Pathology - Phase C

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  1. how do you differentiate the two non-neoplastic lesions of the vulva? Which one has the risk to progress to VIN
    Lichen sclerosis: leukoplakia with parchment paper like skin (thin epidermis), some Cancer risk

    Lichen simplex chronicus: leukoplakia with thich leathery skin (epithelial hyperplasia). no Ca risk. Just think "simple is better"
  2. etiology of vulvar condylomatas (warts) (2)
    • condylomata lata (syphilis)
    • condylomata accuminata (HPV, koilocytic cells)
  3. Two causes of vulvar carcinoma
    HPV 16,18 progress to VIN

    longstanding lichen sclerosis progresses to SCC
  4. Histological keys to HPV (2)
    koilocytic cells (raisin nuclei), peri-nuclear halo
  5. Differentiate VIN usual type and VIN differentiated type
    Usual: Entire epithelium is VIN III, irreversiible is carcinoma in situ (not reversible), seen in young women with HPV, poorly differentiated SCC

    Differentiated: potential for a very rapid cancer usually associated with lichen sclerosis and appears in postmenopausal women, well differentiated SCC
  6. What does extramammary paget's disease look like? How is it different from the mammary type? (3 points for both)
    • -red, itchy, crusty lesions
    • -you will think it is eczema, but if it sticks around for 2+/52, it is important to biopsy
    • -mammary always has an underlying carcinoma while the vulvar variety rarely has an underlying ca.
  7. How do you differentiate extramammary pagets from melanoma? Why is it important to do so?
    Melanoma is S100 positive, important to do so because it is an aggressive cancer. Prognosis is dependent on the depth of the invasion
  8. DDx of vulvar leukoplakia (5)
    • lichen sclerosis
    • lichen simplex chronicus
    • vulvar carcinoma
    • vitiligo
    • benign dermatosis (psoriasis, etc)
  9. DDx of inflammatory vaginitis (big 3)
    • Candidiasis
    • Trichomaniasis
    • Bacterial Vaginosis
  10. 2 types of Vaginal cancer (or VaIN)
    Vaginal adenosis: clear-cell carcinoma, intrauterine exposure to DES, due to persistence of columnar epithelium in upper 1/3 of vagina

    Sarcoma botroyides (ebryonal rhabdosarcoma): peds tumor, grape-like mass hanging out of vagina (is a skeletal muscle tumor)
  11. What gene mutation is can commonly cause ovarian and fallopian tube cancers?
  12. Describe salpingitis
    • -Usually gonococcal infection
    • -acute phase: fever, abdo pain, tubo-ovarian abscess
    • -Chronic phase: scarring with tubal obstruction, sterility, tubal pregnancies
  13. Most common cause of ectopic preg? What do you need you need to diagnose (histologically)
    1) oviduct obstructions (PID, endometriosis, tumors)

    2) chorionic villi
  14. Most common benign tumor of the fallopian tube? FT tumor that is associated with BRCA1 mutation?
    benign: adenomatoid tumor 

    BRCA1: papillary serous carcinoma of FT
  15. Describe the 2 broad categories of placental infections
    ascending: most common, usually mycoplasm or candida, associated with PROM

    Hematogenous: TORCHES, listeriosis
  16. Prevalence of ectopic pregnancy
  17. If you see hCG levels WAY higher than you would expect for gestational age, what should be on your differential (3)
    • Hydatiform mole (complete or incomplete)
    • Invasive mole
    • Choriocarcinoma

    Progressively higher titres as you go down the list. More likely to be cancer as you go down (last one is)
  18. Three things you see in a hydatiform mole
    • - no fetal heart sounds
    • - grape-like structures (the edematous villi) passing through the os
    • - "snow storm" on U/S
  19. Describe the 2 types of hydatiform moles (4 and 3 points each)
    Complete: 2 sperm in an empty egg (46 chrom), all chorionic villi are abnormal, 2-3% cancer risk, most common gestational trophoblastic disease

