Lecture 8.1: Female GU (unedited) Flashcards
Carcinoma of the Vulva: What are the 2 main categories? Which is more common?
1) HPV-related
2) Non-HPV related: more common
Vulvar carcinoma
HPV related (least common)
VIN or vulvar intraepithelial neoplasia- (considered pre-cancerous) → carcinoma in situ → may progress to invasive carcinoma (not inevitable)
Risk factors- smoking & immunodeficiency
Vulvar carcinoma
dVIN : differentiated vulvar intraepithelial neoplasia – characterized by cytologic atypia in the basal layer and abnormal keratinization→ may give rise to well differentiated keratinized squamous cell carcinoma
Risk factors - Age (older) & H/o reactive epithelial changes (lichen sclerosis)
Clinical manifestations
Leukoplakia (25 % are pigmented)
Paget’s Disease of the Vulva
Intraepidermal proliferation of epithelial cells
Extramammary –vulva (usually no association w/ carcinoma)
Breast- almost always associated w/ underlying carcinoma
Clinical manifestation:
Red, scaly, crusted plaque
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Premencarchal vaginal bleeding:
1) What does a pt need if FB?
2) What if you suspect sexual abuse?
1) Pt needs pelvic exam – if done by a provider, this likely requires anesthesia
2) Sexual Abuse: You are required by law to report if you suspect. You are not the detective. Suspicion = report
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Precocious puberty:
Central: early maturation of hypothalamic-pituitary-gonadal axis
Peripheral: excess secretion of sex hormones, adrenal glands, germ cell tumor, ovarian cyst
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Vaginal Atrophy get a good history and physical exam
Endometrial Cancer must have documented counseling on this
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Pregnancy: Vaginal bleeding in pregnancy will be addressed separately
Vaginal Atrophy: Who is it common in? Why?
Common occurrence in elderly patients
Secondary to falling estrogen levels after menopause
What are 2 reasons for 1st trimester vaginal bleeding? Explain
1) Ectopic pregnancy
2) Spontaneous abortion: Nonviable pregnancy
2nd / 3rd Trimester Vaginal Bleeding: Abruption
Abruption
Path: premature separation of placenta from endometrium
Pt: painful vaginal bleeding before labor; no contractions
Careful, there can be cases of abruption with no vaginal bleeding when placenta remains attached with hematoma forming behind it
2nd / 3rd Trimester Vaginal Bleeding” Previa:
1) What is the path?
2) How does it present?
1) Vasa previa/placenta previa os is covered by one of these structures Os dilates during delivery blood vessels (that belong to baby) get torn
2) Painless vaginal bleeding in early labor; there are contractions
2nd / 3rd Trimester Vaginal Bleeding: Uterine rupture
Path: contractions are so strong that the uterus rips baby is delivered into the abdomen
Pt: Sudden onset of new and severe pain with loss of fetal station!
Probably had prior cesarean and TOLAC
Abruption:
1) Define it
2) What are the risks? Explain
1) Separation of placenta from uterine wall after 20 weeks but before delivery
2) Maternal HTN
-Abd trauma
-Smoking (nearly doubles risk)
-Substance abuse (esp. cocaine)
-Age over 40 yo
-Sudden uterine decompression: Rupture of membranes in woman with polyhydramnios, delivery of first baby in multiple gestation
Carcinogenesis(HPV related)
1) What precedes cancer by years to decades?
1) Begins with precancerous epithelial change
SIL-Squamous intraepithelial lesion -precedes cancer by years to decades
Peak incidence of SIL-30 years of age
Peak incidence of invasive carcinoma-45 years of age
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1) What is an established component of PID?
