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Y2B3 - Reproductive 📘 > Pathology 🩺 > Flashcards

Pathology 🩺 Flashcards

1
Q

what are congenital anomalies of Male genital system?

A
  • Phimosis.
  • Hypospadias. (Most common)
  • Epispadias. (Least common)
  • Cryptorchidism

All corrected by surgery

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2
Q

what is the definition of Phimosis?

A
  • Narrowing of the opening of the prepuce which causes inability to retract foreskin over glans
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3
Q

what are the complications of Phimosis?

A
  • Balanitis (inflammations of glans penis).
  • Urinary tract obstruction.
  • Squamous cell carcinoma of penis (Due to no circumcision)
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4
Q

what is the definition of hypospadias?

A

Urethra opens at ventral surface of penis

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5
Q

what are the complications of hypospadias?

A
  • Urinary tract obstruction.
  • Sterility.
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6
Q

what is the definition of epispadias?

A

Urethra opens at dorsal surface of penis

(Usually associated with phimosis)

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7
Q

what are the complications of epispadias?

A
  • Urinary tract obstruction.
  • Sterility.
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8
Q

what is the definition of cryptochidism (Undescended testis)?

A

Arrest of one or both testicles in a point during their descent to scrotum

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9
Q

what are the causes of cryptochidism (Undescended testis)?

A
  • Deficiency of gonadotrophic hormone of pituitary.
  • Organic obstruction.
  • Testicular defect.
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10
Q

M/E of cryptochidism (Undescended testis)

A
  • Atrophy of seminiferous tubules. “Due to high tempertaure”
  • Fibrosis.

in most cases, people with one testicle can get someone pregnant. Remember, one testicle can provide enough testosterone for you to get an erection and ejaculate. This is also enough to produce adequate sperm for fertilization.

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11
Q

what are the complications of cryptochidism (Undescended testis)?

A
  • Infertility (in bilateral cases).
  • Malignancy (precancerous for seminoma).
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12
Q

what are inflammations related to male genital system?

A
  • Prostatitis. (swollen prostate)
  • Seminal vasculitis.
  • Funiculitis: inflammation of spermatic cord.
  • Orchitis: inflammation of testis.
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13
Q

what are the causes of orchitis?

A
  • Bacterial: syphilis. “sexual virus”
  • Viral: Mumps orchitis.
  • Traumatic orchitis.
  • Autoimmune orchitis
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14
Q

what is the definition of Benign prostatic hyperplasia?

A
  • Hyperplastic enlargement of prostate.
  • Senile prostatic hyperplasia.

some notes:

  • Treatment is TURP
  • A transurethral resection of the prostate (TURP) is a surgical procedure that involves cutting away a section of the prostate. The prostate is a small gland in the pelvis only found in men.
  • One of the complications of TURP is postoperative retrograde ejaculation, which accounts for not only male infertility but also impaired sexual satisfaction [17]. The rate of retrograde ejaculation after TURP approximated 70–90% [18, 19].
  • https://youtu.be/nZxVvKw1IdU (The operation)
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15
Q

Incidence of Benign prostatic hyperplasia

A

Common in fifth decade of life and increase with age

All obes affected except posterior: BPH

Posterior lobe only affected: Prostatic cancer

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16
Q

what are the causes of Benign prostatic hyperplasia?

A

Absolute or relative increase of estrogen

absolute: increasedsecretion

Relative: decreased metabolism

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17
Q

N/E of Benign prostatic hyperplasia

A

Nodular, firm,greyish white with small cystic finely cystic C/S

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18
Q

M/E of Benign prostatic hyperplasia

A

Hyperplasia of both stroma and glands.

1) Glands:
* Increase in number.
* Variable in size and shape
* papillomatosis.
* Cysts contain corpora amylacea.

2) Stroma:
* Hyperplasia of smooth muscles and fibroblasts.

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19
Q

what are the complications of Benign prostatic hyperplasia?

A
  • Prostatism. (In 5-20% of patients)
  • Gradual urinary tract obstruction.
  • No relation to malignancy.
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20
Q

what characterizes prostatism?

A
  • Frequency (i.e., only small amounts are voided at a time)
  • Nocturia (urinating at night, same reason)
  • Difficulty starting and stopping urination
  • Incontinence (dribbling)
  • Dysuria (painful urination)
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21
Q

results of gradual urinary tract obstruction

A

1) Urethra: elongated, compressed to a mere slit.

2) Urinarybladder: trabeculations, diverticulations, cystitis, stones.

3) Bilateral hydroureter, pyoureter.

4) Bilateral hydronephrosis, pyonephrosis.

5) Chronic renal failure.

For more info: https://youtu.be/XyldGZdp0Sk

around 24:00

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22
Q

what is the incidence of Prostatic carcinoma?

A
  • One of commonest male cancers.
  • Age> 50 years
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23
Q

what are the causes of Prostatic carcinoma?

A
  • Genetic (Familial Predisposition)
  • Excess androgen
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24
Q

N/E of Prostatic carcinoma

A

Site: Posterior lobe

  • grayish white firm irregular mass
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25
Q

M/E of Prostatic carcinoma

A

Adenocarcinoma

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26
Q

spread of Prostatic carcinoma

A
  • Local
  • lymphatic
  • Blood: osteosclerotic bone metastasis with increased alkaline phosphatase.

(May cause sciatica)

Blood spread to Bone, Lung, Adrenals, Brain & Liver

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27
Q

what are prostatic tumor markers?

A

✓ Prostate specific antigen (PSA). (very specific)
✓ Carcinoembryonic antigen (CEA).
✓ Acid phosphatase.
✓ Alkaline phosphatase.

Most men without prostate cancer have PSA levels under 4 ng/mL of blood. When prostate cancer develops, the PSA level often goes above 4. Still, a level below 4 is not a guarantee that a man doesn’t have cancer. About 15% of men with a PSA below 4 will have prostate cancer if a biopsy is done.

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28
Q

what are testicular tumors?

A
  • Germ cell tumors (90%)
  • Non-germ cell tumors (3%)
  • Lymphoma (7%)
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29
Q

what are germ cell tumors?

A
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30
Q

what are non-germ cell tumors?

A

Leydig cell tumor: produce androgen (precocious puberty)

Sertoli cell tumor: produce estrogen (feminizing characters as gynecomastia)

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31
Q

what is the definition of varicocele?