    Incomplete: 2 sperm in viable egg (69 chrom), contains fetal parts, some normal chorionic villi
  20. Describe an invasive mole (3 points)
    • -more locally invasive complete moles
    • -harder to remove by D&C, track with hCG
    • -may embolize and head to different organs like a metasteses
  21. Describe choriocarcinoma (4 points)
    • -very aggresive malignant tumor
    • -can arise in 2 ways: germ cell tumor, or as a complication of gestation
    • -Presents as a bloody, brownish discharge with higher B-hCG titres even than a complete mole
    • -Have usually metastisized by the time they are detected
  22. Describe how you can morphologically differentiate moles and choriocarcinoma (2)
    • -CC has hemorrhagic, necrotic masses
  23. Describe the difference in treatment efficacy in choriocarcinoma arising from gestation and those arising from the gonad (germ cell tumor)
    Gestation: responds well to chemo (probably due to paternal antigens acting as an adjunct to chemo)

    Gonad: very poor response to chemo
  24. How can you differentiate Placental site Trophoblastic tumor from Choriocarcinoma and moles
    Trophoblastic tumors do not give off elevated levels of B-hCG

    Instead they give off high levels of placental lactogen
  25. Describe Pre-eclampsia, eclampsia, and HELLP
    • Pre-eclampsia: HTN, proteinuria, and edema in the 3rd trimester, starts in 24-25th weeks
    • Eclampisa: Pre-eclampsia + seizures
    • HELLP: Pre-eclampsia + thrombotic microangiopathy involving liver
  26. What is the biggest complication you are worried about in eclampsia?
  27. 2 placental changes you see in eclampsia
    • -higher number  of infarcts
    • -acute arthrosis of the placental arteries
  28. Biggest concern with DIC
    renal necrosis
  29. Describe Leiomyomas (fibroids) (4 points)
    • -benign prolif of SM arising from myometrium due to estrogen and progesterone
    • -pre-menopausal women with no kids prototypically
    • -usually asymptomatic, but can present with AUB, infert, pelvic mass
    • -multiple lesions with white whorls
  30. Describe endometrial polyps (3 points)
    • -present with AUB
    • -may progress to cancer (<2% in premeno, <6-7% in postmeno)
    • -contain thick-walled BVs
  31. Describe adenomyosis (2)
    • -Basically divurticuli of endometrial tissue into the myometrium
    • -It is the basalis layer that invades
  32. How do you treat leiomyoma?
    GnRH analogs, block the effects of progesterone
  33. Describe endometriosis (5 points)
    • -endometrial glands AND stroma outside of the uterus
    • -dysmenorrhea, pelvic pain, and sometimes infertility
    • -usually in 20-30 year olds
    • -most common site is the ovariy (chocolate cyst)
    • -When not on the ovary look for blue and red "power burn" lesions
  34. Describe the 3 theories of endometriosis pathogenesis
    • 1) retrograde menstruation: menstrual stuff going the wrong way, most accepted theory
    • 2) Celomic metaplasia: diff of mesothelial cells into endometrium-like tissue
    • 3) lymphatic spread
  35. Why does endometriosis happen in some women and not others? (3)
    • -genes
    • -acquired properties of the endometrium
    • -poor immune clearance.
  36. What are the three sources of estrogen for endometrial foci in endometriosis
    • 1) The foci themselves (main source)
    • 2) Ovary
    • 3) skin and fat
  37. What are two malignancies that are associated with endometriosis?
    • -Endometrioid ca
    • -clear cell carcinoma (super aggressive)
  38. Do adenomyotic foci respond to the cyclic variation in hormones? Is there hemorrhage in the foci?
  39. How does adenomyosis is different from endometriosis
    adenomyosis is the basalis layer, which does not respond to hormones and that is why there is not bleeding

    endometriosis is the functional layer, which is why you see all the sx
  40. Define DUB. 3 causes
    Bleeding resulting from proliferative endometrium as a result of anovulation or abnormality of follicle development in the absence of any organic disease.

