Lecture 8.1: Female GU (unedited) Flashcards

1
Q

Carcinoma of the Vulva: What are the 2 main categories? Which is more common?

A

1) HPV-related
2) Non-HPV related: more common

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2
Q

Vulvar carcinoma

A

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

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3
Q

Vulvar carcinoma

A

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)

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4
Q

Clinical manifestations
Leukoplakia (25 % are pigmented)

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5
Q

Paget’s Disease of the Vulva

A

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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6
Q

slide 9

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8
Q

Premencarchal vaginal bleeding:
1) What does a pt need if FB?
2) What if you suspect sexual abuse?

A

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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9
Q

slide 12

A

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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10
Q

SLIDE 12

A

Vaginal Atrophy  get a good history and physical exam

Endometrial Cancer  must have documented counseling on this

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11
Q

slide 12

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Pregnancy: Vaginal bleeding in pregnancy will be addressed separately

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12
Q

Vaginal Atrophy: Who is it common in? Why?

A

Common occurrence in elderly patients
Secondary to falling estrogen levels after menopause

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13
Q

What are 2 reasons for 1st trimester vaginal bleeding? Explain

A

1) Ectopic pregnancy
2) Spontaneous abortion: Nonviable pregnancy

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14
Q

2nd / 3rd Trimester Vaginal Bleeding: Abruption

A

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

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15
Q

2nd / 3rd Trimester Vaginal Bleeding” Previa:
1) What is the path?
2) How does it present?

A

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

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16
Q

2nd / 3rd Trimester Vaginal Bleeding: Uterine rupture

A

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

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17
Q

Abruption:
1) Define it
2) What are the risks? Explain

A

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

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18
Q
A
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19
Q

Carcinogenesis(HPV related)
1) What precedes cancer by years to decades?

A

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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20
Q

slide 23
1) What is an established component of PID?

A

1) Inflammation of the endometrium
2)

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21
Q

slide 23

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22
Q

Hypotheses of endometrial dispersion include what? Explain

A

1)

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23
Q

slide 28

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24
Q

30

A

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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31 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
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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)
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Cardiovascular: Decrease in SVR
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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
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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
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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
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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
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How much does HR increase in pregnancy? Why do we care?
By about 10-20 BPM over baseline; tachycardia
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63 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
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Thalidomide 1) What was it used for? 2) What happened?
1)
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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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slide 82
Warfarin Hypoplastic nose Skeletal abnormalities Ocular abnormalities Neonatal bleeding Mental retardation
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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
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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
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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
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Teratogenic drugs
1) Antibiotics Bactrim Fluoroquinolone Tetracycline Acne Isotretinoin Statins Early reports indicated these were teratogenic, but this is currently being reconsidered
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True or false: Chemotherapy is harmful to the fetus This will be managed by specialty
True
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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 *
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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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92 Chronic Hypertension Predating Pregnancy
Path Primary hypertension Pt Diagnosis of HTN before becoming pregnant
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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
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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
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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
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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
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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
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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
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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
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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
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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)
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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
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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)
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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
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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
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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
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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
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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
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Hep C
Transmission via blood Vertical transmission can occur, there’s nothing we can do about it C-Section Doesn’t help
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HIV
Path: HIV retrovirus Pt: Mom with HIV Now baby has HIV Tx: Start with a screen Tx = PPx
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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
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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
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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
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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
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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
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