Findings in CT Scan in HIV

A

Toxoplasmosis, hypodense, multiple sclerosis and ring-enhancing lesions

385
Q

Investigations in HIV

A
  • Laboratory evaluation of immune status
  • Smears, appropriate cultures and biopsy for more definitive diagnosis.
  • Testing for HIV infections
386
Q

Laboratory evaluation of immune status in HIV

A

(white cell count and helper/suppressor T-cell ratio).

➥ There is immunosuppression if helper/suppressor ratio is < 1, and there are fewer than 500 helper T cells.

387
Q

Methods of testing for HIV infections

A
  • HIV culture
  • Detection of HIV antibodies
  • Detection of HIV antigen
388
Q

HIV culture

A
  • Cultivation of host lymphocytes in presence of interleukin.

➥ It is the most accurate but difficult & expensive.

389
Q

what is the most accurate method for HIV Testing?

A

Culture

390
Q

Detection of HIV antibodies

A
391
Q

When do most people develop antibodies to HIV?

A
  • Within 2 to 8 weeks (average of 25 days), but it can take from 3 to 6 months.
392
Q

Detection of HIV antigen

A

(P24 in the core of the virus) by ELISA and PCR.

393
Q

Serologic testing for HIV currently involves …..

A
  • Serologic testing for HIV currently involves a screening test (ELISA) followed by a confirmatory test (Western blot) for all positives.
394
Q

When are patients Excluded from having HIV?

A

HIV antibody negative + have Normal T helper lymphocyte counts and Normal T helper : T suppressor ratios.

395
Q

Criteria for diagnosis of AIDS in adults

A
396
Q

Criteria for diagnosis of AIDS in Children

A
397
Q

Prevention for HIV infection

A

➥ Prevention of sexual transmission
➥ Prevention of non sexual transmission
➥ Prevention of vertical transmission

398
Q

Prevention of vertical transmission

A
399
Q

TTT of AIDs

A
400
Q

what reduces the chance of HIV transmission to her newborn?

A

Reverse Transcriptase Inhibitors

401
Q

Indications for initiation of anti-HIV drugs

A
402
Q

primary goals of antiretroviral therapy

A
403
Q

Classes of anti-retroviral drugs

A
404
Q

Passive immunization for HIV

A
  • Immunomodulators to restore T cell functions as IF, IL-2, Isoprenosine.
405
Q

Indications for change of drug

A
406
Q

Future vaccines for HIV

A
  • Subunit vaccines by recombinant DNA technology.
  • Liver recombinant microorganisms
407
Q

Genome of Cytomegalovirus

A

DNA ds

408
Q

Family of Cytomegalovirus

A

Herpesviridae family

409
Q

Transmission of Cytomegalovirus

A

intimate contact with infected body fluids including semen

410
Q

Can Cytomegalovirus survive in Frozen & Thawed semen?

A

Yes

411
Q

Is CMV A possible causative agent of hematospermia?

A

Yes

412
Q

What is the most important agent responsible for viral congenital infection and damage?

A

CMV

413
Q

What is responsible for most prenatal and perinatal virus infections?

A

CMV

414
Q

Effect of CMV on AIDS

A
  • Increases the risk of AIDS, possibly by activating CD4+ cells such that HIV-1 is produced.
415
Q

Hepatitis B virus

  • Family
  • Genome
  • Relation to STDs
A
  • Hepadnaviridae family
  • DNA ds
  • HBV DNA was integrated into the DNA of spermatozoa and mononuclear cells
416
Q

Hepatitis C virus

  • Family
  • Genome
  • Relation to STDs
A
  • Flaviviridae family
  • RNA ss+
  • HCV-specific antigens and RNA have also been detected in semen and the supernatant of spermatozoa, cell pillet and spermatids with chronic hepatitis C. However, it may be absent after Percooll selection
417
Q

Maternal Transmission of HCV

A
  • Maternal transmission of HCV could be observed in babies born to mothers with high level viraemia and infection through assisted reproduction and cryopreservation occurs.
418
Q

Hepatitis G virus

A

Hepatitis G virus (HGV) and HGV RNA are present in semen, with HIV-1-infected homosexual men.

419
Q

Def of Sexual Medicine

A
  • It is the branch of medicine that deals with the sexual health and sexual dysfunctions.
420
Q

What is Sexual act?

A
  • complex physiologic response that is dependent upon the integration of vascular, endocrine, psychological, and neurogenic mechanisms.
421
Q

what is Desire (libido)?