    • Causes
    • -Chronic anovulation: peri menarchal, perimenopausal
    • -unopposed estrogen (endometrial hyperplasia)
  41. Describe endometrial hyperplasia (4 points)
    • -caused by unopposed estrogen
    • -usually in (peri)menopausal women
    • -usually preceeds endometrial adenocarcinoma (most cases do not progress though)
    • -high gland to stroma ratio (3:1)
  42. Morphological diganostic criteria for endometriosis (3)
    • Need 2/3 of the following:
    • -endometrial glands
    • -endometrial stroma
    • -hemerosiden laden microphages
  43. Most common cause of AUB?
    ovarian dysfunction
  44. Describe the 2 types of endometrial ca (4 points each)
    • -Type 1: endometriod
    •   -arises from endometrial hyperplasia
    •   -more common of the two (80%)
    •   -good prognosis (90% 5 yr survival)
    •   -usually in 50-60 year olds
    • -Type 2: Papillary serous
    •   -aggresive
    •   -p53 mutation
    •   -70+ years old (due to atrophy)
    •   -Metastisize easily
  45. How does HPV infection cause cervical cancer
    they produce proteins E6 and E7 which knock out p53 and Rb proteins which usually act as a check in the cell cycle.
  46. Describe LSIL (3) and HSIL (4)
    • -in both you see nuclear enlargement and atypia
    • LSIL: 
    •  -CIN I
    •  -LOWER 1/3 of epidermis only
    •  -30% persist, 10% progress
    • HSIL
    •  -CIN II and III
    •  -2/3 to full thickness involvement
    •  -60% persist, 10% progress
    •   -CIN III is more associated with invasive cancer
  47. Describe the staging of cervical SCC
    • Stage 0: HSIL/CINIII
    • Stage I: limited to cervix
    • Stage II: limited to upper 1/3 of vagina
    • Stage III: has extended to lower vagina
    • Stage IV: has extended beyond true pelvis
  48. clinical criteria for PCOS
    • need 2/3 of:
    • 1) oligo or anovulation
    • 2) clincal or biochemical signs of hyperandrogenism
    • 3) PC ovaries on U/S and exclusion of other causes.
  49. Describe the pathophysiology of PCOS (5 steps)
    • We don't really know, but a good way to remember is:
    • 1) There is increased LH (for some reason that we dont know the GnRH pulsatility is increased)
    • 2) Increased LH decreases FSH causing LH:FSH >2
    • 3) Increased LH causes increased androgen production by the thecal cells
    • 4) adipose tissue converts androgen to estrone which will further decrease the FSH
    • 5) decreased FSH causes granulosa cells to decrease estrogen production which causes follicular degeneration
  50. How is CA 125 useful in ovarian epithelial tumors?
    NOT useful for screening! IS useful for tracking treatment efficacy and if the disease returns.
  51. Describe what every woman should know about ovarian cancer
    • -super treatable if it is caught early (90% survival), but only 24% are caught early.
    • -4th leading cause of  cancer death in women
    • -difficult to diagnose until pressure sx start
  52. Why are ovarian carcinomas associated with ascites?
    because they have a propensity to seed the peritoneal cavity
  53. Describe a Malignant Mixed Mullerian Tumor (2)
    • -Have both epithelial and stromal tumors
    • -stromal components may be cartilagenous or SM-like
  54. Most common type of adrenal cancer?
    mets, usually from the lungs
  55. What is usually responsible for acute adrenal insuff? What if they are on long term steroids?
    Waterhouse-Friedriechsen syndrome due to meningococcal sepsis. 

    If on long term steroids, the adrenals atrophy and withdrawing steroids or times of increased demand (e.g. after surg) will result in acute adrenal insufficiency
  56. If you see a baby that has the sx of pheochromocytoma, what should you be thinking?
    neuroblastoma (most common extracranial solid tumor in kids). Usually presents as an enlarging abdominal mass
  57. If you are operating on a pituitary tumor in someone with pituitary probs and "machine oil" spills out what should you be thinking?
  58. When you do an FNA of someone with hashimoto's, what do you see (3)? Why is important to do the FNA?
    • You see:
    • -Lymphocytic infiltration
    • -atrophy of thyroid follicles
    • -Hurthle cells (cells with abundant pink granular cytoplasm)

    Do FNA because these people are at 80x more risk for B-cell lymphoma
  59. If someone has a big, painful thyroid, what are you thinking?
    Subacute granulomatous (DeQuervains) thyroiditis
  60. What causes a multinodular goitre?
    Some problem with making thryroid hormone (e.g. decreased iodine intake) cause increased TSH which causes some areas to enlarge (differential response to TSH)
  61. Do thyroid adenomas transform into carcinomas?
  62. What are the 4 types of thyroid carcinomas in order of prevalence
    • 1) Papillary thyroid (75-85%)
    • 2) Follicular carcinoma (10-20%)
    • 3) Medullary ca (5% of ca)
    • 4) anaplastic (rare, usually old people)
  63. What are the 4 radiological signs of breast cancer in mammography?
    • 1) Densities (DCIS)
    • 2) archetectual distortion (LC)
    • 3) calcifications (DCIS)
    • 4) changes over time
  64. List 4 RF's for breast cancer. sum it up in a sentence
    • 1) gender (99% female)
    • 2) age (steady rise after menopause)
    • 3) geographic influence
    • 4) estrogen exposure

