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Roy's Pathology (G3) > Female Repro Patho 3 > Flashcards

Female Repro Patho 3 Flashcards

1
Q

What are the disorders of early pregnancy (2) ?

A

Spontaneous Abortion
Ectopic Pregnancy

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2
Q

What is Spontaneous Abortion?
Loss of pregnancy within __ weeks of gestation without ___?

Most occur within __ Weeks?

A

Loss of pregnancy within 20 weeks of gestation without outside intervention

Most occur within 12 Weeks

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3
Q

How common is spontaneous abortion?

A

15% of pregnancies and additional 20% abort without notice (don’t even know baby was there)

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4
Q

What are the causes of spontaneous abortion?

A

Uterine defects: fibroids and polyps
Endocrine factors
Systemic: HTN and Diabetes
Fetal Chromosomal Abnormalities
Infections: TORCH

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5
Q

When to do chromosomal analysis?

A

Habitual or recurrent abortions → spontaneous loss of three or more pre-viable pregnancies

Malformed foetus

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6
Q

What is ectopic pregnancy?

A

Implanation of fetus at any site other than normal intrauterine location (1:150 pregnancies)

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7
Q

What are some prediposing factors of ectopic pregnancy? (many, know a few)

A
  • Chronic salpingitis (gonoccocal) → obstruction → tubo-ovarian masses/hydrosalpinx/ hydrosalpinx follicularis
  • Peritubal adhesions (appendicitis)
  • Leiomyomas → most common benign neoplasms → worsen from progesterone and pregnancy → grow due to nuclear oestrogen receptor but regress when postmenopause
  • Previous surgery
  • Benign cysts and tumours of tube
  • IUCD
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8
Q

What are some clinical features of ectopic pregnancy?

A
  • Amenorrhoea 6-8 weeks
  • Abdominal pain
  • Vaginal bleeding
  • Rupture leading to Hemorrhagic shock (Hematosalpinx, Hemoperitoneum)
  • Tubal abortion → contents of pregnancy expelled into abdominal cavity where it can be reabsorbed → spontaneous regression of pregnancy
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9
Q

How to diagnose ectopic pregnancy?

A

hCG titres -> elevated in normal and ectopic pregnancy

Pelvic ultrasound → swelling of tubes appreciated

Endometrial biopsy -> no evidence of pregnancy in endometrial cavity except secretory changes

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10
Q

Sites of ectopic pregnancy

A

> 50% may appear normal looking but are actually pathogenic

90% within tubes, some can be ovarian, some can be abdominal

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11
Q

What are the disorders of late pregnancy? (3)

A

Placental inflammations/infections
Toxemias
Placental abnormalities

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12
Q

What are the 3 types of placental inflammation? (Think Placenta, Membranes, Umbilical cord)

A

Villitis (placenta)
Chorioamnionitis (chorion and amnion membranes)
Funisitis (umbilical cord)

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13
Q

What are the two types of infections you can get in placental infection/inflammation?

A

Ascending infections
Haematogeneous infections

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14
Q

Which type of infection is more common for placental infections (ascending or haematogeneous)

A

Ascending

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15
Q

What are the 4 different types of Ascending infections and examples?

A

STD (Chlamydia, Syphilis)
Viral (Rubella, CMV)
Bacterial (Strep, Listeria)
Protozoa (Toxoplasmosis)

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16
Q

What are the haematogeneous infections?

A

TORCH
Toxoplasmosis
Other (HEP B)
Rubella
CMV
Herpes

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17
Q

What are the consequences of placental infections (to baby)

A

IUGR (intrauterine growth retardation)
Low birth weight
Premature delivery
Congenital abnormalities

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18
Q

What is toxemia of pregnancy?

A

Systemic syndrome characterised by widespread maternal endothelial dysfunction

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19
Q

Who is more susceptible to toxemia?

A

3-5% of pregnant women
In primiparous (first time giving birth)

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20
Q

When does toxemia usually occur?