A

Varicosity of pampiniform plexus of veins around spermatic cord

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32
Q

N/E of varicocele

A

bag of worm-like mass in the scrotum

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33
Q

what are the causes of varicocele?

A

Primary: in young unmarried men.

Secondary:
- Renal tumor compressing on spermatic vein
- Venous thrombosis.
- RSHF

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34
Q

what are the complications of varicocele?

A

Defective spermatogenesis due to increased temp in scrotum (infertility)

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35
Q

what is the definition of Spermatocele?

A

Small cysts filled with clear or milky fluid containing sperms in relation to epididymis (spermatozoa + albumin)

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36
Q

site of Spermatocele

A

more related to head of epididymis, less often in body or tail

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37
Q

what are the causes of Spermatocele?

A
  • Embryological remnants
  • Post inflammatory obstruction of epididymis
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38
Q

what is the definition of hydrocele?

A

Collection of serous fluid within Tunica vaginalis

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39
Q

what are the causes of hydrocele?

A

Primary: Unknown

Secondary:
- Diseases of testis, epididymis, spermatic cord
- generalized edema

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40
Q

what are the complications of hydrocele?

A

1- Pressure atrophy of testis (infertility).

2- secondary infection (pyocele)

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41
Q

what is the definition of hematocele?

A

Collection of blood within Tunica vaginalis

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42
Q

what are the complications of hematocele?

A

1- Pressure atrophy of testis (infertility).

2- secondary infection (pyocele)

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43
Q

what are the causes of hematocele?

A

Primary:
- Unknown

Secondary:
- Trauma
- Blood disease
- Malignant tumor

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44
Q

what is the definition of chylocele?

A

Collection of lymphatic fluid within tunica vaginalis

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45
Q

what are the causes of chylocele?

A

Lymphatic obstruction: e.g. filariasis

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46
Q

What are the diseases of vulva?

A

Benign lesions:

  1. Condyloma Accuminata which is virus related (Low risk HPV 6, 11).
  2. Squamous cell papilloma is not of viral origin.
  3. Hydradenoma Papilliform: Benign glandular proliferation.

Malignant lesions:
1. Squamous cell carcinoma.
2. Adenocarcinoma.
3. Malignant melanoma.

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47
Q

Hydradenoma Papilliform

A

Benign glandular proliferation.

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48
Q

what is Squamous cell carcinoma of the vulva related to?

A

It is related to (High risk HPV 16, 18).

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49
Q

Precursor lesion of Squamous cell carcinoma of the vulva

A

Vulvar Intraepithelial Neoplasia “VIN”

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50
Q

what are diseases of the Vagina?

A
  • Squamous cell carcinoma
  • Clear cell carcinoma
  • Embryonal Rhabdomyosarcoma (Sarcoma Botryoides)
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51
Q

What is squamous cell carcinoma of the vagina related to?

A

These tumors are related to (High risk HPV).

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52
Q

what is the precursor lesion of squamous cell carcinoma of the vagina?

A

Vaginal Intraepithelial Neoplasia “VaIN”

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53
Q

what is the nature of clear cell carcinoma of the vagina?

A

This is a variant of adenocarcinoma.

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54
Q

what is the precursor lesion of clear cell carcinoma of the vagina?

A

Vaginal adenosis which is an area of vaginal mucosa not covered by squamous epithelium.

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55
Q

what causes clear cell carcinoma of the vagina?

A
  • it is uncommon but is seen in patients exposed in utero to DES (Di-Ethyl Stilbestrol).
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56
Q

what is Embryonal Rhabdomyosarcoma (Sarcoma Botryoides)?

A

It is uncommon tumor occurring in girls from birth to adolescence (90% under 5 years of age). It is the least malignant of Rhabdomyosarcomas.

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57
Q

N/E of Embryonal Rhabdomyosarcoma (Sarcoma Botryoides)

A

Large - Polypoid - Reddish - Soft grape-like mass arising from submucosa.

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58
Q

M/E of Embryonal Rhabdomyosarcoma (Sarcoma Botryoides)

A

Malignant embryonal cells (Small cells with oval nuclei) with Rhabdomyoblastic differentiation (Striated muscle) in a Myxoid stroma

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59
Q

what are the diseases of the cervix?

A
  • Inflammations (Acute & Chronic Cervicitis)
  • Endocervical polyps
  • Micro-glandular hyperplasia
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60
Q

inflammation of cervix

A

Some degree of cervical inflammation may be found in virtually all women, and it is usually of little clinical consequence.

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61
Q

what organisms cause inflammation in cervix?

A
  • Infections by Gonococci, Chlamydia, Mycoplasma & Herpes simplex virus may produce significant acute or chronic cervicitis.
  • Important is to identify their association with upper genital tract disease, complications
    during pregnancy, and sexual transmission.
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62
Q

what does cervical inflammation produce (Concerning the epithelium)?

A

Cervical inflammation produces reparative and reactive changes of the epithelium.

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63
Q

what is Endocervical polyps?

A

Benign exophytic growths that arise from the endocervix.

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64
Q

what do Endocervical polyps cause?

A

They can cause irregular vaginal bleeding.

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65
Q

N/E of Endocervical polyps

A

Soft Mucoid lesions.

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66
Q

M/E of Endocervical polyps

A

Fibrous stroma + Dilated Mucus-secreting Endocervical glands + Inflammation.

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67
Q

what is Micro-glandular hyperplasia?

A

It is benign condition of the cervix in which there is closely packed proliferation of endocervical glands.

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68
Q

What causes Micro-glandular hyperplasia?

A

Caused by Progesterone administration such as during pregnancy, postpartum period or oral contraceptive pills administration.

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69
Q

Incidence of Carcinoma of the cervix

A
  • One of the commonest cancers in females especially in developing countries.
  • The age beak of incidence is 45 years.
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70
Q

what is the etiology of Carcinoma of the cervix?

A

Human Papilloma Virus (HPVI Is the most common in seyuallu active women

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71
Q

Pathogenesis of Carcinoma of the cervix

A
  • High risk HPVs (16 & 18) are the single most important factor in cervical oncogenesis.
  • HPVs infect immature basal cells of the squamous epithelium in areas of epithelial breaks, or immature sauamous cells present at the squamo-columnar junction
  • Intearation Of HOV DNA interferes with the P53 & Rb genes.
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72
Q

what are the risk factors of Carcinoma of the cervix?

