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Repro/Endocrine/ Etc. > MHD2 Exam 4 Rapid Review > Flashcards

MHD2 Exam 4 Rapid Review Flashcards

1
Q

Cell type for normal extocervix? Normal endocervix?

A

Ecto: nonkeratinized stratified squamous

Endo: Simple columnar

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2
Q

Key high risk HPV types (2 +2)

Key low risk HPV types (2)

A

HR: 16/18 and 31/33

LR: 6, 11

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3
Q

Low risk HPV leads to what type of growth?

High risk?

A

Low: Condyloma

High: Inc. neoplasm risk

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4
Q

What are the key HPV oncoproteins and what role do they play in causing cancer?

A

E6 and E7

They bind/ neutralize p53 and Rb

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5
Q

What cell type is characteristically associated with Condyloma? What are the (4) characteristics of this cell type?

A

Koilocyte

  1. Hyperchromasia
  2. Nuclear enlargement
  3. Irregular nuclear membrane contour (raison-like)
  4. Perinuclear halo

(Head Negus In Peds)

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6
Q

What are the grades/categories for neoplasia of the cervix? How does this correlate to treatment?

Peak incidence for cervical cancer?

A

Cervical Intraepithelial Neoplasia (CIN)/ Squamous Intraepithelial Lesion (SIL)

CIN1 (aka low grade SIL): Low chance of invasion; will likely remain CIN1; Tx: observation

CIN2/3 (aka high grade SIL): High chance of invasion; Tx: Must remove!

Peak incidence: 45y

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7
Q

Cancer types most associated with HPV

Tx

A

SCC (75%)

Adenocarcinoma (15%)

Tx: Hysterectomy and LN dissection

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8
Q

Cervical Cancer Staging

A

Stage 0: Carcinoma in-situ

Stage 1: Confined to cervix

Stage 2: Extends beyond cervix but not to pelvic wall or lower 1/3rd of vagina

Stage 3: Includes pelvic wall and lower 1/3rd of vagina

Stage 4: Extends beyond true pelvis and involves bladder or rectum

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9
Q

Vulva vs Vaginal SCC

  1. RFs
  2. Precursor
  3. Presentation
  4. Mets
A
  1. RF: Vulva: HR HPV or Lichen Sclerosis / Vaginal: HR HPV
  2. Precursor: Vulva: Vulvar Intraepithelial Neoplasia (VIN)/ Vaginal: Vaginal Intraepithelial Neoplasia (VAIN)
  3. Presentation: Vulva: Leukoplakia/ Vaginal: vaginal bleeding and discharge
  4. Mets: Regional LNs
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10
Q

Describe the characteristics of Paget Disease of the Vulva. Key markers which distinguish this disease from Melanoma?

A
  • Intraepidermal proliferation of malignant cells (with risk of LN spread)
  • PAS+ and Cytokeratine+ (which distinguishes it from melanoma)
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11
Q

Describe the histo of Paget disease

A

Single cells with pale vacuolated cytoplasm with abundant glycosaminoglycans

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12
Q

Clear cell adenocarcinoma

  1. Associated with what?
  2. What is the precursor lesion?
  3. How does it present?
A
  1. DES-associated
  2. Vaginal adenosis = precursor lesion
  3. Presents as agranular areas adjacent to normal, pink, vaginal mucosa
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13
Q

Embryonal Rhabdomyosarcoma of Vagina

  1. Age of appearance
  2. Presentation
  3. What key markers?
A
  1. Appears before 20 y/o (usually before 5)
  2. Presents as bleeding, soft, grape-like mass protruding through the vagina
  3. Skeletal muscle markers (rhabdoMYOblasts)
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14
Q

Cell type present in chronic endometritis

Main etiologies?

Longterm complications?

A

Plasma Cells (Lymphocytes present in normal epithelium)

Etiologies: Ascending infxn, IUDs, Retained products of conception post-delivery

Long-term” infertility/ ectopic pregancy

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15
Q

Top theory for cause of endometriosis

Other theories? (2)

A

Menstraul backflow (regurg)

Other theories: metaplastic or Vascular/Lymphatic dissemination

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16
Q

Survival factors for Endometriosis (4)

Needed criteria?

A

AIIM

  1. Aromatose activity of stromal cells (inc. estrogen production)
  2. inc. Inflammatory mediators
  3. dec. Immune clearance
  4. activated Macrophages to establish/maintain

Need 2/3: Endometrial glands, endometrial stroma, hemosiderin pigment

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17
Q

What is Adenomyosis? When do you treat?

A

When endometrial glands and stroma are present within the myometrium, leading to uterus enlargement. Only treat if severe.

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18
Q
  1. Endometrial Hyperplasia is the result of what?
  2. Describe the (2) Histo types
  3. What is the key gene mutation assc?
  4. Sx?
A
  1. Results from estrogen excess
  2. Nonatypical (low short term risk of endometrial cancer); Atypical (aka endometrial intraepithelial hyperplasia/neoplasia– high cancer risk)
  3. Key mutation for atypical: PTEN
  4. Sx: Postmenopausal bleeding
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19
Q

Describe the histo/cytology for Atypical hyperplasia

A
  • Glandular crowding
  • Cytologically atypically rounded, vesicular nuclei, w/ prominent nucleoli
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20
Q

Endometrioid vs Serous Endometrial Cancer

  1. What does it arise from?
  2. Mutations associated
  3. Key histological feature
A
  1. Endometrioid: Arises from endometrial hyperplasia; Serous: Sporadic
  2. Endometrioid: PTEN; Serous: p53
  3. E__ndometrioid: appears reminiscent of “normal” endometrium; Serous: Papillary structures
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21
Q

Endometrial Polyps are often associated with what drug?

A

Tamoxifen (breast cancer drug)

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22
Q

Leiomyoma

  1. Arises from what cell type?
  2. Appearence?
  3. Chromosomal abnormalities?
  4. What stimulates growth?
  5. Usually seen in singles or multiples?
A
  1. Arises from myometrial smooth muscle cells
  2. Appears well circumscribed and whorled
  3. Chromosomal abnormalities: 6, 12 rearrangements
  4. Stimulated to grow by Estrogen (so associated with premenopause)
  5. Usually seen in multiples

BENIGN

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23
Q

Leiomyosarcoma

  1. Arise from?
  2. Patient demographic
  3. Clinical course?
  4. Usually seen in singles or multiples?
A
  1. Arise denovo (NOT leiomyomas gone bad)
  2. Postmenopausal women
  3. Recur after removal and often metastasize to the lung
  4. Usually single
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24
Q

