Lecture 8.1 MJ slides Flashcards
Vulvitis:
1) What is the pathogenesis? Give examples of causes
2) What is a complication? How does this happen?
1) Reactive inflammation in response to exogenous stimulus
-Irritant; allergen; infectious; sexually transmitted (HPV, HSV, N. gonorrhea, chlamydia, Treponema pallidum), non-sexually transmitted (Candida)
2) Bartholin’s cyst
Obstruction of the secretory ducts → blockage → painful dilation of the glands
Lichen sclerosis:
1) What characterizes it?
2) What does it increase the risk of developing?
1) Thinning and hardening of the epidermis
Zone of acellular, homogenized, dermal fibrosis
Band-like mononuclear inflammatory cell infiltrate
2) SCC
Lichen Simplex Chronicus:
1) What is it?
2) What Sx is it associated with?
1) Epithelial thickening , aka hyperplasia. Hyperkeratosis
2) Pruritus
Vaginitis:
1) What is its main characteristic?
2) What are 3 causes?
1) Characterized by vaginal discharge (leukorrhea)
2) Bacterial pathogens
Fungal pathogens
Parasitic pathogens
Frequent offenders of vaginitis: List and describe 2 frequent offenders
1) Candida albicans → curdy white discharge.
Presence indicates predisposing influence or superinfection
2) Trichomonas vaginalis → copious gray-green discharge
STD
Flagellated protozoa visible with microscopy
Cervicitis:
1) What are the 2 classes?
2) What is it usually associated with?
3) What are the 5 potential infections? (hint: all are STIs)
4) How do you Tx?
1) Infectious and noninfectious
2) Purulent discharge (e.g., leukorrhea)
3) Chlamydia, Neisseria gonorrhea, Trichomonas Vaginalis
HSV 2*, certain HPV
4) Usually treat for GC, and may find Trichomonas Vaginalis
1) Explain how HPV is causative of cervical neoplasia
2) List risk factors for HPV and cervical carcinoma
3) Why can one of these be serious?
1) Transformation zone: squamocolumnar junction → eversion @ puberty →exposing the columnar cells of endocervix→ squamous metaplasia (normal process)
Suppression of p53 and RB proteins
2) HPV infection
-Multiple sex partners
-Male partner w/ multiple previous partners
-High risk strains of HPV (16,18,31,33)
-Cigarette smoking
Immunodeficiency
3) HSV can be serious b/c of maternal fetal transmission and systemic HSV infections in the newborn
Cervical Neoplasia:
1) What are the high risk types? Explain
2) What can prevent? What can detect?
1) 16, 18, 31, 33
-E6 & E7 viral oncoproteins of high-risk variants inhibit p53 & R8 (tumor suppressors)
2) HPV vaccine effective against types that are associated w/ carcinoma
Pap testing → good for detection of SIL and carcinoma
Carcinogenesis (HPV related): What are the 2 types? Which did each used to be called?
1) LSIL (low grade): formerly CIN I
2) HSIL (high grade): formerly CIN II & III
HPV-related carcinogenesis: Is LSIL (low grade) pre-malignant? Explain
-Not treated as a pre-malignant lesion
-Does not progress directly to carcinoma, and only a small % progress to HSIL.
HPV-related carcinogenesis:
1) What does HSIL (high grade) demonstrate? (3 things)
2) What is it considered a high risk for?
1) ↑ proliferation, arrested epithelial maturation, and ↓ levels of viral replication
2) Progression to carcinoma
Non-neoplastic Disorders of the Endometrium: What are 2 of these?
Adenomyosis and endometriosis
Adenomyosis:
1) What is it?
2) What is it often seen with?
3) What may the Sx be when it’s extensive?
1) Growth of endometrium into the myometrium
Often seen with uterine enlargement
3) Extensive growth may be w. menorrhagia, dysmenorrhea & pelvic pain
Endometriosis:
1) What is this?
2) What does it most often involve?