A
  1. Smoking: Reduces local cervical immunity.
  2. Multiple sexual partners - Early age at first
    intercourse.
  3. Having a portner with sexually transmitted disease.
  4. Presence of another sexually transmitted disease lke HIV & Genital herpes.
  5. Long term Oral contraceotive pills - Multible pregnancies.
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73
Q

what are Precancerous lesions of carcinoma of the cervix?

A
  • Cervical Intra-epithelial Neoplasia
    “CIN”
  • Adenocarcinoma in situ “AIS”
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74
Q

Cervical Intra-epithelial Neoplasia (CIN)

A
  • The precancerous lesion of cervical squamous cell carcinoma.
  • It is classiled as CIN1 - CIN2 - CIN3 according to the upward extension or the abnormal cells in the epithelium.
  • The dysplastic cells show Loss of normal maturation, Increased Nuclear/Cytoplasmic ratio, Nuclear hyperchromatism, pleomorophism, frequent mitotic activity
  • CIN3 is the most severe where the atvoical cells involve the whole thickness of the epithelium
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75
Q

Adenocarcinoma in situ (AIS)

A

It is the precancerous lesion of invasive adenocarcinoma

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76
Q

CIN grading

A
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77
Q

Modified Simpler Bethesda classification of Carcinoma of the cervix

A
  • Low-grade Squamous Intra-epithelial Lesion (LSIL) = CIN I
  • High-grade Squamous Intra-epithelial Lesion (HSIL) = CIN Il and CIN III
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78
Q

what are the types of carcinoma of the cervix?

A

The most common types are squamous cell carcinoma (80% & Adenocarcinoma 15%)

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79
Q

what are the sites of Carcinoma of the cervix?

A
  1. Squamo-columnar junction.
  2. Endocervix with Squamous metaplasia
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80
Q

what is the shape of carcinoma of the cervix?

A
  1. Carcinoma in situ: Focal thickening.
  2. Invasive carcinoma:-
    a) Fungating “Exophytic”
    b) Ulcerating “Malignant ulcer”.
    c) Infiltrating “Endophytic” with induration & deformity of cervix.
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81
Q

Microscopic picture of carcinoma of the cervix

A

1) Squamous cell carcinomas (80%): Either Keratinizing or Non-keratinizing.

2) Adenocarcinomas (15%): Characterized by formation of irregular glandular structures.

3) Other types (5%): Adeno-squamous carcinoma - Neuroendocrine carcinoma

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82
Q

Spread of carcinoma of the cervix

A
  1. Local: Peritoneum - Bladder - Rectum
  2. Lymphatic: Regional LNs.
  3. Distant metastasis: Lung - Liver - Bone
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83
Q

Prognosis of carcinoma of the cervix

A
  • Because of screening programs, Most of patients are discovered in early stages.
  • Patients with stage 4 cancer die as a result of local extension of the tumor (e.g. Urethral obstruction - Pyelonephritis - Uremia) rather than Distant Metastases.
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84
Q

Prevention of Carcinoma of the cervix

A
  1. Vaccination against HPV introduced to girls at school age hopefully may reduce the
    cervical cancer risk
  2. Screening proarams:-
  • Aim: Detect precancerous lesions or abnormal cells early.
  • Method: PAP smear - HPV testing
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85
Q

what are the manifestations of uterine disease?

A
  1. Abnormal Uterine Bleeding.
  2. Pain Associated with Menstruation.
  3. Infertility & Spontaneous Abortion.
  4. Uterine Masses.
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86
Q

abnormal uterine bleeding

A

Any departure from a normal menstrual cycle pattern.

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87
Q

what are the key characteristics used in determination of abnormal uterine bleeding?

A

Regularity - Frequency - Heaviness - Duration of flow.

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88
Q

what are the causes of abnormal uterine bleeding?

A

Organic (Structural) abnormality:
- Chronic endometritis
- Submucosal leiomyoma
- Endometrial polyp
- Endometrial neoplasms.

Functional disturbances (Dysfunctional uterine bleeding):
- Result from abnormalities in the menstrual cycle or systemic diseases.

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89
Q

what are nonstructural causes of abnormal uterine bleeding?

A

1) Disorders of endometrial origin (Disturbances of the molecular mechanisms responsible for regulation of the volume of blood lost at menstruation).

2) Disorders of the hypothalamic-pituitary-ovarian axis.

3) Disorders of hemostasis (Coagulopathies).

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90
Q

FIGO classification for causes of abnormal uterine bleeding

A
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91
Q

what is endometritis?

A

Inflammation of the endometrial lining of the uterus.

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92
Q

what is what is endometritis divided into?

A
  1. Pregnancy-related endometritis.
  2. Endometritis unrelated to pregnancy (Pelvic inflammatory disease PID).
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93
Q

what causes acute endometritis?

A

Uncommon - Caused by bacterial
infections after delivery or miscarriage

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94
Q

what are the predisposing factors of acute endometritis?

A

Retained products of conception are the usual predisposing factors.

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95
Q

what does progression of acute endometritis Lead to?

A

Progression leads to puerperal sepsis

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96
Q

what are the clinical characters of chronic endometritis?

A

Bleeding - Pain - Discharge - Infertility.

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97
Q

M/E of chronic endometritis

A

Plasma cells

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98
Q

what does chronic endometritis occur in?

A

It occurs in:-

1) Chronic PID.

2) In post-partum or post- abortion patients with retained gestational tissues.

3) Intrauterine contraceptive device.

4) TB - Syphilis.

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99
Q

what is endometriosis?

A

Presence of endometrial tissue at a site other than the lining of the uterine cavity.

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100
Q

what is the ectopic endometrial tissue Composed of?

A

The “Ectopic” endometrial tissue is usually composed of both epithelial and stromal cells.

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101
Q

What characterizes ectopic endometrial tissue?

A

It responds to ovarian hormones somewhat like the uterine endometrium.

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102
Q

what are the types of endometriosis?

A

External Endometriosis: Presence of endometrial tissue (Glands & Intervening Stroma) outside the uterus.

Internal Endometriosis (Adenomyosis): Presence of endometrial tissue (Glands & Stroma) in the myometrium of uterine wall.

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103
Q

what is the definition of external endometriosis?

A

Presence of endometrial tissue outside the uterus.

