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OMS II - Becom Exam 4 > Hef's Lectures > Flashcards

Hef's Lectures Flashcards

1
Q

what is the most common form of germ cell tumor?

A

seminoma

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2
Q

classical seminoma

A
  • 15-35 y/o and PAINLESS

- “fried egg” due to collagen -> large cells w/ clear cytoplasm and central nuclei

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3
Q

spermatocytic seminoma

A
  • 60 y/o

- NO fried egg appearance (no glycogen)

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4
Q

embryonal carcinoma

A
  • 20-30 y/o and PAINFUL
  • high hCG or AFP or both
  • HEMORRHAGE and NECROSIS -> Acute abdomen
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5
Q

yolk sac tumor

A
  • <4 y/o
  • high AFP
  • Schiller-Duval bodies
  • AFP and alpha 1 antitrypsin markers
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6
Q

choriocarcinoma

A
  • 20s and PAINFUL
  • mimic placental tissue
  • high hCG -> GYNECOMASTIA
  • blood metastasis to lungs
  • syncytiotrophoblasts and cytotrophoblasts
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7
Q

Teratoma

A
  • more than 1 of the 3 germline layers

- high hCG or AFP or both

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8
Q

Leydig cell tumors

A
  • 20-60 y/o
  • precocious puberty or gynecomastia
  • GOLDEN BROWN cholesterol nodules
  • crystalloids of Reinke
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9
Q

testicular lymphoma

A
  • men >60 y/o
  • metastis in testes
  • diffuse large B cell type
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10
Q

where do carcinomas arise from in prostate?

A

peripheral zone

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11
Q

where does BPH arise from in prostate?

A

transitional zone

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12
Q

what is the main androgen leading to BPH?

A

DHT

-formed by type 2 5a-reductase stromal cells

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13
Q

BPH

A
  • benign, men >50 y/o
  • NOT premalignant
  • DHT activates FGF and TGF-B
  • BRCA, HOXB13, PTEN, TP53 mutations
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14
Q

prostatic intraepithelial neoplasia (PIN)

A
  • cancer has NOT invaded BM

- can progress to prostatic adenocarcinoma

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15
Q

adenocarcinoma of the prostate

A
  • a-methylacyl-coenzyme A-racemase (AMACR) markers

- grading based on architecture alone, not nuclear atypia

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16
Q

are prostatic crystalloids a sign of good or bad prognosis?

A

-GOOD prognosis -> highly differentiated and less invasive

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17
Q

where does prostate cancer like to spread to?

A

-bone (osteoblastic), lungs, kidneys, Brain

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18
Q

prostatic biomarkers

A
  1. PAP
  2. PSA (>10 -> cancer)
  3. PCA3
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19
Q

what type of epithelium is the outside of the cervix compared to inside?

A

outside -> stratified squamous

inside -> columnar

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20
Q

acute vs. chronic cervicitis

A

acute -> neutrophil infiltrate

chronic -> lymphocytes, plasma cells, Mac infiltrate

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21
Q

squamous intraepithelial lesion (aka cervical intraepithelial neoplasia)…CIN

A

-NOT invading BM

  • CIN 1 -> <1/3
  • CIN 2 -> <2/3
  • CIN 3 -> full thickness (CIS)
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22
Q

cervical dysplasia

A
  • iodine stains of glycogen are BROWN
  • acetic acid stains WHITE (no glycogen)

test with Pap smear from the transformation zone

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23
Q

most common type of invasive cervical carcinoma?

A
  • SCC

- Adenocarcinoma is 2nd

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24
Q

when is dysfunctional uterine bleeding most worrisome?

A
  • post-menopausal women

- can indicate cancer

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25
Q

endometriosis

A
  • ectopic endometrial tissue OUTSIDE the uterus
  • usually due to retrograde menstruation
  • usually in ovaries -> CHOCOLATE CYSTS
  • gun powder nodules
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26
Q

adenomyosis

A

-endometrial tissue in myometrium

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27
Q

endometrial hyperplasia

A
  • precursor to endometrial carcinoma
  • unopposed estrogen
  • associated w/ Cowden syndrome & PTEN mutations
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28
Q

endometrial carcinoma

A
  • post-menopausal bleeding >40 y/o
  • unopposed estrogen
  • type I (endometrioid) -> PTEN mutations…less aggressive (high differentiation) and arises from endometrial hyperplasia
  • type II (serous) -> p53 mutations…more aggressive (poor differentiation) and arises from endometrial atrophy
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29
Q

Leiomyoma aka fibriod

A
  • BENIGN
  • tumor of smooth muscle
  • “Whorled pattern”
  • Red degeneration -> ACUTE ABDOMEN
  • pre-menopause
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30
Q

Leiomyosarcoma

A
  • MALIGNANT
  • tumor of smooth muscle
  • MED12 mutations
  • do NOT arise from leiomyomas
  • post-menopause
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31
Q