A
  • This stage in which a man or a woman begins to want or “desire” sexual activity
422
Q

Duration of Desire (libido)

A
  • May last from a moment to many years
423
Q

Requirements for the successful completion of the sexual act

A
  • sexual drive (libido)
  • an attractive partner
  • a suitable environment that provide freedom from distraction & anxiety
424
Q

what are the phases of physiologic sexual response cycle (sexual act)?

A
  • Excitement phase
  • Plateau phase (full sexual excitement)
  • Orgasmic phase
  • Resolution phase
425
Q

What creates Desire (libido)?

A
  • Sexual stimuli can create sexual desire
426
Q

Characters of Excitement phase in males

A
427
Q

Characters of Excitement phase in both

A
428
Q

Characters of Excitement phase in females

A
429
Q

Characters of Plateau phase
(full sexual excitement) in males

A
430
Q

Characters of Plateau phase
(full sexual excitement) in females

A
431
Q

Characters of Orgasmic Phase in males

A
432
Q

Characters of Orgasmic Phase in females

A
433
Q

Characters of Plateau phase
(full sexual excitement) in both

A
434
Q

Characters of Orgasmic Phase in both

A
435
Q

Characters of Resolution phase in males

A
436
Q

Characters of Resolution phase in females

A
437
Q

Characters of Resolution phase in both

A
438
Q

what is the Refractory period?

A
  • Occurs only in males,
439
Q

Difference between Ejaculation and Orgasm

A
440
Q

Characters of Refractory period

A
  • During which further erection & ejaculation are inhibited.
441
Q

Stimuli for Erection

A
442
Q

Center for Erection

A

Sacral segments (S2 - S4) of the spinal cord (parasympathetic system).

443
Q

Afferent for Erection

A
444
Q

Efferent for Erection

A
445
Q

what does cGMP cause in Erection?

A
  • Relaxation of the smooth muscles of the incoming arterial walls.
  • Filling the erectile tissue to with blood.
446
Q

Vascular response in Erection

A

1- Cavernosal artery dilatation leading to increased blood flow.

2- Relaxation of the smooth muscles of the blood sinusoids of corpora cavernosa.

3- Mechanical venous occlusion.

447
Q

Response in Erection

A
448
Q

Phases of Ejaculation

A
  • Emission
  • Bladder Neck Closure
  • Ejaculation Proper
449
Q

Significance of Phosphodiesterase 5 (PDE5) in Erection

A

is an intracellular enzyme that degrades cGMP → The penis returns to its flaccid state.

450
Q

What is Ejaculation?

A

Ejaculation is the process of semen expulsion from the sex organs to the outside, and this occurs through 3 rapidly successive phases which are reflex in nature

451
Q

Emission in Ejaculation

A
  • expulsion of semen into the posterior urethra (sympathetic control from T10 - L2 through the hypogastric plexus).
452
Q

Bladder neck closure in Ejaculation

A
  • to avoid retrograde ejaculation with formation of posterior urethral chamber (sympathetic control from T10 - L2).
453
Q

Ejaculation proper

A
  • Propulsion of semen out of the urethra.
  • This involves opening of external urethral sphincter, contraction of bulbourethral muscles and contraction of pelvic floor muscles (somatic control from S2 - S4 through pudendal nerve).
  • Ejaculation of the semen from the penis marks the height of orgasm.
454
Q

what is Orgasm?

A

A cortical sensory experience. It is the sum of the reactions and sensations in the body at climax that evokes feelings of release and pleasure.

455
Q

Def of Erectile dysfunction

A
  • Consistent inability to achieve or sustain an erection of sufficient rigidity for sexual intercourse to the point of satisfaction of both partners.
456
Q

Etiology of ED

A
  • With the introduction of new diagnostic techniques, the old theory that 90% of ED cases are due to psychogenic causes has become obsolete.
  • It is now estimated that organic causes are present in approximately 70% of cases of ED. However, both organic and psychogenic factors are involved in many cases.
457
Q

why is The term erectile dysfunction (ED) is more preferred than the term impotence?

A

because the latter is a comprehensive label for disturbances which may occur in libido erection, ejaculation, or orgasm.