1) Inflammation of the endometrium
2)
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Hypotheses of endometrial dispersion include what? Explain
1)
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Inflammation of fallopian tubes
Almost always infections resulting from PID
G and C
Blood borne infections- happen when staph, strep penetrate the wall of the tubes allowing for hematogenous spread to distant sites
Signs and symptoms
Fever, lower abdominal/pelvic pain, masses, distended tubes
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May lead to ↑ risk of tubal ectopic or sterility
Primary adenocarcinoma of the fallopian tube
Once uncommon, but now thought to be the site of origin for high grade serous carcinoma that was once thought to be from the ovary
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Polycystic Ovarian Syndrome(PCOS)
Complex endocrine disorder characterized by Hyperandrogenism
Menstrual Abnormalities
Polycystic ovaries
Chronic anovulation
↓ fertility
2) After menarche, in teenagers or young adults
Oligomenorrhea
Hirsutism
Infertility
Obesity
List the 3 places ovarian tumors can occur and describe each
1) Epithelium
Most common malignant type (90%)
More common age >40
Primarily serous, mucinous, or endometroid
2) Sex cord–stromal cells
May display differentiation toward granulosa, Sertoli, Leydig, or ovarian stromal cell type.
Depending on differentiation, they may produce estrogens or androgens.
3) Germ cells
Mostly cystic teratomas
Most common ovarian tumor in young women; the vast majority are benign.
may differentiate toward oogonia (dysgerminoma), primitive embryonal tissue (embryonal), yolk sac (endodermal sinus tumor), placental tissue (choriocarcinoma), or multiple tissue types (teratoma)
Cardiovascular: Decrease in SVR
Cardiovascular: Decrease in SVR
Mean Arterial Pressure = Cardiac Output x Systemic Vascular Resistance
Cardiac Output = Heart Rate x Stroke Volume
Stroke volume = Contractility x Preload
What are 2 changes that affect SVR in pregnancy? Describe each. How does your body compensate?
1) Progesterone: Smooth muscle dilator
2) Placental growth: New vessels are added which effectively increases mean small vessel diameter
-Placenta stops growing at ~wk 26
Cardiovascular: Increase in Volume in pregnancy
1) What system further compensates for falling SVR? Explain
2) When does it match the pace of falling SVR?
1) Renin/ang/aldo system: aldo sodium volume PRELOAD stroke volume
2) After week 26
Describe BP in pregnancy
The BP falls until about week 26 due to progesterone and placental growth, then returns gradually to nearly reach baseline before term
How much does HR increase in pregnancy? Why do we care?
By about 10-20 BPM over baseline; tachycardia
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1) What should cause weight gain in pregnancy?
2) How much weight gain is normal?
1) Amniotic fluid, placenta, fetus, maternal adipose stores
2) If underweight to begin with, gain more to build up adipose stores
-If overweight to begin with, gain less; adipose stores are adequate, and weight gain should be due to fluid, placenta, fetus
Thalidomide
1) What was it used for?
2) What happened?
1)
Diethylstilbestrol
Was given for at risk pregnancy
Their children got vaginal adenosis/adenoma, sarcoma botryoides (cancer of vagina), clear cell carcinoma (vaginal cancer)
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Warfarin
Hypoplastic nose
Skeletal abnormalities
Ocular abnormalities
Neonatal bleeding
Mental retardation
Eplieptic meds
Weigh risk: drug vs. disease
It’s better to come off drugs if mom can
Levetiracetam and Lamotrigine
Levels will vary throughout pregnancy because estrogen affects their metabolism– must be monitored
Epileptic meds
1) Phenytoin = severely teratogenic
Phenobarbital = severely teratogenic
Topiramate = severely teratogenic
2) Valproate = cardiac defects
Not indicated for grand mal seizures
In other words – it is better for mom to tolerate “minor” seizures than for baby to have side effects;
3) Carbamazepine = Stop it if you can, but this is the only seizure med indicated for tic douloureux
Extremely painful; but consider tolerating the illness while pregnant
Teratogenic drugs:
1) What HTN drug?
2) What is the only FDA approved diabetes drug? What is the second line?