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104
Q

site of external endometriosis

A

Pelvic organs - Laparotomy scar.

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105
Q

pathogenesis of external endometriosis

A

Suggested theories are:

Regurgitation theory:
- During menstruation, viable endometrial fragments pass via fallopian tube to implant on peritoneum

Metaplastic theory:
- Endometrial metaplasia of serosal cells leads to peritoneal lesions.

Vascular & Lymphatic dissemination theory:

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106
Q

N/E of external endometriosis

A
  • Hemorrhagic lesions (As the endometrial tissue undergoes cyclic menstrual bleeding.
  • It excites excessive fibrosis around it.
  • Ovarian Endometriosis (Chocolate Cysts) appears as cyst with dark red brown altered blood content.
  • The blood may organize leading to fibrous adhesion with surroundings.
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107
Q

ovarian endometriosis (Chocolate cyst)

A

appears as cyst with dark red brown altered blood content.

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108
Q

M/E of external endometriosis

A
  • Lesion consists of endometrial glands and stroma with hemosiderin.
  • Fibrosis + Hemosiderin laden macrophage.
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109
Q

definition of adenomyosis

A

Presence of endometrial tissue in the myometrium of uterine wall.

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110
Q

Site of adenomyosis

A

Myometrium of body of uterus.

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111
Q

Pathogenesis of adenomyosis

A

The basal zone of endometrium dips into adiacent myometrium.

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112
Q

N/E of adenomyosis

A
  • Uterus is symmetrically enlarged, Thick uterine wall
  • The lesions form dark red foci.
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113
Q

M/E of adenomyosis

A

Nests of endometrial glands and stroma in myometrium between muscle bundles.

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114
Q

What are the characters of endometrial polyp?

A
  • Endometrial polyps are sessile masses that project into the endometrial cavity.
  • They may be single or multiple.
  • It may cause abnormal bleeding.
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115
Q

what are the types of endometrial polyp?

A
  1. Functional endometrium.
  2. Hyperplastic endometrium, in association with endometrial hyperplasia.
  3. Endometrial polyps in association with the administration of tamoxifen, an anti-estrogen therapy of breast cancer.
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116
Q

what is the definition of endometrial hyperplasia?

A
  • Increased proliferation of the endometrial glands relative to the stroma, resulting in an increased gland-to-stroma ratio when compared with normal proliferative endometrium.
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117
Q

what is endometrial hyperplasia considered as?

A

It is an important cause of abnormal uterine bleeding.

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118
Q

what are the causes of endometrial hyperplasia?

A

Prolonged unopposed estrogen stimulation:-

  1. Repeated Anovulatory menstrual cycles.
  2. Obesity.
  3. Estrogen secreting tumors.
  4. Polycystic ovarian disease.
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119
Q

N/E of endometrial hyperplasia

A

Endometrial hyperplasia appears as increased endometrial thickness.

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120
Q

M/E of endometrial hyperplasia

A

Characterized by:

  • Glandular proliferation and crowding.
  • Increased gland to stromal ratio.
  • Varying degree of atypia.

Can be divided based on:
- Architecture (Simple - Complex).
- Cytologic features (With - Without atypia).

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121
Q

what is endometrial hyperplasia divided into?

A
  1. Simple hyperplasia without atypia.
  2. Simple hyperplasia with atypia.
  3. Complex hyperplasia without atypia.
  4. Complex hyperplasia with atypia.
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122
Q

what are the most common cancer of the female genital tract?

A

Endometrial carcinoma

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123
Q

compare between type I and type II endometrial carcinoma

A
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124
Q

what are precursor lesion of Type I carcinoma?

A

Atypical endometrial hyperplasia (Endometrial Intraepithelial Neoplasia, EIN).

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125
Q

what is the precursor lesion of type II carcinoma?

A

Surface endometrial lesion is called Endometrial Intraepithelial Carcinoma, EIC (Minimal Serous Carcinoma).

126
Q

what are other tumors that affect the endometrium?

A
  1. Carcino-Sarcoma (MMMT).
  2. Adeno-Sarcoma.
  3. Endometrial stromal tumors:-
    a) Benign: Stromal nodule.
    b) Malignant: Endometrial Stromal Sarcoma (ESS).
127
Q

what are tumors of the myometrium?

A

Benign: Leiomyoma

Malignant: Leiomyosarcoma

128
Q

Etiology of leiomyoma “Fibroid”

A

The tumor is linked to prolonged Hyperestrinism.

129
Q

site of leiomyoma “Fibroid”

A
  • Commonly arise in the body of uterus and cervix.
  • May be (Intramural - Submucous - Subserous - Leiomyomatous polyp - Parasitic)
130
Q

N/E of leiomyoma “Fibroid”

A
  • Rounded mass.
  • Pseudo-capsulated (Compressed uterine muscles & Interstitial tissue)
  • C/S: Whorly appearance
131
Q

M/E of leiomyoma “Fibroid”

A
  • Interlacing bundles of (Smooth muscle cells + Fibroblasts)
  • Secondary changes: Hyaline degeneration - Cysts - Necrosis - Calcification
  • Red degeneration (Hemorrhagic infarction) occurs during pregnancy
132
Q

what are the characteristics of Leiomyosarcoma?

A

Atypia - Increased mitotic figures - Coagulative necrosis

133
Q

what are gestational trophoblastic disease?

A

Group of diseases characterized by:-

  1. Proliferation of pregnancy-associated trophoblastic tissue.
  2. Has a malignant potential.
134
Q

classification of gestational trophoblastic diseases

A
135
Q

compare between complete hyaditiform mole & Partial mole in terms of:

  • Etiology
  • N/E
  • M/E
  • Prognosis
A
136
Q

What is another name of invasive mole?

A

(Chorio-adenoma Destruens)

137
Q

what does invasive mole complicate?

A

complicates complete mole

138
Q

what characterizes invasive mole?

A

Villi become more invasive to myometrium and blood vessels and spread to distant sites.

139
Q

what is the definition of choriocarcinoma?

A

Malignant neoplasm of trophoblastic cells.