458
Q

Phsychogenic causes of ED

A
459
Q

Organic causes of ED

A
  • Congenital penile deformities
  • Mechanical Causes
  • Endocrinal Causes
  • Metabolic Causes
  • Neurogenic Causes
  • Vasculogenic Causes
  • Exercise Intolerance
  • Iatrogenic Causes
460
Q

Congenital penile deformities which cause ED

A
461
Q

Mechanical causes of ED

A
462
Q

Endocrinal Causes of ED

A
463
Q

Metabolic Causes of ED

A
464
Q

what is Metabolic syndrome?

A
  • Is the name for a group of risk factors

(obesity, overweight, ↑ blood pressure, ↑triglycerides, dyslipidaemia & ↑ fasting glucose)

  • that increase the chance for heart disease, diabetes, stroke & erectile dysfunction.
465
Q

Neurogenic causes of ED

A
466
Q

Vasculogenic causes of ED

A
467
Q

Exercise intolerance as a cause of ED

A
468
Q

Iatrogenic Causes of ED

A
469
Q

Dx of ED

A
  • Thorough sexual, medical and drug History
  • Examination
  • Investigations
470
Q

How to differentiate organic from psychogenic impotence?

A

Onset, course, and duration:

  • Organic impotence is of insidious onset and there is progressive loss of erectile capacity in all sexually arousing situations (many men cannot get an erection from time to time, and this is normal).

Presence of morning, nocturnal, psychogenic, and reflex erections
- (defective in organic impotence).

471
Q

How to determine the etiology of ED?

A

− History of systemic disease, e.g., diabetes, hypertension, peripheral neuropathy or
organ failure.

− Risk factors for atherosclerosis such as smoking, hypertension and hyperlipidemia.

− History of marital troubles, drug intake, trauma or surgery.

472
Q

Examination in ED

A
473
Q

Differences between Psychogenic vs Organic ED

A
474
Q

History taking in ED

Extensive

A
475
Q

How to confirm the diagnosis by ED?

A
  1. Proper history and examination
  2. International index of erectile function questionnaire (15 questions)
  3. Intracavernous vasoactive drugs testing
476
Q

Drugs for Intracavernous injection (ICI)

A
  1. Papaverine hydrochloride.
  2. Prostaglandin E1 (Alprostadil)
  3. Phentolamine Mesylate.
  4. Atropine sulphate
477
Q

what does +ve test after Drugs for Intracavernous injection (ICI) exclude?

A

exclude significant vascular lesion

478
Q

Side effects of Drugs for Intracavernous injection (ICI)

A
  • Priapism
  • Fibrosis
  • Injury
  • Pain
  • Transient hypotension
479
Q

How to search for the etiology of ED?

A
480
Q

How to Assess the type & degree of ED?

A

Specialized methods for investigation

481
Q

Specialized methods for investigation of ED

A
  • Psychological testing
  • Monitoring of nocturnal erections
  • Penile-brachial pressure index.
  • Doppler studies
  • Cavernosometry and Cavernosography
  • Internal pudendal arteriography:
  • Biothesiometry
  • Neurologic evaluation of afferent and efferent pathways of erection
482
Q

Psychological testing

(ED)

A

for measurement of psychosexual functioning

483
Q

When do nocturnal erections happen?

A
  • Occur during rapid eye movement sleep to differentiate organic from psychogenic impotence.
484
Q

How are nocturnal erections monitored?

A
  • This is done by Rigiscan device examination.
485
Q

Doppler studies

ED Investigations

A
486
Q

Biothesiometry

A

Vibration sense in penis

487
Q

Cavernosometry and Cavernosography

ED

A

To study the venous drainage system of the penis
(the veno-occlusive mechanism of the corpus cavernosum).

488
Q

TTT of ED

A
  • Avoiding risk factors
  • Treatment of underlying causes
  • TTT of Psychogenic erectile dysfunction
  • TTT of Organic erectile dysfunction
489
Q

Neurologic evaluation of afferent and efferent pathways of erection

A

Biothesiometry, Electromyography, Verve conduction studies, Thermal or Vibratory threshold and Bulbocavernosus latency.