Polycystic Ovarian Syndrome

  1. Characterized by what (3) things?
  2. Key component of pathogenesis?
  3. Histo
  4. Clinical sequela (5)
A
  1. (1) Excess secretion of androgenic hormones, (2) Persistent anovulation, (3) Subcapsular ovarian cysts
  2. Increased LH secretion (leading to inc. androgens)- key component
  3. Histo shows follicles lined by granulosa cells with hyperplastic theca (interna)
  4. Sequela: (1) Hirsutism, (2)chronic anovulation/oligomenorrhe/infertility, (3)insulin resistance, (4)obesity, (5)endometrial hyperplasia/cancer
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25
Q

Endometrioid vs Brenner

  1. Behavior?
  2. Gross?
  3. Histology?
  4. Assc. Tumor Suppressor Gene?
  5. May arise from what underlying condition?
A
  1. E: malignant; B: benign (usually)
  2. E: Solid/cystic; B: unilateral, solid, encapsulated
  3. E: Glands similar to endometrium; B: Nests of transitional urothelium (urinary tract epithelium)
  4. E: PTEN
  5. E: Estrogen Excess
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26
Q

Key Tumor marker for ovarian tumors?

A

CA-125 (used for tx and recurrence)

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27
Q

Struma Ovarii

A

When a large portion of a teratoma is composed of thyroid tissue

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28
Q

Dysgerminoma

  1. Behavior
  2. Tumor marker
  3. Male counterpart
A
  1. Malignant and Radiosensitive
  2. LDH tumor marker
  3. Male counterpart = testis Seminoma; associated with gonadal dysgenesis
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29
Q

Endodermal Sinus Tumor (Yolk Sac Tumor)

  1. Behavior
  2. Key Histo
  3. Tumor marker
A
  1. Malignant
  2. Schillar-Duvall Bodies (glomerulus like structure)
  3. AFP Tumor marker
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30
Q

Choriocarcinoma

  1. Behavior
  2. Histo
  3. Tumor marker
  4. How common is a pure choriocarcinoma?
A
  1. Malignant; Early met (cells are primed for invasion); often fatal
  2. Like placental tissue with trophoblasts and syncyciotrophoblast (NO VILLI!)
  3. hCG
  4. Pure choriocarcinoma is rare (usually is a component of other germ cell tumor)
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31
Q

Embryonal Carcinoma

  1. Behavior
  2. Histo
  3. Gross
A
  1. Malignant aggressive
  2. Large primitive cells
  3. Malignant and aggressive
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32
Q

Granulosa cell tumor

  1. Key histology
  2. Hormone produced
  3. Presentation
A
  1. Call-exner bodies (gland like structures filled with eosinophilic material)
  2. Estrogen production
  3. Sx based on age: Prepuberty- precocious puberty; repro age- bleeding; postmenopause- endometrial
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33
Q

Sertoli-Leydig cell tumor

  1. Histo (key crystal type)
  2. Hormone type produced
  3. Presentation
A
  1. Reinke crystals
  2. Androgen production
  3. Block female sexual development in children; Hirsutism/virilization
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34
Q

Thecoma-Fibroma

  1. What (2) specific cell types are present?
  2. Hormons produced
  3. Key syndrome associated
A
  1. Fibroblasts (fibroma)/ Lipid-laden theca cells (thecoma)
  2. May produce estrogen
  3. MEIGS SYNDROME: (1) right sided pleural effusion; (2) Ascites; (3) Ovarian mass
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35
Q

Key Met to Ovaries

A

Gastric adenocarcinoma is most common- (Krukenberg tumor)

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36
Q

Name the (2) layers of the placenta, and where it attaches.

A

Amnion (inner); Chorion (outer)

Chorion attaches to the decidua (the endometrium of pregnancy)

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37
Q

Chorionic VIlli

  1. What is it?
  2. What is it made of? (include the two layers of epithelium)
A
  1. Placental component which sprouts from chorion to provide large contact area between fetal and maternal circulations
  2. Made of central stroma and (2) layers of epithelium (trophoblasts): syncytiotrophoblasts and cytotrophoblasts
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38
Q

Twins

  1. Dichorionic vs Monochorionic (what does each imply?)
  2. Diamnionic vs monoamnionic (what does each imply?)
  3. What is an vascular anastomose?
A
  1. Dichorionic means there are two seperate outer layers. This can be present for both identical and fraternal twins. Monochorionic implies monozygosity (thus is reserved for identical twins)
  2. Diamnionic implies two seperate inner layers. This is determined by the time of the split so is common to have a diamnionic state. Monoamnionic also implies monozygosity
  3. Vascular anastomose- twin-twin transfusions where one twin receives more blood than the other
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39
Q

Placenta Accreta

  1. What is it?
  2. Predisposing factors?
A
  1. When the placental villous tissue adheres directly to the myometrium (partial/complete abscence of decidua). This can lead to post partum bleeding.
  2. Predisposing factors: (1) Placenta previa (placenta blocking the cervix/lower uterus), (2) Hx of previous C-section
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40
Q

Abruptio Placenta

  1. Pathogenesis
  2. Clinical effect (3)
A
  1. Premature seperation of placenta prior to delivery, often due to a retroplacental bloodclot
  2. Effect: (1) Decreased blood supply to fetus, (2) painful maternal bleeding, (3) potential fetal death
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41
Q

What (3) characteristics define Preeclampsia? What is the main etiology?

A

Characterized by (1) HTN, (2) Proteinuria, (3) Edema during pregnancy

Result of issue with the placenta, often associated with ischemic injury including fibrinoid necrosis and macrophage associated inflammation

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42
Q
  1. Preeclampsia vs severe preeclampsia
  2. Preclampsia vs eclampsia
  3. Define HELLP syndrome
A
  1. Preeclampsia: HTN, edema, proteinuria; Severe preeclampsia: preeclampsia + HA and vision changes
  2. Eclampsia: preeclampsia + convulsions
  3. HELLP syndrome: Seve preeclampsia + _H_emolysis, _E_levated _L_iver enzymes, and _L_ow _P_latelets
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43
Q

Tx and longterm sequelae of Preeclampsia

A

Mild: expectant management

Severe: delivery regardless of fetal age

Can be some long term sequelae including HTN/microalbuminemia and inc. heart/brain vascular disease risk

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44
Q

In general, what is the pathological state of the chorionic villi and trophoblasts in hydatiform moles?