3) Where is it rarely located?
4) How many theories are there abt it?
1) Endometrial glands and stroma located outside of the uterus
-Tissue is displaced and abnormal
2) Most often involves pelvic or abdominal peritoneum
3) Rarely distant sites and lungs
4) 4 theories (next slide)
Endometriosis involves cyclic bleeding and is a common cause of dysmenorrhea and pelvic pain
*Endometrial Hyperplasia: List the risk factors
important
1) Anovulatory cycles
2) Polycystic ovary syndrome
3) Estrogen-producing ovarian tumor
4) Obesity
5) Estrogen therapy without counterbalancing with progestin
(all have estrogen exposure in common)
Endometrial Carcinoma: What are the 2 main types? What is each associated with? What mutations are involved in each?
1) Endometrioid carcinoma:associated with estrogen excess and endometrial hyperplasia.
Mutations in DNA mismatch repair genes and thetumor suppressor PTENgene.
2) Serous carcinoma(older women): usually is associated with endometrial atrophy and a distinct precursor lesion, serous endometrial intraepithelial carcinoma (SEIC).
-Mutations in theTP53gene are an early event, usually being present in serous endometrial intraepithelial carcinoma as well as invasive serous carcinoma.
Out of the 2 types of endometrial carcinoma, which has a worse prognosis and why?
Serous endometrial carcinoma(older women): Manifests more frequently with extrauterine extension
PCOS:
1) What is the inheritance pattern?
2) Etiology?
3) What does it sometimes include?
1) Complex inheritance pattern
2) Not completely understood
3) Cysts
1) What hormones happen normally for ovulation?
2) What about in PCOS?
1) Normal: GnRH > FSH/LH > ovary releases egg to uterus
2) GnRH released rapidly and daily instead of cyclically > LH goes up and FSH goes down > ovary makes more testosterone > hirsutism and acne, inhibited ovulation
What does the same genetic mechanism behind PCOS appear in recent studies to also act upon? What does this lead to?
The body’s insulin receptors > serine phosphorylation (don’t need to know that name) > insulin resistance develops
What happens to each of the following cardiovascular factors in pregnancy?
1) Systemic vascular resistance
2) HR
3) Blood volume and preload
1) Goes DOWN
2) Goes UP (a little)
3) Blood volume goes UP, so Preload goes UP
What happens to each of the following cardiovascular factors in pregnancy?
1) Stroke volume
2) Cardiac output
3) BP
1) Goes UP
2) Gradually goes UP
3) Falls to 26 weeks, then it gradually (and nearly) returns to baseline
More fluid during pregnancy leads to what 2 things?
1) Daytime pedal edema
2) Nocturia/frequent nighttime urination
1) Why does daytime pedal edema occur in pregnancy?
2) What about nocturia?
More fluid leads to
1) Daytime pedal edema
Water obeys the law of gravity fluid collects in the feet
Also, late term uterus compresses IVC less venous return more peripheral edema
2) Nocturia/frequent nighttime urination
When excess blood volume that was in her legs all day when this finally returns, she gets a “fluid bolus”
Increased venous return increased preload increased cardiac output increased renal perfusion pressure increased GFR more urine
Hemoglobin:
1) What is hemoglobin like pre-pregnancy?
-What does this look like on a lab?
2) What about early pregnancy until ~wk 26?
-What does this look like on a lab?
1) Normal amount of hemoglobin and normal volume
-Normal hemoglobin on lab
2) Same amount of hemoglobin as before, but increased blood volume
-Hemoglobin concentration falls on lab
Hemoglobin:
1) What is hemoglobin like at ~week 26 of pregnancy?
2) What about after week 26?
3) What’s the Tl;dr of hemoglobin in pregnancy?
1) Hemoglobin production has increased by now, but it still can’t keep up with blood volume
Hemoglobin concentration reaches its lowest point
2) RBC production begins catching up to blood volume
Toward the end of term, hemoglobin returns to normal
3) Mild anemia is common
Hypercoagubility:
*1) Estrogen regulates gene transcription in the liver, telling it to make more of which clotting factors and fewer what?