3)
Hypertension:
ACE/ARB both teratogenic
Diabetes
Only FDA approved drug is insulin
If insulin is not an option – second line is metformin
Teratogenic drugs
1) Antibiotics
Bactrim
Fluoroquinolone
Tetracycline
Acne
Isotretinoin
Statins
Early reports indicated these were teratogenic, but this is currently being reconsidered
True or false: Chemotherapy is harmful to the fetus
This will be managed by specialty
True
Fetal alcohol syndrome (FAS)
Causes hallmark congenital abnormalities:
Short palpebral fissure and smooth philtrum
Growth Retardation
Neurobehavorial disorder
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Increased ADHD
Increased Autism Spectrum
Developmental Delay
Intellectual disability
Oppositional defiant disorder
Conduct disorder
Mood disorder: depression, bipolar
Impulsive behavior
Reactive attachment disorder and PTSD *
What is nicotine associated with in pregnancy?
Placental abruption
Preterm premature rupture of membranes
Placenta previa
Preterm labor
Low birth weight
Ectopic pregnancy
Possibly Miscarriage
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Path
Primary hypertension
Pt
Diagnosis of HTN before becoming pregnant
Gestational HTN / preeclampsia / HELLP / eclampsia spectrum:
1) What is the pathology?
2) What are some changes the pt would notice?
1) Not well understood
Spectrum that begins at gestational HTN preeclampsia without severe features preeclampsia with severe features eclampsia / HELLP
2) HA, vision changes, swelling in face and hands
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Gestational HTN sustained readings of 140/90 after week 20
GET MICROSCOPIC URINE AND LOOK FOR PROTEIN
Almost 50% of women with gestational HTN go on to develop preclampsia
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Preeclampsia without sustained readings of 140/90 after week 20 + proteinuria
GET MICROSCOPIC URINE AND LOOK FOR PROTEIN
Protein to creatinine ratio: positive if > 0.3
More than 300 mg protein on 24-hour collection
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Dx Cont.
Preeclampsia with sustained readings of 160/110 + any one
Platelets < 100
AST or ALT 2x UNL
RUQ or epigastric pain
Cr > 1.1 or 2x baseline
Pulmonary edema
HA or vision changes
Items 2, 3, and 4 are the beginning of HELLP Syndrome (stay tuned)
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HELLP Preeclampsia + Elevated Liver Enzymes AND Low Platelets
Eclampsia Preeclampsia + Seizure
Alloimmunization: What happens during pregnancy #1?
1) Fertilization between Rh-negative female and an Rh-positive male
2) If baby inherits Rh + gene from father, baby will be Rh +
3) Baby’s blood does not leave the placenta
Mom’s immune system is unaware that there is any Rhesus antigen present in baby’s blood
Nor is there any natural immunity that occurs against Rhesus antigen
Therefore, in order for Mom’s immune system to become primed against Rhesus antigen, she must be exposed
What are some examples of first exposures for alloimmunization? What do they lead to?
Delivery
Loss
Procedures
Trauma
IgM Antibodies Against Rhesus antigen > IgG Antibodies Against Rhesus antigen
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Extramedullary hematopoiesis
Remember that RBCs are made primarily in bone marrow
But Bone marrow cannot keep up
Liver and Spleen attempt to aid in production
These organs hypertrophy hepatosplenomegaly
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Hemolysis Increased bilirubin
Kernicterus: infant brain damage resulting from high levels of bilirubin in blood
Fetal Demise
Prevention:
Prevent mom’s immune system from exposure!
Routine screening establishes Rh status
If Mom is Rh positive, you’re DONE
If Mom is Rh negative, determine dad’s status
If Dad is Rh negative, you’re DONE
If Dad is Rh positive or unknown give Rhogam
How does Rhogam work?