A

There is swelling of the villi and proliferation of the trophoblasts

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45
Q

Key lab value that is increasd in hydatiform moles

A

HCG

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46
Q

Invasive mole

  1. Pathology
  2. Sx
  3. Tx
A
  1. A mole in which the Hydropic chorionic villi invade the uterine wall (myometrium) and embolize to distant sites
  2. Sx: Vaginal bleeding and risk of uterine rupture (HCG persistently increased)
  3. Tx: Chemo
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47
Q

Gestational Choriocarcinoma

  1. What is it?
  2. Presentation
  3. Tx
  4. How does this differ from ovarian or testicular choriocarcinoma?
A
  1. A malignant/rapidly invasive neoplasm of trophoblast derived cells (cysto and syncytio) that is necrotic and hemorrhagic
  2. Presents as vaginal blood and brown fluid spotting
  3. Tx: CHEMO IS EXTREMELY EFFECTIVE! (surgery is also an option)
  4. Ovarian/testicular are NOT responsive to chemo
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48
Q

1 etiology for hyperpituitarism?

Other dz’s on the differential?

A

1 = Functional anterior pituitary ademoma!

All the major causes are as follows:

  1. Fxnal anterior pituitary adenoma
  2. Anterior pituitary hyperplasia (prego)
  3. Carcinoma
  4. Extrapiuitary tumors
  5. Hypothalamic pathology

FACE Hormones

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49
Q

Name the aldosterone-sensitive tissues

What enzyme do they express?

A

Kidney, salivary glands, and colon

Enzyme = 11B-HSD2

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50
Q

What tissue types express 11B-HSD1? What is its fxn?

A

Liver (as well as adipose tissue and brain) all express 11B-HSD1.

Responsible for converting cortisone back into cortisol (its active state)

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51
Q

What (3) genetic etiologies can be potentially associated with an anterior pituitary adenoma?

A
  1. They can be sporadic (vast majority)
  2. Familial: MEN1 assc. (5%)
  3. GNAS gene mutation (constitutive activation of stimulatory G protein leading to unchecked cellular proliferation)
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52
Q

Prolactinoma

  1. What is it?
  2. Sx (based on sex)
  3. Tx
A
  1. Prolactin secreting adenoma
  2. Sx: Female- galactorrhea, amenorrhea, and infertility; Male- impotence and infertility
  3. Tx: Dopamine; surgery (for macroadenomas)

MOST COMMON FXNING ADENOMA

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53
Q

Somatroph cell adenoma

  1. What does it secrete
  2. Sx
  3. Dx
  4. Tx
A
  1. Secretes GH (leading to inc. IGF-1 secretion
  2. Sx: Pre-pubertal - gigantism; post-pubertal- acromegaly
  3. Dx: IGF-1 test; GH test (less reliable); Oral glucose tolerance test (GH normally supressed by oral glucose)
  4. Tx: Surgery or Somatostatin analogs (GH-inhibitory hormone)
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54
Q

Nelson Syndrome

  1. What is it?
  2. Sx?
A
  1. Adrenal glands removed in tx of cushing, but an unknown corticotroph microadenoma is present. WIthout the adrenal glands, there is a loss of any sort of feedback and the adenoma grows massively
  2. Sx: Mass effect, hyperpigmentation, no coritsol secretion
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55
Q

Pituitary apoplexy

What is it and what is the main risk associated

A

Acute hemorrhage into a nonfxnal adenoma. Leads to loss of ACTH, and thus cortisol, constituting and EMERGENCY DROP IN BP

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56
Q

What is usually the first clinical clue of Sheehan syndrome?

A

Lactation failure

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57
Q

What is the affect of SIADH on blood volume?

A

There is a euvolemic hyponatremia– blood volume remains nearly normal

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58
Q

From what embryological components do the anterior and posterior pituitary originate from?

A

Anterior- Rathke pouch

Posterior- Neurohypophyseal bud

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59
Q

Craniopharyngioma

  1. Pathology
  2. Usual location
  3. Key histo
  4. Who gets it and how often does it recur
A
  1. Benign tumor which arises from vestigial remants of Rathke’s pouch
  2. Usually found in the suprasellar location
  3. Histo: Palisading of squamous epithelial cells
  4. Bimodal age distribution and tends to recur after resection (can be locally invasive)
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60
Q

Pathology of Rathke cleft cysts

A

Developmental failure of Rathke’s pouch obliteration

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61
Q

Adrenal cortex derives from which embryological layer? Adrenal medulla?

A

AC: Mesoderm

AM: Neuroectoderm

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62
Q

Most common etiology of Cushing’s syndrome?

A

Administration of exogenous glucocorticoids

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63
Q

Cushing’s syndrome vs Dz

How often is the hypothalamus involved?

A

Syndrome: hypercortisolism

Dz: syndrome due to corticotroph secreting microadenoma, macroadenoma, or hyperplasia in the pituitary!

VERY RARE to have the HYPOTHALAMUS be the cause (via CRH secretion)

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64
Q

Other than a Cushing’s Dz causing Adenoma, what are the other endogenous causes of Cushing’s syndrome (2)

A
  1. Paraneoplastic Cushing syndrome (Ectopic ACTH, usually by SCC
  2. Primary adrenal neoplasms (Causes ACTH independent Cushing Syndrome)
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65
Q

What are the top (2) primary causes of hyperaldosteronism (i.e. causes unrelated to the RAA system)

A
  1. Bilateral idiopathic hyperaldosteronism: Bilateral nodular hyperplasia of adrenal glands (most common)
  2. Adrenocortical Neoplasms: aldosterone producing adenoma (Conn syndrome)
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66
Q

Clinical manifestations of Hyperaldosteronism

A
  1. HTN w/ longterm CV issues
  2. Hypokalemia w/ possible neuromuscular manifestations
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67
Q

Congenital Adrenal Hyperplasia (CAH)

  1. Heredity
  2. Pathology
  3. Clinical features
A
  1. Autosomal recessive
  2. Hereditary defect in enzyme (usually 21-hydroxylase), leading to dec. cortisol and thus inc. ACTH. This causes ADRENAL HYPERPLASIA
  3. infant females: clitoral hypertrophy/pseudohermaphroditism; older females: masculization + oligomenorrhe, acne, and hirsutism; males: precocious puberty + enlargement of external genitalia
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68
Q

Addison’s disease

A

aka Chronic Adrenal Insufficiency

Chronic destruction of the adrenal cortex (via multiple etiologies) leading to hypofxn (> 90% destruction). Could result from infxn, autoimmune adrenalitis (atrophy of all cortisol zones w/ spared medulla), sarcoidosis, metastasis, etc

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69
Q

Value for a normal blood sugar

A

70-120 mg/dl

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70
Q

DM diagnostic criteria (4)

A
  1. Random glucose > 200 (+ classic signs/sx)
  2. Fasting glucose > 126 mg/dl
  3. Abnormal glucose tolerance test (carbo load [75g glucose] and check 2h later. (+) if > 200mg/dl)
  4. HgbA1C > or equal to 6.5
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71
Q

Pre-DM criteria (3)

A
  1. Impaired fasting glucose (100-125 mg/dl after overnight fast)
  2. Impaired glucose tolerance test (post-parandial glucose– 140-199mg/dl)
  3. HgbA1C 5.7 to 6.4
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72
Q

Role of Adipose cells in T2DM

A

Adipose cells normally secrete Adipokines which aid in maintaining insulin sensitivity. Obese patients actually have dec. adipokine secretion leading to dec. insulin sensitivity

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73
Q

Describe the histological expectation for T2DM

A

Unlike T1DM, you don’t expect inflammation/ infiltrate (insulinitis), but you can often have amylin which ican replace some B-cells.

