Patho- Exam 2- PCOS Flashcards

1
Q

What are two common non neoplastic and functional lesions of the ovaries?

A

Functional ( benign ) cysts and tumors , these are normal in females to a certain degree

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The ova develop in the cortical lesion, why is this important clinically?

A

That if cyst form they will be in the cortex and budge outward, they could rupture into the peritoneum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Follicle Cysts (Cystic follicles)

A

Follicle Cysts are so common, they are considered normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the possible Pathogenesis of Follicle Cysts ?

A

Unruptured graafian follicles or Follicles which ruptured and seal off immediately

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the graafian follicles?

A

Unruptured follicles with a lot of granulosa cells and estrogen in the antrum, but It never has the LH surge that causes the release of the egg, instead it just gets larger in size which will cause increased pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are some Characteristics of Follicle Cysts?

A

Occur in multiples
Contain Clear serous fluid
May be associated with increased estrogen production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Luteal Cysts

A

Luteal Cysts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Are Luteal Cysts common/ normal?

A

Granulosa luteal cysts are normally in the ovary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are Luteal Cysts lined with and what do they look like?

A

Lined with luteinized granulosa cells: bright yellow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a possible outcome of a Luteal Cysts?

A

Occasionally rupture: peritoneal manifestations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

When Luteal Cysts are chornic or old what do they look like?

A

Old hemorrhage and fibrosis look like endometirotic cysts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Polycystic ovarian syndrome

A

Polycystic ovarian syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Polycystic ovarian syndrome is aka as:

A

Stein-Leventhal syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Polycystic ovarian syndrome is considered a Heterogeneous disorder, what does this mean?

A

There is a number of thing going on/ wrong at once.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the size of the ovaries in Polycystic ovarian syndrome ?

A

Ovaries 2X size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What happeneds to the cortex during Polycystic ovarian syndrome ?

A

Thick fibrotic cortex- as the cyst is forming the ovarie has to restructure its self

17
Q

What is the etiology of Polycystic ovarian syndrome ?

A

Unclear etiology- has to do with genetic mutations and or the environmental influances.

18
Q

what does Polycystic ovarian syndrome Manifests with?

A

Numerous cystic follicles
Ovulatory dysfunction: anovulation
Androgen excess: hirstuism
Obesity : 40% - DMII plays a role in PCOS but not in everyone

19
Q

What is the Pathogenesis of Polycystic ovarian syndrome ?

A

Current theory: complex genetic trait with variants &

environmental factors

20
Q

What is the pathogenesis of Polycystic ovarian syndrome ?

A

the start of PCOS is a defect up in the hypothalamus and ant pit resulting in a lot of LH compaired to FSH which will stimulate thecal cells to produce a lot of androgens which will cause the follicle to arrest , premature follicular atresia, you get multiple cyst and they never release an egg so you have an Anovulatory state. The increased androgens also leads to Hyperandrogenism leads to hirsutism, acne, alopecia

Androgens cause:
Premature follicular atresia
Multiple follicular cysts
Anovulatory state
Hyperandrogenism leads to hirsutism, acne, alopecia
21
Q

What is the genetic mutation that leads to PCOS?

A

There is a genetic mutation that leads to an increase in frequency of GNRH paulses
This goes to the anterior pit gland, causing a lot of LH ( not as much FSH)
This goes to the ovaries
FSH: causes proliferation and a little estrogen production
LH: the HUGE amount affects the thecal cells and turns on the enzyme for androgen production.

The increased androgens will cause 3 things,
Increased hair, acne, alopecia
In the body androgens are converted to estrogen
Stop follicular growth (androgens stop follicular growth!)

22
Q

What effect does increased estrogen have?

A

It will go to the uterus and cause proliferation and thinking→ DUB→Hyperplasia→Endometiral CA.

23
Q

How does Obesity affect PCOS?

A

People with DMII have a lot of insulin, the insulin just does not work, the insulin does turn on an enzyme in the thecal cells to produce more androgens.

24
Q

So why does metfromin work for people with PCOS?

A

Metformin increases insulin sensitivity, causing insulin levels to go down, less available to stimulate the thecal cells, and therefore the symptoms of PCOS decrease

25
Q

What urine test can you do for PCOS?

A

There will be increased LH in the urine in patients with PCOS

26
Q

Review of the pathogenenisis of PCOS (From TBBs notes)

A

Accelerated GnRH activity with heightened pituitary response
Accelerated GnRH caused by ??
Insulin & IGFs
Rapid frequency of pulses favors LH
Frequency is not affected by BMI (only amplitude is) therefore BMI does not influence LH release
Excess LH activity in urine and plasma of women with PCOS
LH receptor is overexpressed in thecal and granulosa cells from polycystic ovaries
Genetic variants of the LH-beta subunit found in PCOS patients