PCOS

A
  • excess androgens -> hirsutism
  • associated w/ DM and obesity
  • hyperinsulinemia -> displace IGF
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32
Q

cystadenoma

A
  • 30-40 y/o
  • benign
  • SINGLE layer, FLAT lining
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33
Q

brenner tumor

A
  • bladder-like epithelium

- benign

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34
Q

borderline tumor

A
  • low malignant potential

- MULTIPLE layers

35
Q

cystadenocarcinoma

A
  • JAGGED lining
  • Psammoma bodies
  • CA-125 marker
36
Q

Dysgerminoma***

A

-ovarian counterpart of testicular seminoma

  • 20-30 y/o
  • “fried egg” appearance
  • all are MALIGNANT
  • high hCG and LDH
37
Q

granulosa theca cell tumor

A
  • Call-Exner bodies
  • coffee-bean nuclei
  • excess androgens and estrogen
  • FOXL2 gene mutations
38
Q

fibroma

A
  • benign tumor of fibroblasts
  • Meigs syndrome (ascites, effusion)
  • Gorlin syndrome
39
Q

Sertoli-Leydig tumor

A
  • mimics testicles
  • reinke crysals
  • produce androgens -> virulization and hirsutism
40
Q

Krukenberg tumor

A
  • metastatic mucinous tumor (GI/breast) -> spread to ovary
  • mucin -> SIGNET RING
  • bilateral
41
Q

fibroadenoma

A
  • benign

- MOBILE marble like mass (slippery)

42
Q

intraductal papilloma

A
  • benign
  • fibrovascular stalks -> BLOODY discharge from nipple
  • 2 layers (epith. + myoepith.)
43
Q

Phyllodes tumor

A
  • benign or malignant (based on STROMA)

- “leaf-like” due to overgrowth of fibrous part

44
Q

mutations in what are at high risk for breast cancer?

A
  • BRCA 1 and BRCA 2

- p53

45
Q

ductal carcinoma in situ (DCIS)

A
  • NO invasion of BM
  • microcalcifications
  • NO mass
  1. solid -> plugging
  2. comedo** -> CHEESY necrotic debris in center w/ calcification
  3. papillary -> lack fibrovascular stalk
  4. cribriform -> fenestrations
46
Q

Paget disease

A

if DCIS travels to the epidermis in the nipple

-always associated w/ carcinoma of breast

47
Q

invasive ductal carcinoma

A

HAS MASS

  1. NST
    - extensive FIBROSIS -> DESMOPLASIA
    - Peau d’ Orange (dimpling)
    - form ducts
    - NO myoepithelial layer (single)
  2. Medullary
    - SOFT & fleshy (encephaloid carcinoma)
    - most Anaplastic, BEST prognosis
  3. Mucinous
    - islands of cells “floating” in mucin
  4. tubular
    - no myoepith. layer
    - VERY good prognosis
48
Q

Lobular carcinoma in situ

A
  • NO invasion of BM
  • loosely cohesive cells (lack cadherin)
  • mucin -> SIGNET RING
  • ER+ and PR +, no HER2
49
Q

invasive lobular carcinoma

A
  • INDIAN FILE -> single file spread of cells

- bad prognosis

50
Q

do ER/PR negative tumors have a good or bad prognosis?

A

BAD

-want ER+ and PR+ tumors to treat w/ anti estrogen therapy (ex. tamoxifen)

51
Q

HER2

A
  • receptor seen on some types of breast cancer

- respond to anti-HER2 Abs (trastuzumab/herceptin) if present

52
Q

where does breast cancer 1st metastasize to?

A

AXILLARY lymph nodes

-disseminate to lung, liver, bone, brain

53
Q

thyroid follicular adenoma

A
  • benign & encapsulated
  • COLD nodule
  • Hurthle cell type -> seen in parathyroid lesions also
  • Atypical type -> indicate malignancy
54
Q

thyroid carcinoma

A
  • multiple types
  • COLD nodules
  • normal TSH values
  • FNA if nodules 1-4 cm (>4 -> surgery)
  • arise from follicular cells (except Medullary)
55
Q

most common type of thyroid carcinoma

A

PAPILLARY thyroid carcinoma

56
Q

Papillary thyroid carcinoma

A
  • TRANSLOCATION/inversion of RET
  • gain of function mut. in BRAF
  • RADIATION is risk factor
  • fibrovascular core
  • ORPHAN ANNIE EYE nuclei
  • Pseudo-inclusion bodies
  • PSAMOMMA bodies
57
Q

Follicular thyroid carcinoma

A
  • q13;p25 translocation -> fusion of PAX8 w/ PPARG
  • IODINE DEFICIENCY is risk factor -> stimulate TSH
  • produces more T3, T4 -> suppress TSH
  • INFILTRATE through capsule
  • COLLOID follicles
  • HOT iodine scan
58
Q

Anaplastic thyroid carcinoma

A
  • undifferentiated
  • B-catenin activation mutation
  • WORSE PROGNOSIS -> aggressive
  • ELDERLY (65 y/o)
59
Q

Medullary thyroid carcinoma

A
  • arise from PARAFOLLICULAR C cells -> Calcitonin
  • high Calcitonin w/ NORMAL Ca2+ levels
  • point mutations in RET (sporadic) or germline mut. in RET (MEN-2A/B)
  • markers: CEA and CALCITONIN
  • AMYLOID deposits -> SOFT
60
Q

Are most thyroid nodules malignant or benign?