490
Q

Avoiding risk factors

TTT of ED

A

drugs, smoking, weight reduction and alcohol

491
Q

Treatment of underlying causes

TTT of ED

A

hypogonadism, surgical correction of correctable causes, control of diabetes, hypertension

492
Q

TTT of Psychogenic erectile dysfunction

TTT of ED

A
  • Psychotherapy, Behavior modification therapy, Sexual education & counseling and/or the use of a variety of medications. Such counseling is useful, even if the sexual dysfunction has a strictly organic basis.
493
Q

TTT of Organic erectile dysfunction

TTT of ED

A
  • Hormonal pharmacotherapy
  • Non-hormonal pharmacotherapy
  • Hemodynamic treatment
  • Penile prosthesis
  • Other treatment options
494
Q

Hormonal pharmacotherapy in TTT of ED

A
  • Androgens
  • Bromocriptine
495
Q

Non-hormonal pharmacotherapy in TTT of ED

A
  • PDE5 inhibitors
  • Intracorporal pharmacotherapy
  • Systemic therapy
496
Q

uses of androgens in TTT of ED

A
  • Hypogonadism is the principal indication.
  • Most impotent men have normal testosterone levels; so, the administration of testosterone to these individuals provides no benefit.
497
Q

Examples of PDE5 inhibitors

A

sildenafil, avanafil, vardenafil and tadalafil

498
Q

Uses of Bromocriptine in TTT of ED

A
  • erectile impotence secondary to hyperprolactinemia.
499
Q

uses of PDE5 inhibitors in TTT OF ED

A
  • These drugs inhibit PDE5 that degrades cGMP in the smooth muscle cells of the penis → accumulation of cGMP → good penile erection.
500
Q

Explain Intracorporal pharmacotherapy

A
  • Induction of artificial erection can be done, in selected cases, by injection of vasoactive drugs into corpora cavernosa to induce vasodilatation & erection.
  • Papaverine, phentolamine and prostaglandin E1 are commonly used for intracorporal injection.
501
Q

Systemic therapy in TTT of ED

A

yohimbine (alpha 2-adrenergic blocking agent).

502
Q

Hemodynamic treatment of ED

A

For treatment of vasculogenic impotence).

  1. Arterial reconstructive surgery.
  2. Venous reconstructive surgery.
503
Q

Penile prosthesis as TTT of ED

A
  • Penile implants are reserved for erectile impotence that is not amenable to any other form of therapy.
  • They are divided into inflatable and noninflatable devices.
  • Noninflatable devices include rigid rods and malleable devices.
504
Q

Other treatments (Pharma) for ED

A
  • vacuum-constriction devices and Electrostimulation therapy
505
Q

TTT of ED

PPT

A
506
Q

Def of Priapism

A
  • Uncommon disorder characterized by a painful prolonged and persistent (further than a time interval of 4 hours) penile erection in the absence of sexual interest or excitation.
507
Q

Pathophysiology of Priapism

A
508
Q

Etiology of Priapism

A
509
Q

Types of Priapism

A

So, there are 2 types of priapism depending on the cause:

  • Ischemic type: caused by: sickle cell disorders, leukemia & drugs
  • High flow type: caused by: Trauma
510
Q

Investigations for Priapism

A
  • Duplex examination and blood gas measurement of the blood from the penis.
511
Q

Managment of Priapism

A
512
Q

TTT of Priapism

A

conservative as ice packs, blood aspiration, drugs, or surgery

513
Q

what are Disorders of ejaculation?

A
  • Premature ejaculation
  • Delayed ejaculation
  • Retrograde ejaculation
514
Q

Def of Premature Ejaculation

A
  • It is the inability to control ejaculation for a sufficient length of time during vaginal penetration before the man wishes to ejaculate.
  • It is ejaculation which always or nearly always occurs prior to or within about 1 minute (for primary PE) and 3 minutes of vagina penetration (for secondary PE).
515
Q

Physiological PE

A
  • in younger men with a new partner but usually this is self-resolving with simple reassurance.
516
Q

what are causes of Premature Ejaculation?

A
  • Physiological PE
  • Psychological PE
  • Primary lifelong PE
  • Acquired or Secondary PE
517
Q

Def of Primary lifelong PE

A
  • occurring from the 1st sexual experience & persists over life.
518
Q

Psychological PE

A

Can occur in association with anxiety. It was once thought that almost all PE was psychological.

519
Q

Characters of Primary lifelong PE

A

characterized by -ve personal consequences (distress, bother, frustration and/or the avoidance of sexual intimacy).

520
Q

What is Primary lifelong PE associated with?

A
  • It is thought to be associated with diminished serotonergic neurotransmission & higher serum leptin levels. (neurobiologically - and possibly genetically- determined).
521
Q

TTT of Primary lifelong PE

A
  • Selective serotonin reuptake inhibitors
    (e.g., paroxetine) are effective in some cases.
522
Q

Def of Acquired or Secondary PE

A
  • Occurring at some point during life after a period of normal ejaculatory functioning.
523
Q

What causes Acquired or Secondary PE?

