MHD2 Exam 4 Rapid Review Flashcards
1
Q
Cell type for normal extocervix? Normal endocervix?
A
Ecto: nonkeratinized stratified squamous
Endo: Simple columnar
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
3
Q
Low risk HPV leads to what type of growth?
High risk?
A
Low: Condyloma
High: Inc. neoplasm risk
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
5
Q
What cell type is characteristically associated with Condyloma? What are the (4) characteristics of this cell type?
A
Koilocyte
- Hyperchromasia
- Nuclear enlargement
- Irregular nuclear membrane contour (raison-like)
- Perinuclear halo
(Head Negus In Peds)
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
7
Q
Cancer types most associated with HPV
Tx
A
SCC (75%)
Adenocarcinoma (15%)
Tx: Hysterectomy and LN dissection
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
9
Q
Vulva vs Vaginal SCC
- RFs
- Precursor
- Presentation
- Mets
A
- RF: Vulva: HR HPV or Lichen Sclerosis / Vaginal: HR HPV
- Precursor: Vulva: Vulvar Intraepithelial Neoplasia (VIN)/ Vaginal: Vaginal Intraepithelial Neoplasia (VAIN)
- Presentation: Vulva: Leukoplakia/ Vaginal: vaginal bleeding and discharge
- Mets: Regional LNs
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)
11
Q
Describe the histo of Paget disease
A
Single cells with pale vacuolated cytoplasm with abundant glycosaminoglycans
12
Q
Clear cell adenocarcinoma
- Associated with what?
- What is the precursor lesion?
- How does it present?
A
- DES-associated
- Vaginal adenosis = precursor lesion
- Presents as agranular areas adjacent to normal, pink, vaginal mucosa
13
Q
Embryonal Rhabdomyosarcoma of Vagina
- Age of appearance
- Presentation
- What key markers?
A
- Appears before 20 y/o (usually before 5)
- Presents as bleeding, soft, grape-like mass protruding through the vagina
- Skeletal muscle markers (rhabdoMYOblasts)
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
15
Q
Top theory for cause of endometriosis
Other theories? (2)
A
Menstraul backflow (regurg)
Other theories: metaplastic or Vascular/Lymphatic dissemination
16
Q
Survival factors for Endometriosis (4)
Needed criteria?
A
AIIM
- Aromatose activity of stromal cells (inc. estrogen production)
- inc. Inflammatory mediators
- dec. Immune clearance
- activated Macrophages to establish/maintain
Need 2/3: Endometrial glands, endometrial stroma, hemosiderin pigment
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.
18
Q
- Endometrial Hyperplasia is the result of what?
- Describe the (2) Histo types
- What is the key gene mutation assc?
- Sx?
A
- Results from estrogen excess
- Nonatypical (low short term risk of endometrial cancer); Atypical (aka endometrial intraepithelial hyperplasia/neoplasia– high cancer risk)
- Key mutation for atypical: PTEN
- Sx: Postmenopausal bleeding
19
Q
Describe the histo/cytology for Atypical hyperplasia
A
- Glandular crowding
- Cytologically atypically rounded, vesicular nuclei, w/ prominent nucleoli
20
Q
Endometrioid vs Serous Endometrial Cancer
- What does it arise from?
- Mutations associated
- Key histological feature
A
- Endometrioid: Arises from endometrial hyperplasia; Serous: Sporadic
- Endometrioid: PTEN; Serous: p53
- E__ndometrioid: appears reminiscent of “normal” endometrium; Serous: Papillary structures
21
Q
Endometrial Polyps are often associated with what drug?
A
Tamoxifen (breast cancer drug)
22
Q
Leiomyoma
- Arises from what cell type?
- Appearence?
- Chromosomal abnormalities?
- What stimulates growth?
- Usually seen in singles or multiples?
A
- Arises from myometrial smooth muscle cells
- Appears well circumscribed and whorled
- Chromosomal abnormalities: 6, 12 rearrangements
- Stimulated to grow by Estrogen (so associated with premenopause)
- Usually seen in multiples
BENIGN
23
Q
Leiomyosarcoma
- Arise from?
- Patient demographic
- Clinical course?
- Usually seen in singles or multiples?
A
- Arise denovo (NOT leiomyomas gone bad)
- Postmenopausal women
- Recur after removal and often metastasize to the lung
- Usually single
24
Q
Polycystic Ovarian Syndrome
- Characterized by what (3) things?
- Key component of pathogenesis?