140
Q

incidence of choriocarcinoma

A
  1. 50% arise in hydatiform mole.
  2. 25% in previous abortions.
  3. 22% in normal pregnancies.
141
Q

N/E of choriocarcinoma

A
  • Uterus contains a soft, friable, fleshy mass invading the uterine wall
  • Very hemorrhagic & necrotic.
142
Q

M/E of choriocarcinoma

A
  • Tumor tissue consists of malignant Cytotrophoblasts & Syncytiotrophoblasts which do not keep their normal relation but occurs as separate large sheets.
143
Q

what are the non-neoplastic cysts of the ovary?

A
  • Polycystic ovary (Stein - leventhal syndrome)
  • Follicular cysts
  • Corpus luteum cysts
  • Theca lutein cysts
  • Endometriotic cyst (Chocolate cyst)
144
Q

who does PCOS affect?

A
  • Affects young women.
145
Q

what is the most common cause of anovulatory infertility?

A

PCOS

146
Q

what is PCOS associated with?

A

*Associated with irregular menstrual periods, hyperandrogenism, hirsutism, acne, obesity, and insulin resistance

147
Q

what causes endometrial hyperplasia in PCOS?

A
  • Elevated serum androgens are converted to estrogens, unopposed estrogen may lead to -›Endometrial hyperplasia.
148
Q

morphology of PCOS

A
  • Multiple cystic follicles covered by a dense fibrous capsule lined by luteinized theca cells
149
Q

clinical picture of follicular cysts

A
  • Usually asymptomatic and incidental.
  • May present with symptoms related to hyper-estrogenism
150
Q

morphology of follicular cysts

A
  • Bilateral, multiple (may be single) filled with clear fluid.
151
Q

what are follicular cysts Lined by?

A
  • Lined by inner granulosa cells and outer theca cells
152
Q

what causes corpus luteum cysts?

A
  • Dilatation of degenerated corpus luteum.
153
Q

clinical picture of corpus luteum cysts

A
  • Can be asymptomatic or present with menstrual irregularities, abdominal pain, mass (large cyst), acute abdomen and hemoperitoneum (ruptured cyst).
154
Q

morphology of corpus luteum cysts

A

Usually single, large & filled with blood or serous fluid.

155
Q

what are corpus luteum cysts lined by?

A

Lined by an inner luteinized granulosa cells and outer theca cells

156
Q

what causes Theca lutein Cysts?

A

*Caused by elevated serum level of human chorionic gonadotropin (HCG)

157
Q

what are Theca lutein Cysts Associated with?

A

High association with gestational trophoblastic disease.

158
Q

morphology of Theca lutein Cysts

A

Bilateral, multiple, large cysts lined by luteinized theca cells

159
Q

what is the definition of endometriotic cyst?

A
  • Cystic changes of ovarian endometriosis.
160
Q

morphology of endometriotic cyst

A
  • Bilateral or unilateral.
  • Multiple small or single large cyst with fibrotic wall, and dark brown contents (chocolate cyst)
161
Q

M/E of endometriotic cyst

A
  • Characterized by endometrial glands, endometrial stroma and hemosiderin laden macrophages
162
Q

what is another name of endometriotic cyst?

A

(Chocolate cyst)

163
Q

what is another name of PCOS?

A

(Stein - leventhal syndrome)

164
Q

what are types of ovarian tumors?

A
165
Q

classification of tumors derived from surface epithelium of the ovary

A
166
Q

what is the traditional pathogenic view of the cause of tumors derived from the surface epithelium of the ovary?

A
167
Q
A
168
Q

Classification of epithelial ovarian carcinomas

A
169
Q

Compare between Begnin surface epithelium tumors Serous cystadenoma & Mucinous cystadenoma in terms of:

  • Age
  • Size
  • Shape
  • Surface
  • Pedicle
  • C/S (Wall - Lining - Content)
  • M/E
  • Complications
A
170
Q

What are the characteristcs of borderline surface epithelium tumors?

A
171
Q

What are the characteristcs of malignant surface epithelium tumors?

A
172
Q

what are tumors derived from germ cells (Totipotent cells)?

A
  • Undifferentiated Germ Cell Tumor (Dysgerminoma)
  • Differentiated along embryonic pathway (Teratoma)
  • Differentiated along Extra Embryonic Pathway
173
Q

Charachteristcs of undiffrentiated germ cell tumor (Dysgerminoma)

A

Uncommon malignant non-functioning neoplasm.

174
Q

Incidence of undiffrentiated germ cell tumor (Dysgerminoma)

A

Occurs in children & young adults.

175
Q

Microscopic appearence of undiffrentiated germ cell tumor (Dysgerminoma)

A

(Similar to Seminoma of testis)

  • Formed of: Lobules of Large Polygonal cells with Hyperchromatic nuclei
  • Cytoplasm: Abundant - Rich in Glycogen
  • Separated by: Fibrous septa infiltrated by Lymphocytes
176
Q

whata re types of tumors derived from germ cells that diffrentiated along embryonic pathway (Teratoma)?

A
  • Mature Teratoma: Benign - Cystic (Dermoid cyst).
  • Immature Teratoma: Malignant - Solid.
  • Monodermal Teratoma
177
Q

what charachterizes Monodermal teratoma? and give an example of it

A

One-sided development (One Tissue Line)

Example: Struma Ovarii (Thyroid tissue)

178
Q

what are types of tumors derived from germ cells that diffrentiated along extra-embryonic pathway?

A
  • Choriocarcinoma
  • Endodermal Sinus Tumor “Yolk Sac Tumor”
  • Embryonal Carcinoma
179
Q

Diffrentiation of choriocarcinoma

A

Differentiation towards Trophoblast (Placenta).

180
Q

What does choriocarcinoma secrete?

A

HCG hormone.

181
Q

Diffrentiation of Endodermal sinus tumor (Yolk sac tumor)

A

Differentiation towards yolk sac.

182
Q

what does Endodermal sinus tumor (Yolk sac tumor) secrete?

A

secretes Alpha Feto-Protein (AFP).

183
Q

what are types of tumors derived from sex cord and stromal cells?

A
  • Pure sec cord tumors
  • Pure stromal tumors
  • Mixed sex cord-stromal tumors
  • Meig’s syndrome
184
Q

what are (Pure sex cord tumors)?

A

1) Adult Granulosa cell tumor: Secretes Estrogen

2) Juvenile Granulosa cell tumor

3) Sertoli cell tumor: Secretes Estrogen

185
Q

what are Pure stromal tumors?