A

BENIGN**

61
Q

Adrenocortical Adenocarcinoma

A

-11C-metomidate-PET is diagnostic -> binds to 11B-hydroxylase

62
Q

Pheochromocytoma

A
  • BENIGN -> tumor of adrenal MEDULLA
  • ADULT (20-40)***
  • dark brown in K+ dichromate***
  • Zellballen Pattern***
  • neuron-specific enolase (NSE) marker
  • HTN 90% of time
  • catecholamines in urine (Vanillylmandelic acid and Metanephrines)**
63
Q

Neuroblastoma

A
  • MALIGNANT
  • 4th most common childhood malignancy -> CHILD <5 y/o**
  • small blue tumor cells
  • Schwann cells**
  • Homer-Wright Pseudorosettes**
  • markers: NSE, neurofilaments, chromagranin
  • Raccoon eyes, Heterochromia iridis
64
Q

Pituitary cancers

A
  • BENIGN
  • FUNCTIONAL -> PRL, ACTH, GH
  • nm23 tumor suppressor mutation**
  • c-MYC activating mutation
65
Q

MEN type 1 (Wermer syndrome)

A
  • 3 ps -> parathyroid, pancreatic, pituitary adenomas**

- inactivating mutation in MEN-1 (chrom. 11)

66
Q

Zollinger-Ellison syndrome

A

-gastrinomas (pancreatic tumor) w/ MEN1 mutations -> peptic/gastric ulcers

67
Q

Carcinoid tumors

A
  • MEN1 mutations
  • metastasize -> death
  • no cure
  • release Serotonin** -> 5-hydroxytryptamine metabolite in urine**
  • pallagra, flushing, diarrhea
68
Q

MEN type 2A (Sipple syndrome)

A
  • gain of function mut. in RET
    1. Medullary thyroid carcinoma
    2. Pheochromocytoma
    3. Parathyroid hyperplasia
69
Q

MEN-2B

A
  • M918T variant of RET mut.
  • NO hyperparathyroidism
    1. medullary thyroid carcinoma
    2. pheochromocytoma
    3. mucosal neuromas
    4. Marfanoid Habitus
70
Q

Von Hippel-Linau (VHL) disease

A
  • benign
  • mut. in VHL
  • HEMANGIOBLASTOMAS*** and pheochromocytoma
71
Q

Pancreatic Neuroendocrine Tumors (PanNETs)

A
  • MEN1 and PTEN mutations
  • MONOTONOUS cells
  • AMYLOID deposits
72
Q

pancreatic beta cells

A
  • produce insulin by pro hormone convertase 1/3 (PC1/3)
  • ATP-regulated K+ channels
  • INSULINOMA
73
Q

what drug blocks K+ efflux leading to an increase in insulin

A

SULFONYLUREA

74
Q

pancreatic alpha cells

A
  • secrete glucagon

- GLUCAGONOMA -> Necrolytic Migratory Erythema*** (AA and zinc deficiency)

75
Q

pancreatic delta cells

A
  • secrete Somatostatin

- SOMATOSTATINOMA -> low gastric acid, gallstones, steatorrhea

76
Q

Gastrinoma (Zollinger-Ellison syndrome)

A

-increase acidity, ulcers, high serum gastrin

77
Q

VIPoma (Verner-Morrison syndrome)

A
  • diarrhea -> hypokalemia, dehydration

- treat and image w/ OCTREOTIDE

78
Q

mutations that can cause DM

A
  1. MODY
    - glucokinase mut.
    - hepatic nuclear factor mut.
    - insulin promotor factor 1 mut.
  2. GATA6
  3. DNA 3243
79
Q

HbA1c

A
  • glycated Hb from DM

- high levels -> retinopathy and CV problems

80
Q

type I DM

A
  • HLA-DR3 and HLA-DR4 class II antigens (higher w/ DQ8)***
  • HLA-DQ5 and DQ6 -> protection from type 1
  • hyperglycemia
  • increase risk for Candida
  • DIABETIC KETOACIDOSIS
81
Q

type 2 DM

A
  • insulin resistance due to obesity -> adipokines (resistin and RBP4)**
  • beta cell dysfunction -> AMYLOID deposits*
  • beta cell burnout
  • excess FAs
82
Q

Hyperosmolar Hyperglycemic state

A
  • seen in type 2 DM

- hyperglycemia, dehydrated, uremia, coagulability, rhabdomyolysis -> high mortality

83
Q

AGE from DM

A
  • ECM accumulation -> cross-link ECM type I collagen -> REDUCE ELASTICITY
  • trap LDL proteins -> cholesterol deposits (Kimmelstiel-Wilson Nodules)
84
Q

activation of kinases and cytokines w/ DM

A

High glucose -> increase DAG -> increase PKCbeta -> increase TGFbeta and VEGF -> increase vascular permeability and angiogenesis

-Avastin (VEGF antagonist) -> treat diabetic retinopathy

OMS II - Becom Exam 4 (8 decks)

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