- Histo
- Clinical sequela (5)
A
- (1) Excess secretion of androgenic hormones, (2) Persistent anovulation, (3) Subcapsular ovarian cysts
- Increased LH secretion (leading to inc. androgens)- key component
- Histo shows follicles lined by granulosa cells with hyperplastic theca (interna)
- Sequela: (1) Hirsutism, (2)chronic anovulation/oligomenorrhe/infertility, (3)insulin resistance, (4)obesity, (5)endometrial hyperplasia/cancer
25
_Endometrioid vs Brenner_
1. Behavior?
2. Gross?
3. Histology?
4. Assc. Tumor Suppressor Gene?
5. May arise from what underlying condition?
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
26
Key Tumor marker for ovarian tumors?
CA-125 (used for tx and recurrence)
27
Struma Ovarii
When a large portion of a teratoma is composed of thyroid tissue
28
**Dysgerminoma**
1. Behavior
2. Tumor marker
3. Male counterpart
1. Malignant and _Radiosensitive_
2. LDH tumor marker
3. Male counterpart = testis Seminoma; associated with gonadal dysgenesis
29
**Endodermal Sinus Tumor (Yolk Sac Tumor)**
1. Behavior
2. Key Histo
3. Tumor marker
1. Malignant
2. **Schillar-Duvall Bodies** (glomerulus like structure)
3. AFP Tumor marker
30
_Choriocarcinoma_
1. Behavior
2. Histo
3. Tumor marker
4. How common is a pure choriocarcinoma?
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)
31
_Embryonal Carcinoma_
1. Behavior
2. Histo
3. Gross
1. Malignant aggressive
2. Large primitive cells
3. Malignant and aggressive
32
_Granulosa cell tumor_
1. Key histology
2. Hormone produced
3. Presentation
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
33
_Sertoli-Leydig cell tumor_
1. Histo (key crystal type)
2. Hormone type produced
3. Presentation
1. Reinke crystals
2. Androgen production
3. Block female sexual development in children; Hirsutism/virilization
34
_Thecoma-Fibroma_
1. What (2) specific cell types are present?
2. Hormons produced
3. Key syndrome associated
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
35
Key Met to Ovaries
Gastric adenocarcinoma is most common- (Krukenberg tumor)
36
Name the (2) layers of the placenta, and where it attaches.
Amnion (inner); Chorion (outer)
Chorion attaches to the decidua (the endometrium of pregnancy)
37
_Chorionic VIlli_
1. What is it?
2. What is it made of? (include the two layers of epithelium)
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**
38
_Twins_
1. Dichorionic vs Monochorionic (what does each imply?)
2. Diamnionic vs monoamnionic (what does each imply?)
3. What is an vascular anastomose?
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
39
_Placenta Accreta_
1. What is it?
2. Predisposing factors?
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
40
_Abruptio Placenta_
1. Pathogenesis
2. Clinical effect (3)
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
41
What (3) characteristics define Preeclampsia? What is the main etiology?
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
42
1. Preeclampsia vs severe preeclampsia
2. Preclampsia vs eclampsia
3. Define HELLP syndrome
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
43
Tx and longterm sequelae of Preeclampsia
_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
44
In general, what is the pathological state of the chorionic villi and trophoblasts in _hydatiform moles_?
There is swelling of the villi and proliferation of the trophoblasts
45
Key lab value that is increasd in _hydatiform moles_
HCG
46
_Invasive mole_
1. Pathology
2. Sx
3. Tx
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
47
_**Gestational** Choriocarcinoma_
1. What is it?
2. Presentation
3. Tx
4. How does this differ from ovarian or testicular choriocarcinoma?
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**
48
#1 etiology for hyperpituitarism?
Other dz's on the differential?
#1 = **Functional anterior pituitary ademoma!**
All the major causes are as follows:
1. **_F_**xnal anterior pituitary adenoma
2. **_A_**nterior pituitary hyperplasia (prego)
3. **_C_**arcinoma
4. **_E_**xtrapiuitary tumors
5. **_H_**ypothalamic pathology
FACE Hormones
49
Name the aldosterone-sensitive tissues
What enzyme do they express?
Kidney, salivary glands, and colon
Enzyme = 11B-HSD2
50
What tissue types express 11B-HSD1? What is its fxn?
Liver (as well as adipose tissue and brain) all express 11B-HSD1.
Responsible for converting cortisone back into cortisol (its active state)
51
What (3) genetic etiologies can be potentially associated with an _anterior pituitary adenoma_?
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)
52
_Prolactinoma_
1. What is it?
2. Sx (based on sex)
3. Tx
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
53
_Somatroph cell adenoma_
1. What does it secrete
2. Sx
3. Dx
4. Tx
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)
54
_Nelson Syndrome_
1. What is it?
2. Sx?
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
55
_Pituitary apoplexy_
What is it and what is the main risk associated
Acute hemorrhage into a nonfxnal adenoma. Leads to loss of ACTH, and thus cortisol, constituting and **EMERGENCY DROP IN _BP_**
56
What is usually the first clinical clue of Sheehan syndrome?