A

1) Leydig cell tumor: Secrets Androgen

2) Theca cell tumor (Thecoma): Secretes Estrogen

3) Fibroma

186
Q

what are Mixed sex
cord-stromal tumors?

A

Sertoli-Leydig cell tumor: Secretes Both hormones

187
Q

what is Meig syndrome?

A

Ovarian Fibroma + Ascites + Hydrothorax.

188
Q

Are metastaticv ovary tumors unilateral or bilateral?

A

Usually bilateral.

189
Q

How do tumors reach the ovary?

A

Direct - Lymphatic - Blood - Transcoelomic spread.

190
Q

what are the sites of primary tumors that metastasize to the ovary?

A

GIT - Uterus - GB - Pancreas - Lung.

191
Q

Charachters of Krukenberg tumor

A
  • Bilateral ovarian metastatic tumor.
  • Showing signet ring cells in fibrous stroma.
  • The primary tumor is present in G.I.T, mainly Stomach.
  • It reaches through Trans-coelomic spread.
192
Q

what are the methods of spread of ovarian cancers?

A
193
Q

why does peritoneal dissemenation of ovarian tumors seem to be easy?

A

Peritoneal disseminated metastasis seems to be easier in ovarian cancer because of the lack of anatomical barriers around the primary ovarian tumor.

194
Q

what is Sister joseph’s nodule?

A
  • Umbilical metastasis that may be first manifestation of disease.
195
Q

what are the most common sites of involvment in the spread of ovarian cancer?

A

Contralateral ovary - Peritoneal cavity - Pelvic & Para-aortic LNs - Liver

196
Q

what ismetastasis of ovarian cancer associated with?

A

Metastasis is associated with Malignant ascites - Intestinal obstruction - Ureteral involvement - Hydronephrosis

197
Q

Structure of breast

A
198
Q

Presentations of breast patient

A
  • Lump
  • Pain
  • Discharge
  • Skin manifestations
199
Q

what are common diseases of breast?

A
  • Breast cancer
  • Traumatic fat necrosis
  • Fibrocystic disease of the breast
  • Fibroadenoma
  • Breast abscess
  • Miscellaneous
200
Q

Diffrential diagnosis of breast lump

A

Traumatic: hematoma and traumatic fat necrosis.

Inflammatory: breast abscess, mammary ductectasia and granulomatous as T.B.

Fibrocystic disease of the breast.

Neoplastic mass: Fibroadenoma, duct papilloma, phylloides tumor and breast cancer

201
Q

what are the results of examintion of women seeking evaluation of breast lump?

A
  • No disease - 30%
  • Fibrocystic changes - 40%
  • Miscellaneous(benign) - 13%
  • Fibroadenoma - 7%
  • Cancer - 10%.
202
Q

Predisposing factors of Breast abscess

A
  1. Ignorance of nipple hygiene
  2. Nipple abrasion
  3. Retained milk
203
Q

Pathology of Breast abscess

A
  • Acute, chronic.
  • Single, multiple.
  • Premammary, Intramammary, Retromammary.
204
Q

what is another name of Mammary Duct Ectasia?

A
  • Periductal plasma cell mastitis
205
Q

Characters of Mammary Duct Ectasia

A
  • Dilatation of mammary ducts.
  • Inspissation of breast secretion.
  • Periductal plasma cell infiltrate.
206
Q

what is another name of Fibrocystic disease of the breast?

A
  • Cystic Mammary Hyperplasia
207
Q

Incidence of Fibrocystic disease of the breast

A
  • The most common breast disease.
  • It affects over half the women during reproductive period
208
Q

Prognosis of Fibrocystic disease of the breast

A
  • It is not premalignant.
209
Q

Etiology of Fibrocystic disease of the breast

A
  • Hyperestrogenemia.
210
Q

Pathogenesis of Fibrocystic disease of the breast

A
  • Derangement of cyclic breast changes that occur normally during menstrual cycle.
211
Q

N/E of Fibrocystic disease of the breast

A
  • Unilateral or bilateral.
  • Single or multiple.
  • No-encapsulated, ill defined, rubbery in consistency.
  • Mobile.
  • Grey white in colour.
  • Firm to rubbery.
  • Show variable sized cyst containing serous or hemorrhagic fluid.
212
Q

ME of Fibrocystic disease of the breast

A
  1. Fibrosis.
  2. Adenosis.
  3. Epitheliosis.
  4. Cystic formation.
213
Q

Prognosis of Fibrocystic disease of the breast

A
  • Epitheliosis increase incidence of breast cancer which is more evident with atypical hyperplasia
214
Q

what are begnin tumors of the breast?

A
  • Fibroadenoma
  • Phylloid tumor (Giant fibroadenoma)
  • Duct papilloma
215
Q

what is the most common begnin tumor of the breast?

A

Fibroadenoma

216
Q

Nature of Fibroadenoma

A

Mixed (fibrous and epithelial)

217
Q

Peak incidence of Fibroadenoma

A

Peak incidence is in 3rd decade.

218
Q

what causes Fibroadenoma?

A

estrogen stimulation

219
Q

NE of Fibroadenoma

A
  • Usually single, round or oval.
  • Encapsulated, well-defined.
  • Firm, freely mobile.
  • C/S: well circumscribed, encapsulated, greyish white
220
Q

ME of Fibroadenoma

A
  • Neoplastic acini and ducts separated by fibrous stroma.
  • Surrounded by true capsule.

It may be:

  1. Pericanalicular.
  2. Intracanalicular
  3. Mixed
221
Q

Nature of Phyloid tumor (Giant Fibroadenoma)

A

Fibro-epithelial tumor of unpredictable behaviour

222
Q

ME of Phyloid tumor (Giant Fibroadenoma)

A
  • Intracanalicular but stroma is highly cellular.
  • Cysts may be present
223
Q

Prognosis of Phyloid tumor (Giant Fibroadenoma)

A
  • about 10% metastasize.
  • Metastasis consists of stromal cells only.
224
Q

what is Duct papilloma?

A
  • Intra-ductal growths.
225
Q

what does Duct papilloma cause?

A
  • Frequently causes nipple discharge or small sub-areolar mas
226
Q

Incidence of Duct papilloma

A
  • Usually occur in 4th or 5th decade.
227
Q

Prognosis of Duct papilloma

A
  • Involution.
  • Rarely change to papillary carcinoma.
228
Q

what repesents 20% of all cancers in women?