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74
Q

Although you aren’t worried about DKA, what complication of hyperglycemia are you concerned about with T2DM? Describe it.

Prototypical patient

A

Nonketotic Hyperosmolar Coma

Extreme hyperglycemia (>600) which leads to extreme dehydration, free water deficit and potential for confusion, coma, and seizures

Prototypical patient: NH resident with decreased water access or impaired thirst mechanism

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75
Q

The (3) major pathways of Glucotoxicity in DM complications

A
  1. Formation of Advanced Glycation End products (AGEs) – permanent formations of glycosylation products
  2. Modification of protein C activity
  3. Inc. intracellular glucose
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76
Q

What form does glycosylation take prior to AGE formation?

A

Schiff bases are what is first produced. These are initial glycosylation products which are labile and can dissociate.

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77
Q

What process does AGE formation spark?

A

A sequlae leading to atherosclerosis, thickened BM and microangiopathy

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78
Q

Relationship between hyperglycemia and protein kinase C. What specfically happens?

A

Intracellular hyperglycemia leads to increased protein kinase C. This causes an inc. in VEGF, dec. in endothelial NOS, inc. inTGFB and other proinflamatory cytokines. Leads to new retinal blood vessel formation/ retinopathy.

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79
Q

Affect of high intracellular glucose on eye and nerves

A

Can lead to inc. osmotic intake of water in the eye and subsequent lens swelling and also intracellular oxidative stress (leading to peripheral neuropathy)

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80
Q

Wipple’s Triad

A

Sx associated with Insulinoma

  1. CNS sx associated with hypoglycemia
  2. Glucose <50 mg/dl at measurement
  3. Sx resolve with feeding/glucose
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81
Q

Tx of Primary Adrenal Insufficiency

Secondary?

A

Primary

Cortisol replacement: hydrocortisone (or dexamethasone) + IV electrolyte replacement (acutely)

Fludrocortisone: aldosterone replacement

Secondary

Hydrocortisone (or dex)

In secondary, zona glomerulosa is not typically affected so no need for aldosterone tx

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82
Q

CAH Tx

A

Hydrocortisone and (if necessary) Fludrocortisone

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83
Q

What do you screen amniotic fluid for, in regards to CAH?

A

17-hydroxypregnenolone

(a precursor of cortisol)

84
Q

What is the in-utero tx for females with CYP21 mutation?

A

Dexamethasone (able to cross placenta and feedback to block pituitary secretion of ACTH, thus preventing virilization

85
Q

DOC for Rheumatoid Disorders

A

Prednisolone

86
Q

What drug can be given to treat infant respiratory distress syndrome? Which drug can’t be used and why?

A

Dexamethasone can freely cross the placenta (w/o being metabolized by 11BHSD2) and be used to promote lung maturation.

Prednisone is NOT used because it is converted back to prednisone (after mom activates it) by the placenta and the fetal liver isn’t mature enough to convert it back to predisolone

87
Q

Tx for cerebral edema (from brain tumors, meningitis, radiation, or high altitude)

A

Dexamethasone

88
Q

Mitotane

  1. MOA
  2. Indication
  3. Affect
  4. Contraindication
  5. What drug must be given with it (or soon after)?
A
  1. Destroys mitochondria of adrenocortical cells, leading to adrenocortical necrosis.
  2. Severe Cushing’s dz
  3. Effectively ablates endogenous cortisol production
  4. Contraindicated in pregnancy (permanent fetal adrenal damage).
  5. Must give hydrocortisone eventually, as serum cortisol levels will fall
89
Q

Mifepristone indication and MOA

A

Indication: Tx of refractory Cushing’s Syndrome

MOA: Glucocorticoid Receptor (GR) Antagonist

90
Q

What age is affected by adrenal carcinoma (all be it rarely)?

What inherited syndromes are associated with this rare cancer?

A

Any age

Li-fraumeni syndrome and Beckwith Wiedemann syndrome

91
Q

Describe pheochromocytoma

A

A neoplasm arising from neuroendocrine cells (chromaffin cells) in the paraganglion system (collection of adrenal medulla -like chromafin cells throughout the body).

92
Q

Name and describe the key rule associated with Pheochromocytomas

A

10% rule

  1. 10% have extraadrenal like organs of zuckerkanel or carotid body ( known as paragangliomas)
  2. 10% are bilateral
  3. 10% are malignant
  4. 25% are familial and possibly associated with any one of (6) known genes
93
Q

What are the (6) genes potentially associated with the familial version of pheochromocytoma

A
  1. RET gene (MEN II and III)
  2. NF1 (Type 1 neurofibromatosis)
  3. VHL
  4. Succinate dehydrogenase genes (SDHB, SDHC, and SDHD)
94
Q

Dx of Pheochromocytoma

A

Urinary elevation of metanephrine and VMA

95
Q

Neuroblastoma

  1. Macro:
  2. Micro:
  3. Key clinical features (age and presentation)
A
  1. Macro: Large bulky tumor
  2. Micro: Homer-wright rossettes or sheets
  3. Common childhood neoplasm, often present as large abdominal mass
96
Q

Multiple Endocrine Neoplasia Syndromes

What is it?

Name the (5) main characteristics.

A

Inherited dz w/ lesions (hyperplasia, adenomas, carcinomas) of multiple endocrine glands

  1. Occur at young age
  2. Multiple endocrine organs
  3. Multifocal tumors
  4. May be preceded by asymptomatic stage of endocrine hyperplasia
  5. Aggressive and often recur
97
Q

MEN1

  1. Inheritance
  2. Gene affected
  3. Name the main organs involved and describe their involvement
A
  1. Autosomal Dom.
  2. MEN1 gene (11q13) –> tumor suppressor
  3. 3 P’s: Parathyroid, Pancreas, Pituitary
    • (primary hyperthyroidism- most common)
    • (endocrine tumors of pancreas- leading COD)
    • (pituitary tumors are usually prolactin secreting adenomas)
98
Q

MEN2 (general)

  1. Inheritance
  2. Key mutation
A
  1. Auto. Dom.
  2. Mutation in RET protoncogene (10q11.2)
99
Q

MEN2A vs MEN2B

A

MEN2A: thyroid (medullary carcinoma almost always) + adrenal medulla (pheochromocytoma) + parathyroid (hyperparathyroidism)

MEN2B: Just like MEN2A, with following changes:

  1. Mucosal ganglioneurons + Marfanoid habitus (long axial skeleton)
  2. No parathyroid changes
100
Q

Prophylactic tx for relatives of ppl with MEN2

A

They should get genetic testing for RET, and if positive, have a prophylactic thyroidectomy

101
Q

Most common location for an intramural obstruction

A

Ureteropelvic jxn

102
Q

Metabolic Syndrome

A

Co-occurence of metabolic risk factors for both T2DM and CVD. Includes the following (4) RFs:

  1. Abdominal obesity
  2. Hyperglycemia
  3. Dyslipidemia
  4. HTN
103
Q

Criteria for screening for DM (3)

A
  1. BMI > 25 w/ 1+ risk factor, or
  2. 45 y/o with no risk factor, or
  3. BP>135/80
104
Q

What (3) exams/screens do DM patients need annually?