Mom Rh- and antibody - AND baby Rh+
Give anti rhesus antigen D immune globulin
This is IgG to the rhesus antigen
Yes, the same thing that kills baby #2
Given at the correct time it destroys any Rhesus antigen cells in mom’s blood stream before her immune system ever recognizes them
Toxoplasmosis:
1) What is the pathophys?
2) What are the Sx in mom?
3) What are the Sx in baby?
1) Toxoplasmosis: protozoan toxoplasma Gondii
Pregnant woman in contact with Cat feces (changing litter box) or consumes undercooked lamb or pork
-Virus passed to fetus through placenta during first 6 months of pregnancy
2) Usually asymptomatic, but may have LAD and flu-like symptoms
3) Congenital toxoplasmosis
Describe the Sx of congenital toxoplasmosis
TORCH and:
1) Chorioretinitis: Inflammation of choroid and retina seen on fundoscopic exam
-White and yellow cotton-like scars
2) Hydrocephalus: ICF accumulates and enlarges ventricles macrocephaly
3) Intracranial calcifications: White spots on CT
Syphilis pathophys:
1) What is the organism and how is it spread?
2) What is the primary presentation?
3) What abt secondary?
4) What abt tertiary?
1) Spirochete: treponema pallidum sexual contact
2) Chancre: Labia, anal region, cervix
3) (2-10 weeks): Enters blood stream, generalized LAD
-Maculopapular rash including palms and soles
-Condyloma lata (smooth wart like genital / anal warts)
4) >10 weeks: Granulomatous lesions
-Cardiovascular and Neuro syphilis
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TORCH +
Hydrops fetalis: accumulation of excess fluid in soft tissues still birth
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Early signs: first two years
Maculopapular rash including palms and soles
“Snuffles”: rhinorrhea (lots of treponema in these secretions)
Late Signs: after two years
Frontal bossing: bulging of frontal skull
Saddle nose
Short maxilla
Hutchinson teeth: small notched teeth
Saber shins: bending of LE long bones
Damage to CN VIII: deafness
Rubella:
1) What is the pathophys?
2) Sx in mom?
3) Sx in fetus?
1) Rubella virus; “German Measles”
-Transmitted to mom via respiratory droplets; we vaccinate for this as part of MMR
-Given 12-15 mo; therefore, mom will probably be unvaccinated
2) Fever and maculopapular rash > starts at head and spreads down
-Post-auricular LAD; Polyarthritis (at least 5 joints)
3) TORCH and:
a) Congenital rubella syndrome
b) Deafness
c) Cataracts
d) Congenital heart defects (PDA)
Cytomegalovirus (CMV)
1) Pathophys?
2) Sx in mom?
3) Sx in baby?
1) Sexual contact or organ transplant
Passed to fetus via placenta
2) Usually asymptomatic, may have “mono” type sx
Fever, LAD, sore throat
3) TORCH and:
Deafness and eye abnormalities
Seizure and intellectual disability
Microcephaly
Periventricular calcifications
HSV:
1) Pathophys?
2) Sx in mom?
3) Sx in baby?
Direct contact with infected area of skin or mucous membranes
Spread to baby during childbirth through contact with infected vaginal secretions
Pt
Mom: Genital vesicular lesions on erythematous base
3) Vesicular lesions everywhere; often on scalp, eyelid margins, oral mucosa
Leads to MENINGIOENCEPHALITIS!
Lethargy, irritability, seizures
(Less of a TORCH presentation, because it’s usually contracted at delivery)
Varicella pathophys:
1)
1) Varicella zoster
Respiratory droplets
Direct contact with oral or skin lesions
Rash (chicken pox) secondary reactivation (shingles)
Mom is unvaccinated with no history of infxn
Transmits to baby through placenta during 1st or 2nd trimester
Low rate of 2% transmission
Varicella
Mom: fever, weakness, popular pruritic
Baby: congenital varicella syndrome
Often fatal before 13 weeks 13-20 wks = congenital syndrome after 20 weeks, less serious
Limb hypoplasia
Ciatriccal limb lesion (combination of scar and edema)
Low birth weight
Microcephaly
Eye defect: cataract
Neurological: cortical atrophy intellectual disability
Parvovirus:
1) Pathophys?