A
  • It may occur 2ry to thyroid overactivity or neural or pelvic pathology and in association with prostatitis.
524
Q

Causes of PE

Detailed

A

Neurobiologic defect (↓serotonin), Anxiety & Organic causes as erectile dysfunction, genital infections & hypogonadism

525
Q

what causes Retareded (Delayed) Ejaculation?

A
526
Q

Def of Retareded (Delayed) Ejaculation

A

is a rare sexual disorder in which the man finds it difficult or impossible to ejaculate, despite the presence of adequate sexual stimulation, erection & conscious desire to achieve orgasm.

527
Q

Classification of Retareded (Delayed) Ejaculation

A
528
Q

Managment of Retareded (Delayed) Ejaculation

A
  • Any underlying disease process should be corrected, and medications that may be causing the problem should be stopped, if possible, or substituted.
529
Q

Def of Retrograde Ejaculation

A
  • A sexual act of normal duration, ending with orgasm, in the absence of antegrade ejaculation, but in the presence of postejaculatory urine containing sperm & fructose
530
Q

what happens in Retrograde Ejaculation?

A
  • The emission enters the bladder rather than out of the penile shaft during ejaculation. It occurs when the bladder neck does not close following emission.
531
Q

Causes of Retrograde Ejaculation

A
532
Q

Managment of Retrograde Ejaculation

A
  • It does not require intervention unless a pregnancy is desired. It can be distinguished from anejaculation by the finding of sperm in the post-orgasmic urine.
533
Q

Def of Peyronie’s disease

A
  • It is a localized connective tissue disorder
534
Q

What deos Peyronie’s disease affect?

A
  • the tunica albuginea of the corpora cavernosa of the penis.
535
Q

Investigations in Peyronie’s disease

A
  • Ultrasound & MRI images are helpful to confirm the diagnosis, determine the extent of the plaque and detect calcification.
536
Q

Clinical findings in Peyronie’s disease

A

There is a history of painful bending of the erect penis, the pain usually resolves after 6-18 months. Some men feel a lump and are concerned about the possibility of cancer.

537
Q

Causes of Peyronie’s disease

A
538
Q

Managment of Peyronie’s disease

A
  • Minor degrees usually do not interfere with vaginal penetration, but reassurance is needed.
  • Surgery should be reserved for men with more severe deformity and should be deferred until the acute painful phase has settled.
539
Q

DDx of Genital Ulcers

A
540
Q

What does Each of the following flashcards cause?

Considering it as an STD

Neisseriae gonorrhoea

A

Gonorrhoea

541
Q

Uroplasma Urealyticum

A

NGU

542
Q

Treponema Pallium

A

Syphilis

543
Q

Mycoplasma Hominis

A

NGU

544
Q

Chalmydia Trachomatis

A

LGV - NGU

545
Q

Klebsiella Gramulomatis

A

granuloma inguinale

546
Q

Hemophilus Ducreyi

A

chancroid

547
Q

HPV

A

warts

548
Q

HSV

A

genital herpes

549
Q

Pox virus

A

molloscum Contagiosum

550
Q

HIV

A

AIDS

551
Q

Candida albicans

A

Genital candidiasis

552
Q

Phithirus pubis

A

pediculosis

553
Q

Trichomonas vaginalis

A

Trichomoniosis

554
Q

Sarcoptes scabiei

A

scabies

555
Q

Etiological classification of S.T.D.

A

1- Chancroid (soft sore)
2- Granuloma inguinale (Donovanosis)
3- Lymphogranuloma venereum (LGV)

556
Q

STDs In Tropical Areas

A

1- Chancroid (soft sore)
2- Granuloma inguinale (Donovanosis)
3- Lymphogranuloma venereum (LGV)

557
Q

what is another name for Chancroid?

A

Soft sore

558
Q

Def of Chancroid

A
559
Q

Causitave organism of Chancroid

A
560
Q

IP of Chancroid

A

7 days (ranges from 3 days to 3 weeks)

561
Q

Clinical Manifestations of Chancroid

A
562
Q

Characters of Chancroid Ulcer

A
563
Q

what is the most painful of all genital lesions?

A

Chancroid

564
Q

Dx of Chancroid

A
  • Direct smear stained with Gram’s stain
  • Direct immunofluorescent test (sensitive & Specific)
  • Culture
  • PCR (Improces accuracy)
565
Q

Direct smear in Dx of Chancroid

A
566
Q

DDx of Chancroid

A
567
Q

TTT of Chancroid

A
568
Q

Def of Granuloma Inguinale

A
569
Q

What is another name of Granuloma Inguinale?