What are the tx targets for DM?

A
  1. Pt’s require annual retinal exam, microalbuminuria screening, and foot exam
  2. Targets: A1C
105
Q

Spironolactone MOA

(3) key side effects

A
  1. Androgen-R competitive inhibitor and Aldosterone-R inhibitor
  2. SE: GI hemorrhage, aGranulocytosis and Gynecomastia
106
Q

Main bug associated with acute mastitis

A

Staph aureus (Associated with breast feeding)

107
Q
  1. Most common change in the premenopausal breast. What are the (2) types?
  2. Presentation?
  3. Histo?
A
  1. Fibrocystic change (proliferative and nonproliferative), is common in 20-40 y/o females
  2. Presents as “lumpy breast”, often in upper outer quadrant
  3. Cysts have “blue-dome” appearance on gross exam
108
Q

Describe how the following fibrocystic-related changes are associated with invasive carcinoma risk:

  1. Fibrosis, cysts, and apocrine metaplasia
  2. Ductal hyperplasia and sclerosing adenosis
  3. Atypical hyperplasia
A
  1. No inc. risk (despite metaplasia)
  2. 2x risk
  3. 5x risk
109
Q

Intraductal Papilloma

  1. What is it?
  2. What characterizes it?
  3. How does it present?
  4. What must it be distinguished from?
A
  1. Papillary growth (usually into a large duct)
  2. Characterized by fibrovascular projections lined by epithelial and myoepithelial cells
  3. Classically presents as bloody nipple discharge in a premenopausal woman
  4. Must distinguish from papillary carcinoma (pap. CA lacks myoepithelial cells and is more common in post-menopausal women)
110
Q

Fibroadenoma

  1. How common and in who?
  2. Presentation
  3. Relationship to estrogen
  4. Prognosis
  5. How does histo look?
A
  1. Most common benign neoplasm of the breast, usually seen in premenopausal women
  2. Mobile, marble-like mass
  3. Estrogen sensitive (grows and shrinks with pregnancy and pain during menstration)
  4. Benign (no risk of carcinoma)
  5. Histo: delicate stroma + compressed, slit-like glands
111
Q

Phyllodes tumors

  1. Which component is overgrown?
  2. Common in what population?
  3. Malignant potential?
A
  1. Overgrowth of fibrous component
  2. Common in post-menopausal women
  3. Sometimes malignant

LOOKS LIKE LEAF

112
Q

Risk factors for Breast cancer are mostly related to…

A

Estrogen exposure

+ Obesity and atypical hyperplasia

113
Q

What are the general classifications of Breast Carcinoma (4)

A

In-situ Carcinomas

(1) Ductal carcinoma in-situ; (2) lobular carcinoma in-situ

Invasive Carcinomas

  1. (1) Invasive Ductal Carcinoma; (2) Invasive Lobular Carcinoma
114
Q

Ductal Carcinoma In-situ

  1. What is it?/Dx
  2. What dz is related to it?
A
  1. Malignant proliferation of cells in ducts with no BM invasion. Usually dx via mammographic calcifications
  2. Paget Dz of the breast is DCIS that extends up the ducts to involve the skin of the nipple. Almost always associated with underlying carcinoma.
115
Q

Invasive Ductal Carcinoma

  1. How common?
  2. Presentation
  3. What does biopsy show?
A
  1. MOST COMMON TYPE OF INVASIVE CARCINOMA IN BREAST!!!!! (80%+ of cases)
  2. Presentation: mass detected on PE or mammography. Advanced tumors show dimpling or retraction.
  3. Biopsy shows duct-like structures in desmoplastic stroma
116
Q

Although there is some controversy, when do all experts agree women need to be getting mammographies?

A

Biennially (every 2y, from ages 55-74 y/o

117
Q

Inflammatory carcinoma

  1. What umbrella of breast CA is this under
  2. Characterized by what?
  3. Prognosis
A
  1. Invasive Ductal Carcinoma
  2. Characterized by carcinoma in the dermal lymphatics (and thus, peu d’orange)
  3. Poor prognosis
118
Q

Lobular Carcinoma In Situ (LCIS)

  1. Presentation
  2. Characterization
  3. Tx
A
  1. No mass or calcifications. Usually discovered incidently in biopsy
  2. Characterized by dyscohesive cells lacking E-cadherin adhesins
  3. Tx: tamoxifen (low invasive risk)
119
Q

How does Invasive lobular carcinoma characteristically grow?

A

A single-file pattern due to the loss of E-cadherin

120
Q

What type of gene is HER2/neu? (tumor suppressor or protooncogene)

A

Protooncogene (it is a gene amplifier)

121
Q

After breast conserving surgery is performed to tx breast CA, what is the next tx step?

A

Radiation therapy (daily x 6w)

122
Q

Chemo drugs that can be used for tx of Breast CA. What are potential risks (2 main ones)

A

Cyclophosphamide, Herceptin (trastuzmab), Adriamycin, Taxanes

(CHATing w/ Breast CA patients)

123
Q

Curing tx for metastatic Breast CA

A

It is incurable. 2y survival

124
Q

BRCA1 vs BRCA2

A

1: ch 17, breast and ovary
2: ch. 13, male breast

125
Q

Most common subtype for male breast CA. Presentation?

A

Invasive ductal carcinoma

Presents as subareolar mass in older males.