2) Sx in mom?
3) Sx in fetus?
1) Respiratory droplets
Vertical transmission to baby
Pt:
Pregnant mother: arthritis
Small joints hands, wrists, knees, feet
Symmetrical
Fetus
Decreased production of RBCs Red blood cell aplasia
Anemia Increased HR Increased fetal blood pressure Hydrops fetalis
If baby survives there are rarely any long-term effects
Listeria:
1) Pathophys?
2) Sx in mom?
3) Sx in baby?
1) Bacteria listeria monocytogenes
-Infection occurs after contaminated foods (unpasteurized milk or deli meet)
-Transmitted to fetus through placenta > spontaneous abortion
2) Fever, fatigue, GI sx: diarrhea/vomiting/abdominal cramps
-Amnionitis: infection of the amniotic fluid
-Sepsis
3) Sepsis, Meningitis, Fatal
Hep B
Path:
Mom is chronic carrier transmits virus during delivery
Baby becomes chronic carrier because neonatal immune system cannot clear the infection
Pt:
Baby: asymptomatic carrier that develops cancer later in life
Hep C
Transmission via blood
Vertical transmission can occur, there’s nothing we can do about it
C-Section Doesn’t help
HIV
Path:
HIV retrovirus
Pt:
Mom with HIV
Now baby has HIV
Tx:
Start with a screen
Tx = PPx
Zika:
1) Pathology?
2) Sx of mom?
3) Sx of baby?
1) Mosquito born teratogen
Endemic areas: South America (Brazil), India, Caribbean
2) Zero symptoms
3) Serious birth defects:
Microcephaly
Decreased brain development
Spontaneous abortion
Group B strep:
1) Pathogen?
2) Sx in baby?
3) How to Dx?
1) Path:
GBS is normal vaginal flora for adult woman
Can be transmitted to baby causing severe complications
2) Sepsis > death
3) Screened during prenatal visit at 36 weeks
Differentiate between diabetes mellitus and gestational diabetes
Diabetes Meletus: The type II diabetes that mom already had before she became pregnant
May be referred to as “pregestational diabetes”
Gestational Diabetes: Diabetes that arose during pregnancy
Pregestational diabetes
Path:
Type 1
Beta islet destruction now there’s no insulin
Type 2
Too much sugar insulin resistance develops pancreas has to work too hard to make up the difference, and eventually breaks too
* Genetics also plays a role
Pt:
Known history of diabetes
Dx:
Hgb A1C obtained before conception that shows elevation
> 6.5 = diabetes
< 5.7 = NOT diabetes
In between these two values = prediabetes
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Neonatal hypoglycemia
Path:
Immediately after delivery, baby is getting much less glucose
But there is a lot of insulin on board
Blood sugar tanks
Tx:
Treat with glucagon to oppose insulin and dextrose to support baby while insulin levels are high
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Clinical presentation of breast disease:
1)
1) Symptoms affecting the breasts are evaluated primarily to determine if malignancy is present.
2) Regardless of the symptom, the underlying cause is benign in the majority of cases.
3) Breast cancer is most commonly detected by screening or by palpation of a mass in younger women and in unscreened older women
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Describe breast cysts
Sometimes painful breast mass
May fluctuate in size
May be simple, complicated or complex
The “simpler the better”
However, most cysts or all types are usually benign
Progrowth Signaling Pathways [breast cancer]
BRCA 1 & BRCA 2
Classic tumor suppressor genes
Encode proteins that are required to repair certain DNA damage
BRCA 1-associated with triple negative cancers
BRCA 2-associated with ER mutations
Most carriers will develop breast or ovarian cancer by age 70