2) What does estrogen regulate? What does this tell them to do?
1) Factors 2, 7, 9, 10 and fewer protein C and S
2) Gene transcription in epithelial cells, telling them to make more fibrinogen!
*1) What is the mechanism behind decreased creatinine in pregnancy?
2) What is creatinine generally? What abt during pregnancy? What is considered too high?
3) What is also common?
1) Increased CO > increased renal perfusion > increased GFR > low creatinine
2) Generally, between 0.5-1.0
But in pregnant people 0.4 to 0.8
If she’s over one, it’s too high
3) Mild glucosuria is also common
*Why is there a higher risk of UTI in pregnancy?
Dilation of urinary tract secondary to increased blood volume = greater risk of ascending infxn
*1) Why can constipation occur in pregnancy?
2) What can help?
1) Progesterone is dilater > increased transit time of intestine > colonic relaxion > hard stools > constipation
2) Counsel on dietary fiber
-or Stool softener vs. motility agent
1) Why can GERD occur in pregnancy?
2) What is okay to take for this in pregnancy?
1) LES relaxion plus compression of stomach by gravid uterus > reflux
-Lifestyle changes: caffeine, spicey food, nicotine
2) TUMS are ok to take in pregnancy
What can happen regarding gallbladder disease in pregnancy?
1) Formation of new stones
2) Worsening of stones
3) Cholecystitis
1) When do mammary glands proliferate?
2) When do they differentiate?
3) When do they produce milk?
1) 1st trimester
2) 2nd trimester
3) 3rd trimester
1) What are 2 types of hyperpigmentation that can occur in pregnancy?
2) What are 2 other skin changes? Give an example of one
1) “Mask of pregnancy” also called “melasma”
-Etiology unknown
-Linea nigra
Darkening of skin over linea alba
2) Palmar erythema: spider angiomata
telangiectasia
Incomplete (partial) mole:
1) Are there fetal parts? How many chromosomes?
2) Is there anything wrong with the sperm and egg?
3) What can it do to HCG, and what else can it lead to?
1) There are fetal parts; incompletely chromosomal (69)
2) Incompletely spermal: good egg, bad fertilization
3) Incomplete rise in HCG
-Can lead to choriocarcinoma or invasive hydatidiform moles
Complete mole:
1) What is the number of chromosomes? Is there anything wrong with the sperm and egg?
2) What happens to HCG? What are the 2 effects of this?
3) What can it lead to? (2 things)
1) Completely chromosomal (46)
-Completely spermal: bad egg
2) Completely elevated HCG; HCG can lead to hyperthyroidism or hyperemesis gravidarum
3) Choriocarcinoma or invasive hydatidiform moles
1) How is TORCH syndrome spread?
2) What is TORCH syndrome?
3) What are the 4 main Sx?
1) All diseases are all vertically transmitted via placenta or blood, body fluids, breastmilk,
2) Destructive hematologic pattern driven by hemolysis
3) -Hepatosplenomegaly
-Kernicterus
-Petechia
-Delayed growth
TORCH syndrome:
1) What causes the Sx of Hepatosplenomegaly?
2) What causes the kernicterus?
3) What causes the petechia?
4) What do Caucasian babies with this look like? Why?
5) What does this syndrome cause?
1) Extramedullary hematopoiesis > Hepatosplenomegaly
2) Elevated bilirubin > Jaundice > kernicterus
3) Thrombocytopenia skin lesions petechia
4) Jaundice + petechia + Caucasian baby = blueberry muffins
5) Delayed growth
1) What does hCG + placental growth hormone do in pregnancy?
2) Why?