126
Q

Gynecomastia and male breast CA

A

It is NOT a risk factor for male breast CA

127
Q

Stage of fracture healing

A
  1. Hematoma (hours/days)
  2. Inflammation (w/in 48 hours)
  3. Granulation (2-12 days)
  4. Soft Callus (1w to several months)
  5. Hard callus (1w to several months)
  6. Remodeling (several months)
128
Q

Osteoporosis and mineralization

A

In osteoporosis there is a dec. in trabecular bone mass, despite normal bone mineralization

129
Q

Type I vs Type 2 primary osteoporosis

A

T1: Postmenopause (due to dec. estrogen and subsequent inc. in RANK/RANKL)

T2: Senile (age-related calcium deficiency)

130
Q

What Bone densitometry levels correlate with…

  1. Normal
  2. Osteopenia
  3. Osteoporosis
A
  1. normal:
  2. osteopenia: 1-2.5 SD below young adult mean
  3. osteoporosis >2.5 SD below young adult mean
131
Q

Osteoporosis Tx (6)

A

BEERR Cup

  1. Bisphosphonates
  2. Excercise
  3. Estrogen replacement
  4. Recombinant PTH
  5. RANK-L inhibitor (denosumab)
  6. Calcium/Vit D
132
Q

Rickets vs Osteomalacia

  1. Patient demos
  2. Etiology
  3. Pathophys
  4. Sx
A
  1. Rickets: kids; Osteo: adults
  2. Etiology: Vit D deficiency or bone mineralization defect
  3. Pathophys: Accumulation of osteoid (unmineralized, soft bone)– Ricket specific- osteiod is in growing bones and the growth plate cartilage is not properly reabsorbed. Loss of structural rigidity
  4. Sx: Osteo: same as osteoporosis; Rickets: A bunch! (including delayed fontanelle closure, dental hypoplasia, swelling in wrist/ankle joints, and leg bowing)
133
Q

The presence of dissecting osteitis is a sign of what dz process? What is another name for this sign?

A

The presence of hyperparathyroidism. Also known as railroad tracks. The osteoclasts are cutting through the trabeculue

134
Q

Brown Tumors

A

Lytic lesions (in the setting of excess osteoclast activitiy) that cause hyperparathyroidism.

135
Q

Von Recklinghausen Dz of the Bone

A

Osteitis Fibrosa Cystica

The bone is replaced w/ fibrous tissue and cystic change

136
Q

Paget’s Dz

  1. Path
  2. Etiology
  3. Dx
A
  1. Dz caused by excessive osteoclast driven breakdown of bone tissue, followed by abnormal bone formation.
  2. More often seen in men, with a slow virus infxn (paramyovirus). IL-6 secretion is induced leading to inc. RANK expression.
  3. Dx Radiographics/bone scan and inc. alk phosph
137
Q

What are the (3) stages of Paget dz? (What is the functional cell for each?)

Which stage is assc. with “Cement lines” in the histo?

A
  1. Osteolytic (osteoclasts)
  2. Osteolytic-osteoblastic (mixed)
  3. Osteosclerotic (osteoblasts)

Cement lines = osteosclerotic

138
Q

Paget’s Dz

Presentation

A

SAM Pees In Bushes

  1. Skull thickening (leonitiasis ossea)
  2. _A_xial skeleton, _A_rthritis
  3. Mid-adulthood
  4. _P_ain, _P_roximal femur, _P_latybasia (skull base flattening impinging on foramen magnum)
  5. Incidental finding
  6. Bowing of tibia
139
Q

Paget’s Dz

Potential consequences and Tx

A

Consequences

High output HF: due to hypervascularity of pagetic bones (inc. BF) leading to inc. resting cardiac work

Sarcoma development: osteosarcoma or fibrosarcoma (5-10%)

Tx

  1. Acetominophen/NSAIDs
  2. Bisphosonates (induce osteoclast apoptosis)
  3. Calcitonin (inhibit osteoclast fxn)
140
Q

Which type of OI is autosomal dominant? recessive?

Which type is lethal? not lethal, but severely deforming?

A
  1. Types 1, 3, and 4 are Aut. Dom.Type 2 is Aut. rec.
  2. Type 2 is lethal; Type 3 is the most severely deforming
141
Q

Achondroplasia

  1. What is the defect?
  2. Inheritance
  3. Presentation
A
  1. Mutation in FGF receptor 3, making it constitutively active. This receptor normally inhibits cartilage proliferation, slowing growth plate development
  2. Autosomal dom. (though 80% are de novo)
  3. Dwarfism (failure of long bone growth due to issue of endochondral ossification. membranous ossification is unaffected– so head is normal)
142
Q

Osteonecrosis?

What are some predisposing factors to osteonecrosis of the jaw?

A

Ischemic bone death.

In the jaw, dental disease, dental damage, oral trauma, chemo/corticosteroids all play a role.

(high dose IV bisphosonates)

143
Q

Osteoma

  1. What is it?
  2. Prognosis?
  3. Age
  4. Assc. with what syndrome?
A
  1. Tumor-like mass of abnormally dense bone
  2. Benign
  3. 4th/5th decade
  4. Assc. with Gardner’s syndrome (familial adenomatous polyposis which also includes epidermal cysts, GI polyps, etc.)
144
Q

Osteioid osteoma

  1. Age
  2. Where in the bone does it appear
  3. Presentation
  4. Tx
A
    1. Cortex of long bone
  2. Presents as bone pain that resolves w/ aspirion
  3. Tx w/ excision
145
Q

Osteosarcoma

  1. Incidence
  2. Tumor presentation
  3. Sx (including location and age at presentation)
  4. Dx
A
  1. Most common malignant tumor of the bone
  2. Large, fleshy, or hard, with cavity at the metaphysis
  3. Sx: Painful, tender mass, with 60% located around the knee; age = teens (sometimes elderly)
  4. Codman Triangle on XR (tumor has broken through cortex and lifted periosteum); may also have sunburst appearance
146
Q

Describe the (3) grades of Osteosarcoma

A
  1. Low: Parosteal Osteosarcoma
  2. Intermediate: Periosteal Osteosarcoma
  3. High: Conventional Osteosarcoma (osteoblastic)

As grades inc., so does sunburst pattern, atypia, and disorganization

147
Q

Osteochondroma

Describe the disorder, osteochondromatosis

A

Outgrowth of medullary and cortical bone, covered by a cartilagionus cap. A malformation, more than a true neoplasm.

aka an Exostosis

Osteochondromatosis is an auto dom. dz of many exostoses, causing severe bone deformity. Manifests in adolescence and ceases in adulthood.