A

Donovanosis

570
Q

Caustaive Organism of Granuloma Inguinale

A
571
Q

IP of Granuloma Inguinale

A

9 - 90 days

572
Q

Dx of Granuloma Inguinale

A
  • History of sexual contact.
  • Clinical appearance of the lesion.
  • Smears from scrapings obtained from the margin of the lesion are stained by Wright’s, Giemsa’s or Gram’s stain.
  • PCR testing using swabs rather than biopsy or tissue sample
573
Q

Clinical Manifestations of Granuloma Inguinale

A
574
Q

TTT of Granuloma Inguinale

A
575
Q

Def of Lymphogranuloma venerium (LGV)

A
576
Q

Causative Organism of Lymphogranuloma venerium (LGV)

A
577
Q

Chlamydia trachomatis

  • Family
  • Site
  • Size
  • Contents
  • Serotypes
A
578
Q

IP of Lymphogranuloma venerium (LGV)

A

1-6 weeks

579
Q

CP of Lymphogranuloma venerium (LGV)

A
  • Primary stage
  • Secondary stage
  • Late manifestations
580
Q

Primary Stage of Lymphogranuloma venerium (LGV)

A
581
Q

Secondary Stage of Lymphogranuloma venerium (LGV)

A
582
Q

CP of Inguinal syndrome

A
583
Q

CP of anorectal syndrome

A
  • Characterized by acute proctocolitis and extension of inflammation to the perirectal lymphatics.
  • There are signs and symptoms of proctitis, with anal pruritis, rectal pain and tenesmus.
  • Perirectal abscesses and anal fissure may be the presenting feature.
584
Q

Late manifestations of Lymphogranuloma venerium (LGV)

A
  • Anogenital and rectal syndrome
  • Genital elephantiasis
  • Malignant transformation
585
Q

Anogenital and rectal syndrome

Late manifestations of Lymphogranuloma venerium (LGV)

A
586
Q

what is the most common direct cause of death in LGV patients?

A
  • Bowel perforation followed by acute peritonitis
    is the most common direct cause of death in LGV patients.
587
Q

Malignant transformation

Late manifestations of Lymphogranuloma venerium (LGV)

A
  • Development of cancer following rectal strictures and/or genital elephantiasis may occur in these patients.
588
Q

Genital elephantiasis

Late manifestations of Lymphogranuloma venerium (LGV)

A
  • Lymphatic obstruction may lead to elephantiasis of the external genitalia (vulva, penis and scrotum).
589
Q

Dx of Lymphogranuloma venerium (LGV)

A
590
Q

DDx of Lymphogranuloma venerium (LGV)

A
591
Q

TTT of Lymphogranuloma venerium (LGV)

A
592
Q

Def of Genital Candidosis

A

It is the various clinical conditions caused by Candida, mostly Candida albicans

593
Q

what is the most common cause of abnormal vaginal discharge?

A

Genital Candidosis

594
Q

Predisposing factors for Genital Candidosis

A
595
Q

CP of Genital Candidosis in females

A
596
Q

CP of Genital Candidosis in males

A
597
Q

Dx of Genital Candidosis

A
598
Q

TTT of Genital Candidosis

A
599
Q

Def of Trichomoniasis

A
  • It is a common infection of the female genitourinary tract, It is less often diagnosed in males and is rare in children and after menopause.
600
Q

Etiology of Trichomoniasis

A

Trichomonas vaginalis (a flagellated protozoan)

601
Q

MOI by Trichomoniasis

A
  • Mode of infection in the adults is usually Sexual contact.
  • Accidental infection from improperly sterilized instruments, gloves, moist towels, toilet seats and baths is possible.
602
Q

Trichomoniasis in females

A
603
Q

Trichomoniasis in males

A
  • Males are often asymptomatic, but can transmit the infection. They may develop balanitis or balanoposthitis.
  • Trichomonal urethritis: symptoms and signs are indistinguishable from other causes of NGU.
604
Q

Dx of Trichomoniasis

A
605
Q

TTT of Trichomoniasis

A
  • Metronidazole: 200 mg 3 times a day for one week. OR * Tinidazole: 2gm orally in a single dose.
  • Sex partners should be treated at the same time.

Y3R1 - DALR ✋🏻 (4 decks)

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