1) Antagonize the effect of insulin on the body cells
2) When mom eats, blood sugar goes up; normally, the pancreas would express insulin to usher sugar into cells
-In pregnancy, transcription of insulin receptors are antagonized by Beta-HCG and PG because the placenta wants to steal the sugar from her blood to feed the baby
-More blood sugar for longer period of time = more food for baby
Gestational diabetes:
1) Post-prandial physiology of pregnancy? Why?
2) Pre-prandial physiology of pregnancy? Why?
1) Postprandial hyperglycemia and insulinemia
-Because the body is “hiding” sugar from the cells by keeping it in the blood
2) Pre-prandial hypoglycemia
-Because the placenta is still stealing sugar, trying to feed baby.
1) What causes gestational diabetes?
2) How is it defined?
3) What 3 groups are at higher risk?
1) Exaggeration of normal physiology of pregnancy
2) Elevated blood glucose that starts after 20 weeks gestation
3) Obesity, Hispanic, Southeast Asian
Hyperglycemia complications in pregnancy:
1) What is the physiology?
2) What is the baby’s reaction to hyperglycemia?
1) Insulin does not cross placenta; baby has its own insulin
-Mom has the metabolic disorder and blood sugar is abnormally high (even for pregnancy)
2) Therefore, baby makes additional insulin to handle the elevated glucose load coming through the placenta
Insulin causes baby to grow BIG
Hyperglycemia:
1) Why is macrosomia (when baby grows too big) problematic?
2) Pregnancy with diabetes is closely surveilled, starting at week ____.
1) Complications at delivery:
-Shoulder dystocia > cesarian delivery
-Oligohydramnios
-Baby too big, so space for amniotic fluid too small increased risk of still birth
2) 32
Uncontrolled pregestational diabetes:
1) What body system can have defects when diabetes is uncontrolled? Give examples
2) In all diabetes in pregnancy, what 3 risks are increased in the last 20 wks?
1) Cardiac defects: Transposition of the great arteries, VSD, Tetralogy of Fallot
-Sacral agenesis = baby doesn’t make it to term
2) Eclampsia spectrum, placental abruption, pre-term delivery
Ectopic:
1) What is the pathogen?
2) What happens after implantation?
1) Fertilization > implantation not in uterus
-We tend to think tubal, but could be in peritoneum or cervix (Most of time “ampullary”” in the ampulla of uterine tube)
-Increased risk with any previous scaring, where it may also implant
2) Conceptus begins to grow, while burrowing into the wall of the uterine tube which is not designed to support conceptus with either adequate blood supply or mass
Ectopic:
1) What happens when bleeding occurs?
2) What stops the bleeding? Why?
1) Bleeding occurs, and can pass either into the abdominal cavity by way of fimbriated ends of uterine tube, or into the vaginal canal through uterus and cervix
2) Bc there is adequate space in the abdomen to receive massive hemorrhage, bleeding will not stop until mother progresses through hypovolemic shock and death
1) What is the most common malignancy in women?
2) What is the lifetime risk?
3) The majority (75%) ofthese are diagnosed after the age of _____.
1) Breast Carcinoma
2) 1 in 8
3) 50
The major risk factors for developingbreastcancer are related to what 2 things? Explain
1) Hormonal factors and 2) inherited susceptibility
-Only small percentage of breast cancer is inherited
About 12% of allbreastcancers are caused by identified germline mutations;________ and_________ genes account for _________ of the cases associated with single-gene mutations.
BRCA1; BRCA2; one-half
Adenocarcinoma of the Breast (95% of all breast malignancies): How is it divided? Why?
On the basis of expression of hormone receptors:
1) Estrogen receptor (ER)
2) Progesterone receptor (PR)
3) Human epidermal growth factor receptor 2 (HER 2)
-Receptor expression patterns are helpful because of differences in cancers
Adenocarcinoma of the Breast: What are the 3 major groups of receptor expression?
1) ER +
2) HER2 +
3) Triple negative ( ER, PR, and HER2 negative in 10-20 % of cancers)
The most common location of tumors within the breast is where?
Upper outer quadrant (50%)