148
Q

Chondrosarcoma

  1. Sx/presentation
  2. Prognosis/ Grading
  3. Tx
A
  1. Sx: >40y, men. Painful enlarging masses.
  2. Prognosis is related to grade/size. (Grade 1- 90% 5y; Grade 2- 43% 5y)
  3. Tx: Surgery/chemo
149
Q

Ewing/PNET

  1. What is it?
  2. Key translocation
  3. View on X-ray
  4. Histo
  5. Sx
  6. Ddx
  7. Tx
A
  1. Malignant proliferation of poorly-differentiated cells derived from the neural ectoderm
  2. T11;22 (leading to EWS/FLI-1 fusin and thus over-expression)
  3. Onion skin on XR due to periosteal rxn producing layers of reactive bone
  4. Histo (particulary for PNET variant) includes homer-wright rosettes.
  5. Sx: Fever, tenderness/warmth, Inc. ESR, and leukocytosis
  6. DDx:
  7. Lymphoma, osteomyelitis, other sarcomas
  8. Responsive to chemo (and surgery)
150
Q

Benign Fibrosseous Lesions

  1. What is it
  2. Are cases usually monostotic or polyostotic?
A
  1. Benign intramedullary proliferation of fibrous tissue and bone that is irregularly distributed and has no osteoblastic rimming
  2. Most cases are monostotic (single bone); (polyostotic- 20% of cases)
151
Q

McCune-Albright Syndrome

  1. What is the triad of sx
  2. What gene mutation is it assc. with?
A
  1. (1) Polyostotic fibrous dysplasia + (2) endocrinopathies (ex precocious puberty) + (3) cafe-au-lait skin pigmentation
  2. GNAS gene mutation
152
Q

Giant Cell Tumor of Bone

  1. Describe this tumor
  2. Presentation
  3. DDx
  4. Dx
  5. Prognosis/ recurrence
A
  1. Tumor comprised of multinucleated (osteoclast like) giant cells and stromal cells
  2. Presents as young adult (20-40), with pain around knee
  3. DDx: Brown tumor
  4. Dx: Soap bubble appearence on radiology
  5. Locally aggressive tumor– may recur
153
Q

Other than TSH receptors, what else lines thyroid follicles?

A

Parafollicular or “C” cells, which secrete Calcitonin

154
Q

What are the (4) main thyroid hormone fxns?

A
  1. Stimulation of protein synthesis
  2. Upregulation of carb and lipid catabolism
  3. Inc. metabolic rate
  4. Brain development for fetus/ neonate
155
Q

Thyroid storm

A

MEDICAL EMERGENCY

And abrupt onset of hyperthyroidism, usuallly in patient w/ hx of graves during infxn, surgery

156
Q

Interpret the following radioactive iodine uptake results:

  1. diffuse
  2. localized
  3. reduced
A
  1. diffuse = graves
  2. localized = toxic adenoma
  3. reduced = thyroiditis
157
Q

Cretinism vs Myxedema

A

Cretinism: hypothyroidism in kids; impaired skeletal and intellectual development (worse mental issues if it was due to maternal hypothyroidism)

Myxedema: Adult hypothyroidism; gradual slowing of mental/physical activity. Periorbital edema, thick skin, inc. atherogenic profile

158
Q

Which thyroiditis types cause pain? Are painless?

A

Pain:

  1. Infx thyoiditis
  2. Subacute granulomatous thyroiditis (De Quervain thryoiditis)

No Pain

  1. Reidel’s thyroiditis
  2. Hashimoto’s thyroiditis
159
Q

Key antibodies associated with Hashimoto’s dz

A

Thyroglobulin and Thyroid Peroxidase (TPO)!!!, TSH receptor, or iodine receptor

160
Q

Hashimoto’s Thyroiditis

  1. Gross?
  2. On Histo?
  3. Inc. risk for what type of cancer?
A
  1. Gross: Diffusely enlarged gland, somewhat nodular
  2. Histo: Thyroid follicles lined by Hurthle cells/ oncocytes (abundant granular pink cytoplasm)
  3. Risk of Non-Hodgkin B cell lymphoma
161
Q

Subacute/Granulomatous (De Quervain) Thyroiditis

  1. Age
  2. Pathology
  3. How common?
  4. How is it resolved?
  5. Key points about histo.
A
  1. 40-50 y/o
  2. VIral or post-viral inflammatory response, in which viral antigens/viral induced host tissue, stimulates formation of cytoxic T cells which damages thyroid follicular cells
  3. Most common cause of thyroid pain
  4. Causes transient hyperthyroidism which is self-limiting and recovers in a couple of weeks
  5. Histo: Destruction of gland + presence of giant cells

VAIN, PAIN, VIRAL

162
Q

Riedel thyroiditis

A

Rare + extensive fibrosis involving thyroid and contiguous neck structures

163
Q

Key triad for Graves dz

Key antibodies assc.

A

Hyperthyroidism (with goiter) + exopthalmos + pretibial myxedema

Auto-Antibodies: TSI, TGI

164
Q

Multinodular Goiter evolves from what?

What is it called if there is a toxic, autonomous nodule?

A

Evolves from diffuse goiter. Some cells may become autonomous and continue proliferating.

Toxic + autonomous – Plummer’s syndrome

165
Q

Follicular Adenoma

Where is this neoplasia? Common mutation association.

Key buzzword

How does it look on iodine scan?

A

Thyroid.

20% show mutation of RAS or PAX8-PPARG

Buzzword: Capsule

Usually cold on the scan

166
Q

What is the most common type of thyroid CA? What etiology is it associated with?

A

Papillary carcinoma

Assc. w/ radiation exposure

167
Q

Key nuclear features associated with Papillary carcinoma

What’s key about histo of the follucular variant?

A
  1. Longitudinal nuclear grooves (almost like train-track)
  2. Orphan Annie
  3. Intranuclear cytoplasmic inclusions
  4. Marginated nucleolus

Follicular variant- no papillae, better prognosis

168
Q

Medullary Carcinoma

  1. Describe it
  2. What does it secrete
  3. Inheritance?
  4. Tumor markers
A
  1. Neuroendocrine neoplams derived from parafollicular/C-cells
  2. May secrete calcitonin or other polypeptide hormones (hypocalcemia is NOT PROMINENT despite calcitonin presence)
  3. 70% sporadic- 4th/5th decade; 30% familial/MENS assc.
  4. Markers: Calcitonin and CEA
169
Q

What is key to histo for medullary carcinoma?

A

Presence of Amyloid

“Amy played Medussa”

170
Q

Anaplastic Carcinoma

  1. Path
  2. Mortality
A
  1. p53 inactivation or beta cetenin activation
  2. Virtual 100% mortality
171
Q

Thyroglossal duct/cyst

  1. What is it?
  2. Risk?
A

Most common clinically signficant congenital anomaly, due to incomplete atrophy of the duct. Forms midline cyst, at any age. Can lead to infection/abscess risk.

172
Q

Main cell in the Parathyroid gland

A

Chief cell (also oxyphil cells)

173
Q

What is the most common cause of clinically apparent hypercalcemia? Most common cause of incidental hypercalcemia?

A

Apparent: malignancy

Incidental: primary hyperparathyroidism

174
Q

What are the possible types of parathyroid lesion (3) and how common is each?