    Major RF's are hormonal and genetic!
  65. Why are BRCA1 (basal type) tumors hard to treat?
    They are often triple negative tumors (no ER, PR, or HER2/neu)
  66. What should you think if you get a path report coming back saying that there is a comedo-type DCIS?
    These are BAD and HIGH GRADE tumors. Can often express pus from them.
  67. If there is eczema of the nipple what should you think? What is always under this
    Mammary pagets. Always an underlying DCIS
  68. What is a big difference between LCIS and DCIS?
    LCIS has lost e-cadherin. Do a stain!
  69. What is the most important prognostic factor in breast cancer?
    Whether or not there are LN mets
  70. 3 important prognostic and predictive factors in breast cancer
    • 1) LN mets (most important)/other mets
    • 2) invasive vs in situ disease
    • 3) tumor size
  71. How can you easily differentiate paratyroid hyperplasia from adenoma/carcinoma?
    In hyperplasia, all 4 glands are enlarged. Only one or 2 in adenoma/carcinoma
  72. Histologically, how can you tell if there if a neuroendocrine tumor is malignant?
    Invasion of an area it shouldn't be. There is no other way, these tumors are boring.
  73. Based on phosphate and free calcium levels differentiate between primary and secondary hyperparathyroidism
    primary - high calcium and low phosphate

    secondary (usually renal failure) - kidney can no longer excrete phosphate causing a high phosphate level, which LOVES to bind to free calcium, causing a low/normal Ca++ level with elevated PTH as the parathyroid tries to compensate!
  74. What usually causes primary hyperparathyroidism?
    sporadic adenomas or hyperplasia (95%)

    only 5% are due to familial MEN syndromes
  75. How does primary hyperparathyroidism present?
    • 1) usually asymp
    • if there are symptoms, general hypercalcemia sx:
    • -moans (peptic ulcer pain, Ca++ causes increased gastrin production)
    • -bones (pain, osteitis fibrosa cystica)
    • -stones (kidney stones)
    • -psychiatric overtones (depression, seizures)
  76. Most common cause of hypercalcemia
    90% are primary hyperparathyroidism
  77. what is the hallmark of hypocalcemia?
    tetany (neuromuscular irritability)
  78. Describe what you see in Ca++ and PTH levels in:
    -primary hyperparathyroid
    -secondary hyperparathyroid
    -hypercalcemia of malignancy
    • PHP: calcium up, PTH up
    • SHP: calcium N/low, PTH up
    • Hypercalcemia of malig: calcium up, PTH down
    • hypopara: ca down, PTH down
  79. What do you see in an insulinoma?
  80. What do you see in MEN I (wermer's syndrome)
    • -Pituitary adenomas
    • -Parathyroid hyperplasia
    • -Pancreatic endocrine tumores (ZES, insulinoma, etc)
  81. What are the three subtypes of MEN 2. What gene is impaired in all of these? What should you always do if someone is found to have this gene mutation (why?)
    • 1) MEN 2A (Sipple synd) (95% of MEN 2)
    • 2) MEN 2B (william synd)
    • 3) Familial medullary thyroid cancer

    All are a mutation of the RET oncogene. If someone has this mutation in the GERMLINE, do a prophylactic thyroidectomy (all involve medullary thyroid ca)
  82. What do you see in MEN 2A (Sipple)
    • 1) Thyroid medullary ca by age 20 100% of the time
    • 2) Pheo
    • 3) Parathyroid hyperplasia
  83. What do you see in MEN 2B (william/MENIII). What do you NOT see? Timeline compared to MEN 2A (usually in infancy)
    • 1) Pheo
    • 2) Thyroid medullary ca
    • 3) mucocutaneous ganglioneuromas
    • 4) Marfanoid habitus (Abe Lincoln)

    NO HYPERPARATHYROID!! Develops 10 years earlier than MEN 2A
  84. key feature that identifies a neuroendocrine cell
    neuroendocrine granules
Card Set:
Pathology - Phase C
2014-12-01 17:36:48
Pathology Phase
Pathology,Phase C
Pathology - Phase C
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