A

Final trimester

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21
Q

Symptoms of pre-eclampsia (3)

A

HTN (HTN can develop without proteinuria) - Diffuse endothelial dysfunction and vasoconstriction caused

Proteinuria - Increased vascular permeability

Oedema (Facial puffiness) - Increased vascular permeability

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22
Q

Symptoms of Eclampsia (2)

A

Convulsions
DIC (disseminated intravascular coagulation) in Liver kidney heart placenta brain (LKHPB)

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23
Q

Pathogenesis of Eclampsia

A
  1. Primary causes of eclampsia (Immune, genetic??)
  2. Altered placentation and functional obstruction of spiral arterioles (that bring blood back from myometrium to decidua to maternal blood)
  3. Decreased uteroplacental perfusion
  4. Giving rise to 4 changes
    4a. Fall in prostaglandins (prostaglandins vasodilate) → leads to vasoconstriction
    4b. Rise in renin and angiotensin II → vasoconstriction to raise BP
    4c. Thromboxane rise → rise in platelet aggregation
    4d. Endothelin rise and NO fall → vasoconstriction
    5.These 4 changes lead to
    5a. Arterial vasoconstriction → hypertension
    5b. Further fall in uteroplacental perfusion
    5c. Endothelial injury and DIC
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24
Q

What are the consequences of DIC in eclampsia?

A

Liver → Abnormal liver function tests
Kidneys → proteinuria and low GFR
Other organs → ischemia and fibrin + thrombi (heart AMI, brain stroke)
CNS (brain) → seizures and coma
Generalised oedema

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25
Q

Histological features of Liver during toxemia (DIC)

A

Irregular, focal, subcapsular, intraparenchymal haemorrhage + necrosis

26
Q

Histological features of Kidney during toxemia (DIC)

A

Glomeruli show marked swelling of endothelial cell (endothelial damage) and fibrin thrombi

27
Q

Histological features of Brain during toxemia (DIC)

A

Haemorrhage along with small vessel thromboses

28
Q

Histological features of placenta during toxemia (DIC)

A

Generalised uteroplacental malperfusion due to spiral artery kinking - infarcts
Ischemia and vascular injury can be observed - hematomas
Fibrnoid necrosis of vessels (endothelial damage)

29
Q

What are the 3 placental abnormalities

A

Placenta previa
Abruptio Placentae
Placenta accreta

30
Q

What is placenta previa and its consequences?

A

Implantation of planceta over or near internal os, necessitating delivery of placenta before foetus
Antepartum hemorrahge (before childbirth)

31
Q

Two types of placenta previa?

A

Marginal placenta previa (not completing occluding the internal os) → chance that placenta will separate from the os (good)

Complete placenta previa (completely blocking internal os) → C SECTION!!!

32
Q

What is abruptio placentae and its consequences?

A

Premature incomplete or complete separation of normally positioned placenta from uterine wall during pregnancy/antepartum (leads to antepartum haemorrhage)

Concealed or revealed bleeding
- Severe bleeding can lead to shock or DIC
- Several fetal distress can cause death

33
Q

What is placenta accreta and its consequences?

A

Adhesion of normal placental villi to uterine wall due to absence of decidual plate between villi and myometrium –> Leads to failure of placenta to separate during the 3rd stage of labour

Severe post partum haemorrage - shock or DIC
Hysterectomy needed: stop bleeding

34
Q

How is the decidual plate formed usually?

A

Normally the endoemtrial stroma will undergo decidualization → to form the decidua basalis → the chorionic villi will then be attached to the decidua basalis to facilitate gaseous and nutrient exchange

But because of the failure of the formation of decidual plate, the villi will directly adhere to the myometrium..

35
Q

The 3 types of placenta accreta ranked in severity is…

A

Placenta accreta < Placenta Increta < Placenta Percreta

36
Q

What are trophoblasts?

A

outermost layer of cells of blastocyst that attaches fertilised ovum to uterine wall → serves as nutritional pathway of embryo (it wraps around the chorionic villi)

37
Q

What is gestational trophoblastic disease?

A

Spectrum of tumours and tumour-like conditions characterised by proliferation of placental tissue (villous/trophoblastic)

38
Q

What are the 3 types of gestational trophoblastic diseases?

A

Hydatidiform moles
Invasive moles
Choriocarcinoma

39
Q

Who is more likely to get gestational trophoblastic disease?