A
  1. parathyroid adenoma (85-95%)
  2. hyperplasia (5-10%)
  3. parathyroid carcinoma (1%)
175
Q

Familial Hypocalciuric Hypercalcemia

A

Autosomal dominant mutation in parathyroid calcium-sensing receptor gene (CASR), ch.3q

176
Q

What is the main difference between parathyroid hyperplasia and adenoma in terms of number of glands?

A

Adenoma is single gland enlargement; hypertrophy is mullti

177
Q

Potential PTH Sx

A

“Painful bones, Renal Stones, Abdominal groans, and Psychic Moans”

178
Q

Metformin

  1. Key AE
  2. Key contraindications (3)
A
  1. AE: Lactic Acidosis
  2. Contra: Hx of Renal Failure, MI, or CHF
179
Q

Sulfonylureas

  1. Key AE
  2. Key Contraindications
A
  1. AE: Inc. Hypoglycemic risk
  2. Contra: Renal/Liver disease
180
Q

Thiazolidinediones

  1. Key AEs
  2. Key Contraindications
A
  1. AE: Weight gain (sub q); fluid retention; inc. HF risk; inc. bone fracture in women
  2. Contra: Liver dz, CHF, CVD
181
Q

Ureteritis/ Cystitis Cystica

  1. What is it?
  2. Histo?
  3. Gross?
A
  1. Metaplasia of urothelium
  2. Gross: translucent, pearly-yellow cysts
  3. Histo: von Brunn’s nests (circular infiltrate w/ central degeneration)
182
Q

Non-bacterial Cystitis

  1. Who is affected
  2. What is this dz associated with?
  3. Sx?
  4. Dx?
A
  1. 90% female
  2. Assc. w/ allergies and autoimmunity
  3. Intermittent, severe pain + urinary issues (freq, urgency, etc.)
  4. Dx: mucosal ulcers + mast cells
183
Q

Malakoplakia

  1. What is it?
  2. Sx
  3. Histo
A
  1. Rare inflammatory condition w/ plaque, papule, or ulceration usually in GU system
  2. Sx: Recurrent fever, bladder irritability, etc.
  3. Histo: Foamy macrophages + blue targetoid spheruls (Michaelis-Gutmann bodies)
184
Q

Leukoplakia

  1. Gross/ Path
  2. Risk factor for what?
A
  1. Gray-white areas of squamous metaplasia which are the result of long-term irritation or chronic infxn
  2. Risk of SCC
185
Q

Bladder Cancer

  1. Sx (3)
  2. What is the most common etiology
  3. What is the primary pathology?
A
  1. (1) Painless hematuria, (2) Irritative sx (dysuria, frequency, urgency), (3) other (flank pain, pelvic mass, etc.)
  2. Commonoly due to SMOKING!
  3. Papillary (most common!!!)– result of hyperplasia or could be non-papillary (flat)
186
Q

Tx for CIS-high grade bladder cancer

A

Intravesical immnotherapy (BCG); beyond that, must do cystectomy. Good prognosis (if low grade)

187
Q

Prostate Cancer

  1. What type of cancer is it usually?
  2. What genetic changes increase susceptibility? (4)
  3. Key biomarkers
A
  1. Adenocarcinoma
  2. (1) Inc. androgen receptor due to dec. CAG repeats, (2) BRCA repeats, (3) rearrangement putting ETS gene under promoter control [TMPPRSS2]
  3. Biomarkers: PSA, EZH-2, AMACR, PCA3
188
Q

Prostate CA treatment

If organ confined?

If advanced/metastasized?

A
  1. Confined: radical prostatectomy or radiation
  2. Advanced: Androgen deprivation
189
Q

Prostatic Intraepithelial neoplasia (PIN)

  1. What is it?
  2. Relation to prostate CA?
A
  1. Proliferation of neoplastic cells w/in large ducts
  2. Very high assc. w/ prostate CA but not causative
190
Q

Hypospadia vs Epispadia

A

Hypo: Urethral opening on the ventral surface

Epi (get an epidural into your back): Urethral opening on the dorsal surface

191
Q

Phimosis vs Paraphimosis

A

Phimosis- prepuce annot be retracted

Paraphimosis- forcible retraction of phimotic prepuce leading to damage

192
Q

What is the cause of Molluscum Contagiousm?

Which cause is most prevalent? Which is sexually transmitted?

A

Caused by DNA poxvirus, (MCV)

MCV1 = most prevelant

MCV2= sexually transmitted

193
Q

Risk factors for SCC of the penis (4)

A
  1. Poor hygiene phimosis
  2. Acumulation of smegma
  3. Hx of genital warts
  4. HPV types 16/18
194
Q

Cryptorchidism is sometimes associated with what genetic defect?

A

Trisomy 13

195
Q

For a pt with epidymitis, which bugs do you expect if he is…

>35 y/o

A

> 35 y/o: e. coli, pseudomonas

196
Q

Seminoma

  1. How common
  2. Tx
  3. Markers
  4. When do they usually present?
A
  1. Most common germ cell tumor
  2. Extremely radiosensitive
  3. bHCG
  4. Presents at stage I
197
Q

What neoplasia is a risk factor for Testicular Tumors?

A

Intratubular Germ Cell Neoplasia (ITGCN)

Large, atypical, fried-egg like cells

198
Q

Nonseminomatous tumors

(general facts)

  1. Aggression?
  2. Presentation?
  3. Tx?
A
  1. Much more aggressive than seminomatous
  2. Usually present at stage II/III
  3. Radioresistant but 90% cure rate w/ aggressive chemo
199
Q

90% of invasive testicular tumors have what chromosome defect?

A

Isochromosome of the short arm of chromosome 12

200
Q

Embryonal Carcinoma (male)

  1. Age
  2. Gross
  3. Histo
A
  1. 20-30 y/o
  2. Gross: Poorly demarcared, foci of necrosis/hemorrhage
  3. Micro: large anaplastic cells; distinct cells borders arronged in glandular, papillary patterns
201
Q

Yolk sac tumor (male)

Most common testicular tumor in who?

A

Infants up to 3Y

202
Q

Leydig Cell Tumor (male)

  1. How common?
  2. Key micro finding?
  3. What do they produce?
A
  1. Most common sex-cord stromal tumor
  2. Histo: Crystalloids of Reinke
  3. Produce androgen so can lead to precocious puberty or gynecomastia
203
Q

Teratoma (male)

Benign or malignant?

A

ALWAYS MALIGNANT IN MALES!!!

204
Q

Most common testicular neoplasm for men >60?

A

Lymphoma (poor prognosis) – and also the most common bilateral testicular tumor overall!

205
Q

Which are more common in the testis? Mixed tumors or pure histologic types?

A

Mixed

Repro/Endocrine/ Etc. (1 decks)

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