A

Breast Carcinoma

229
Q

what is the most common cause of death in women between 35-55 years?

A

Breast Carcinoma

230
Q

Incidence of Breast carcinoma

A
  • In UK 1 in 10-12 chances
  • 1 in 8 women in US
  • Less incidence in Asia
  • Very rare before age 25
231
Q

where do majority of Breast carcinomas arise?

A
  • Majority of cancers arise in the ducts.
232
Q

Risk factors of Breast carcinoma

A
  • Female sex
  • Age
  • Obesity, high fat diet
  • Maternal relative with breast cancer.
  • Longer reproductive span.
  • Nulliparity, Oral contraceptives
  • Later age at first pregnancy.
  • Atypical epithelial hyperplasia.
  • Previous breast cancer/Endometrial Ca.
  • Geographic factors - country
  • BRCA1 and BRCA2 genes
233
Q

Clinical features of Breast carcinoma

A
  • Physiologic vs Pathologic changes
  • Lump / lumps
  • Discharge in many conditions.
  • Hard, soft, inflammation
  • Skin fixation / Skin retraction
234
Q

Diagnosis of Breast carcinoma

A
  • Mammorgraphy
  • Ultrasound
  • Fine Needle Aspiration cytology
  • Core Biopsy
  • Excision Biopsy
  • Frozen section
  • IHC
  • Molecular techniques – Gene mutation detection.
235
Q

what evidences Genetic & Familial presisposition in Breast carcinoma?

A
  • Younger age
  • First degree relatives
  • Bilaterality
  • Associated with endometrial & ovarian carcinoma
  • Mutation; BRAC1& BRACA2 genes
236
Q

Site of Breast carcinoma

A
  • Upper outer quadrant.
  • Lt breast > Rt one.
  • Bilateral in 4 -10%, mostly in lobular carcinoma.
237
Q

Incidence of different histologic types of Breast carcinoma

A
238
Q

Types of Breast carcinoma

A
239
Q

what is another name of In-situ duct carcinoma?

A
  • Intraduct carcinoma
240
Q

NE of In-situ duct carcinoma

A
  • Small hard masses
  • Bloody or serous nipple discharge.
  • C/S: Dilated ducts containing papillae or necrotic tissues.
241
Q

Prognosis of In-situ duct carcinoma

A
  • Good with complete removal.
242
Q

Definition of In-situ duct carcinoma with paget’s disease

A
  • Duct carcinoma extends along the main mammary duct to infiltrate the epidermis
243
Q

NE of In-situ duct carcinoma with paget’s disease

A

Nipple and areola show eczema.

244
Q

ME of In-situ duct carcinoma with paget’s disease

A
  • Thickened epidermis.
  • Rounded large pale vacuolated cells in the epidermis (Paget’s cells).
245
Q

what are the types of Invasive duct carcinoma?

A
  • Non-Otherwise Specified (NOS) (65-80%)
  • Otherwise Specified
    1. Medullary carcinoma. (1%-5%)
    2. Mucinous (colloid) carcinoma.
    3. Invasive duct carcinoma with paget’s disease.
246
Q

Incidence of Non-Otherwise specified carcinoma

A

the most common (65%-80%)

247
Q

NE of Non-Otherwise specified carcinoma

A
  • Ill-defined mass greyish white.
  • Stony hard in consistency.
  • Fixed.
  • C/S: retracted hard with gritty sensation with hge and necrosis.
  • Skin covering shows peau d’orange.
248
Q

ME of Non-Otherwise specified carcinoma

A
  • small sheets of malignant cells, separated by abundant Collagenous stroma (Dysmoplasia)
249
Q

Incidence of Medullary carcinoma

A
  • 1-5% of all mammary carcinoma.
250
Q

NE of Medullary carcinoma

A
  • large fleshy mass.
  • C/S: soft fleshy with foci of hge and necrosis.
251
Q

ME of Medullary carcinoma

A
  • solid sheets of malignant cells separated by scanty stroma that shows excess lymphocytes
252
Q

Prognosis of Medullary carcinoma

A
  • is relatively good.
253
Q

Characters of Invasive duct carcinoma with paget’s disease

A
  • The epidermis is thickened and infiltrated with Paget’s cells.
  • The dermis is infiltrated with masses of tumor cells.
254
Q

what is another name of In-situ lobular carcinoma?

A

Intra-lobular carcinoma

255
Q

How is In-situ lobular carcinoma usually discovered?

A
  • Usually discovered incidentally
256
Q

when does In-situ lobular carcinoma occur?

A

Occur near the menopause

257
Q

NE of In-situ lobular carcinoma

A

hard breast mass

258
Q

ME of In-situ lobular carcinoma

A

in one or more breast lobules all terminal ductules and acini are distented with malignant cells

259
Q

Site of Invasive lobular carcinoma

A
  • multicentric and bilateral
260
Q

NE of Invasive lobular carcinoma

A
  • Ill-defined breast mass.
261
Q

ME of Invasive lobular carcinoma

A
  • Strands of malignant cells of Indian file pattern separated by fibrous tissue stroma.
  • The cells are small, uniform with little pleomorphism
262
Q

Prognosis of Invasive lobular carcinoma

A
  • worse than invasive duct carcinoma
263
Q

Incidence of Mucinous (colloid) carcinoma

A
  • Occur in older women.
264
Q

NE of Mucinous (colloid) carcinoma

A
  • Slowly growing tumor forming large, soft gelatinous mass.
265
Q

ME of Mucinous (colloid) carcinoma

A
  • Lakes of mucin with scattered small islands of malignant cells
266
Q

Prognosis of Mucinous (colloid) carcinoma

A

good

267
Q

Spread of invasive carcinoma

A
  • Direct spread
  • Lymphatic spread
  • Blood spread
268
Q

Direct spread of invasive carcinoma

A
  • Deep fascia, pect. Ms, pl.& chest wall.
  • Overlying skin causing cancer en cuirasse (thick, hard skin fixed to underlying structures).
269
Q

Lymphatic spread of invasive carcinoma

A
  • Common and early
  • It occurs by 2 ways:
    1. Lymphaticembolization.
    2. Lymphaticpermeation.
270
Q

what does Lymphatic Embolization lead to?

A

It Leads to metastasis in:

a) L.N., axillary, int. mammary, medias. &supraclav.

b) Opposite breast.

c) liver and peritoneum

271
Q

what does Lymphatic permeation (skin lymphatic) lead to?