A

AGE
- More common in extremes of reproductive age (old and young)
- Malignant sequelae frequent in older patient

OBSTETRIC HISTORY
- Term pregnancies and live births have protective effect against trophoblastic diseases
- History of previous mole increases risk
- Half the choriocarcinomas follow a molar pregnancy

40
Q

What is a complete mole?

A

Abnormal conceptus without embryo-fetus with gross hydropic swelling of villi

41
Q

Pathogenesis of complete mole?

A

Complete mole results from fertilisation of egg in which nucleus is lost or inactivated

Most are 46XX some are 46 XY
- XX is either due to two sperm XX or one X sperm after duplication becomes XX
- XY is due to 23X + 23Y both from the male (two sperm)

42
Q

What is a partial mole?

A

Intimate admixture of both normal and abnormal villi. Fetal development may be present

43
Q

Pathogenesis of partial mole?

A

Triploid: 69XXY or 69XXX
23X + 23Y from male + 23X from female = 69XXY
46XY from male + 23X from female = 69XXY
23X + 23X from male + 23X from female 69XXX

44
Q

How to distinguish between the two moles (complete and incomplete)?

A

P57 is a surrogate marker for maternal genome ( can do immunhistochemistry) → if no maternal genome detected = complete mole

45
Q

Comparison between complete vs partial mole

A

Complete vs partial mole
Uterine size large vs Uterine size small
Very elevated serum hcg vs Elevated serum hcg
10-30% persistant GTD vs 4-11% persistent GTD
Embryo/fetus absent vs Embryo/fetus present
Trophoblastic hyperplasia diffuse vs focal

46
Q

Clinical presentations of moles?

A

Uterin hemorhage leading to Vagina bleeding
Pre-eclampsia toxemia in 1/4 of cases
Passage of molar vesicles
Hyperemesis
Hypercoagulation –>Pulmonary embolism
Hyperthyroidism

47
Q

Serology of moles?

A

Raised hcg levels

48
Q

Moles that have continued GTD will –>

A

Continued trophoblastic activity → 16% progress to invasive mole and 2.5% progress to choriocarcinoma

49
Q

Histological features of moles

A

Hydatidiform mole shows trophoblastic proliferation and villi are hydropic and oedematous + marked dilatation

50
Q

What is an invasive mole?

A

Hydatidiform mole in which hydropic villi
a)invade the myometrium or blood vessels
b) are transported to extrauterine sites

51
Q

Do invasive moles metastasise/invade?

A

Low mets risk - (24-40% distant mets to lungs, vulva, broad ligament)
Locally aggressive - Penetrates into myometrium and later blood vessels

52
Q

Prognosis of invasive moles

A

Highly chemosensitive
Usually self-limiting even without chemo
Deaths usually due to uterine perforation or intraperitoneal bleeding

53
Q

What is gestational choriocarcinoma?

A

Aggressive malignant tumour arising from trophoblastic tissue lining chorionic villi

50% of cases are preceded by a complete mole
25% of cases are preceded by abortion
22.5% of cases preceded by normal pregnancy
2.5% due to ectopic pregnancy

54
Q

Gross features of GCC

A

Hemorrhagic friable mass in uterine cavity

55
Q

Histological features of GCC

A

Hemorrhage and necrosis, anaplastic trophoblast, vascular invasion, trophoblastic proliferation

56
Q

Spread of GCC

A

Widespread metastases via blood (similar to choriocarcinoma of testes)
Usually to lung 50%
Vagina 30-40%
Brain liver marrow etc.

Lymphatic mets uncommon

57
Q

Clinical features of GCC

A

Abnormal uterine bleeding
Distant mets leads to haermorhagic events

58
Q

Serology test of GCC

A

hCG levels are elevated

59
Q

Prognosis of GCC

A

Previously fatal → but now with chemo it’s survival is 80-90%

BUT
Distant mets, failure of chemo - POOR PROGNOSIS

choriocarcinoma following term pregnancy - better prognosis

60
Q

figo staging of gcc

A

I- Tumor confined to uterus
II- Extends by mets or direction extension to other genital structures
III- mets to lung
IV - other distant metastases (w or w/o lung)

Roy's Pathology (G3) (2 decks)

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