A

It Leads to:

a) small malignant nodules under the skin.

b) Cancer en cuirasse (widespread)

c) Peau d‘orange due to lymphatic edema of the skin except at site of hair follicle.

272
Q

what does blood spread of invasive carcinoma lead to?

A
  • Occurs early or late.
  • Metastasis to lung, liver, bone, brain & adrenal gland.
273
Q

5 & 7 year survival rates of different types of breast carcinoma

A
274
Q

Skin manifestations of breast carcinoma

A
  • Paget disease of nipple
  • Retraction of nipple
  • Peau-de Orange
  • Cancer en cuirasse.
  • Skin retraction
275
Q

what is Estrogen Receptor expression proportional to?

A
  • differentiation of tumor
276
Q

what is used to treat tumors with estrogen receptor?

A

tamoxifen (receptor antagonist)

277
Q

How are estrogen receptors demonstrated?

A

IHC stain

278
Q

what does HER2 proto-oncogene encode?

A
  • a cell surface receptor that is overexpressed in approximately 25%-30% of breast cancers
279
Q

what is used to treat tumors with extracelluar domain of the HER2 protein?

A
  • Trastuzumab (Herceptin®) is the first monoclonal antibody that targets the extracelluar domain of the HER2 protein
  • It inhibits growth of breast cancer cells that over express this protein.
280
Q

what is Gynecomastia?

A
  • enlargement of male breast
281
Q

Etiology of Gynecomastia

A

Physiological:
- at puberty.

Pathological:
- Increase estrogen level in:
* Liver cirrhosis
* Estrogen producing tumors
* Estrogen therapy
* Digitalis therapy.
* Klienefilter syndrome.

282
Q

NE of Gynecomastia

A
  • Disc like subareolar mass
  • Unilaterl or bilateral
283
Q

ME of Gynecomastia

A
  • Variable degree of epithelial hyperplasia in ducts.
  • Prominent swollen stroma.
284
Q

Incidence of Carcinoma of male breast

A
  • Occurs in old age
285
Q

what causes Carcinoma of male breast?

A
  • Common with estrogen therapy
286
Q

Prognosis of Carcinoma of male breast

A
  • It has bad prognosis as the tumor infiltrate locally early due to small breast size
287
Q

Definition of Gynecomastia

A
  • It is enlargement or swelling of breast tissue in males
288
Q

Causes of Gynecomastia

A
  • High male estrogen level
  • Estrogen imbalance with testosterone levels.
  • Excess secretion of prolactin due to hypothalamic dysfunction or pituitary tumors.
289
Q

Diagnosis of Gynecomastia

A
  • By demonstrating a high prolactin level
290
Q

Treatment of Gynecomastia

A

Medical: dopaminergic drugs→ ↓prolactin secretion.

Surgical: removal of tumor.

291
Q

Effect of prolactin on GTH

A

-ve feed-back on gonadotropins

292
Q

what does the negative feed-back effect of prolactin on GTH cause?

A
293
Q

Definintion of Hypogonadism

A
  • It is diminished functional activity of the gonads (the testes or the ovaries) that may result in diminished production of sex hormones.
294
Q

Types and causes of Hypogonadism

A

Primary hypogonadism
- can result from abnormal ovaries or testes (genetically, surgically removed or destructed)

Secondary hypogonadism
- due to pituitary or hypothalamic disease.

(Both may be before puberty or after puberty)

295
Q

Types of Hypogonadism in females

A
  • Prepubertal hypogonadism (Eunuchism)
  • Postpubertal hypogoandism
296
Q

Manifestations of Hypogonadism in females

A

Prepubertal hypogonadism (Eunuchism):
1- Primary amenorrhoea and sterility.
2- Secondary sex organs remain infantile.
3- Secondary sex characters do not appear.
4- The patient becomes tall due to delayed union of the epiphyses of long bones, span > height.

Postpubertal hypogoandism:
1- Secondary amenorrhoea and sterility.
2- The secondary sex organs regress.
3- The breasts atrophy and become pendulus.
4- The secondary sex characters regress.
5- Osteoprosis and muscle wasting.

297
Q

Definition of Hypergonadism

A
  • Is a condition where there is a hyperfunction of the gonads.
298
Q

Causes of Hypergonadism

A

It is caused by abnormally high levels of testosterone or estrogen, crucial hormones for sexual development.

299
Q

Causes and effects of Hypergonadism in females

A
300
Q

Definition of Subfertility

A
  • is a delay in conceiving , the possibility of conceiving naturally exists, but takes longer than average.
  • It generally describes any form of reduced fertility with prolonged time of unwanted non-conception.
301
Q

Definition of Infertility

A
  • Is the inability to conceive naturally.
302
Q

Definition of Amenorrhea

A
  • Absence of a menstrual period in a woman of reproductive age, most commonly during pregnancy and lactation (lactational amenorrhoea; method of contraception)
303
Q

Types of Amenorrhea

A
  • Primary amenorrhoea
  • Secondary amenorrhoea
304
Q

1ry amenorrhoea

A
  • absence of secondary sexual characteristics by age 14 with no menarche or normal secondary sexual characteristics but no menarche by 16 years of age.
305
Q

2ry amenorrhoea (menstrual cycles ceasing)

A
  • (menstrual cycles ceasing)
  • It is defined as the absence of menses for three months in a woman with previously normal menstruation.
306
Q

Causes of 2ry amenorrhoea (menstrual cycles ceasing)

A
  • hormonal disturbances from the hypothalamus and the pituitary gland, from premature menopause or intrauterine scar formation.
307
Q

Definition of Oligomenorrhea

A
  • Infrequent or very light menstruation.
  • More strictly, it is menstrual periods occurring at intervals of greater than 35 days, with only four to nine periods in a year.
308
Q

Causes of Oligomenorrhea

A
  1. Prolactinomas
  2. Thyrotoxicosis
  3. Hormonal changes in perimenopause.
  4. Polycystic ovary syndrome (PCOS): a condition in which excessive androgens (male sex hormones) are released by the ovaries.
309
Q

Definition of Virilism

A
  • Development of male secondary sex characteristics in a female due to excessive secretion of adrenal androgens.
310
Q

Causes of Virilism

A

Y2B3 - Reproductive 📘 (9 decks)

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