Lactation failure
57
What is the affect of SIADH on blood volume?
There is a euvolemic **_hypo_**natremia-- blood volume remains nearly normal
58
From what embryological components do the anterior and posterior pituitary originate from?
_Anterior_- Rathke pouch
_Posterior_- Neurohypophyseal bud
59
_Craniopharyngioma_
1. Pathology
2. Usual location
3. Key histo
4. Who gets it and how often does it recur
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)
60
Pathology of Rathke cleft cysts
Developmental failure of Rathke's pouch obliteration
61
Adrenal cortex derives from which embryological layer? Adrenal medulla?
AC: Mesoderm
AM: Neuroectoderm
62
Most common etiology of Cushing's syndrome?
Administration of exogenous glucocorticoids
63
Cushing's syndrome vs Dz
How often is the hypothalamus involved?
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)
64
Other than a Cushing's Dz causing Adenoma, what are the other endogenous causes of Cushing's syndrome (2)
1. Paraneoplastic Cushing syndrome (Ectopic ACTH, usually by SCC
2. Primary adrenal neoplasms (Causes ACTH independent Cushing Syndrome)
65
What are the top (2) primary causes of _hyperaldosteronism_ (i.e. causes unrelated to the RAA system)
1. **Bilateral idiopathic hyperaldosteronism**: Bilateral nodular hyperplasia of adrenal glands (most common)
2. **Adrenocortical Neoplasms**: aldosterone producing adenoma (_Conn syndrome_)
66
Clinical manifestations of Hyperaldosteronism
1. HTN w/ longterm CV issues
2. Hypokalemia w/ possible neuromuscular manifestations
67
Congenital Adrenal Hyperplasia (CAH)
1. Heredity
2. Pathology
3. Clinical features
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
68
Addison's disease
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
69
Value for a normal blood sugar
70-120 mg/dl
70
DM diagnostic criteria (4)
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
71
Pre-DM criteria (3)
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
72
Role of Adipose cells in T2DM
Adipose cells normally secrete _Adipokines_ which aid in maintaining insulin sensitivity. Obese patients actually have dec. adipokine secretion leading to dec. insulin sensitivity
73
Describe the histological expectation for T2DM
Unlike T1DM, you don't expect inflammation/ infiltrate (insulinitis), but you can often have **_amylin_** which ican replace some B-cells.
74
Although you aren't worried about DKA, what complication of hyperglycemia are you concerned about with T2DM? Describe it.
Prototypical patient
_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
75
The (3) major pathways of _Glucotoxicity_ in DM complications
1. Formation of Advanced Glycation End products (AGEs) -- permanent formations of glycosylation products
2. Modification of protein C activity
3. Inc. intracellular glucose
76
What form does glycosylation take prior to AGE formation?
Schiff bases are what is first produced. These are initial glycosylation products which are labile and can dissociate.
77
What process does AGE formation spark?
A sequlae leading to atherosclerosis, thickened BM and microangiopathy
78
Relationship between hyperglycemia and protein kinase C. What specfically happens?
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.
79
Affect of high intracellular glucose on eye and nerves
Can lead to inc. osmotic intake of water in the eye and subsequent lens swelling and also intracellular oxidative stress (leading to peripheral neuropathy)
80
Wipple's Triad
Sx associated with _Insulinoma_
1. CNS sx associated with hypoglycemia
2. Glucose \<50 mg/dl at measurement
3. Sx resolve with feeding/glucose
81
Tx of Primary Adrenal Insufficiency
Secondary?
**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
82
CAH Tx
_Hydrocortisone_ and (if necessary) _Fludrocortisone_
83
What do you screen amniotic fluid for, in regards to CAH?
17-hydroxypregnenolone
| (a precursor of cortisol)
84
What is the in-utero tx for females with CYP21 mutation?
Dexamethasone (able to cross placenta and feedback to block pituitary secretion of ACTH, thus preventing virilization
85
DOC for Rheumatoid Disorders
Prednisolone
86
What drug can be given to treat infant respiratory distress syndrome? Which drug can't be used and why?
**_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
Tx for **cerebral edema** (from brain tumors, meningitis, radiation, or high altitude)
Dexamethasone
88
_Mitotane_
1. MOA
2. Indication
3. Affect
4. Contraindication
5. What drug must be given with it (or soon after)?
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
Mifepristone indication and MOA
_Indication_: Tx of refractory Cushing's Syndrome
_MOA_: Glucocorticoid Receptor (GR) **Antagonist**
90
What age is affected by adrenal carcinoma (all be it rarely)?
What inherited syndromes are associated with this rare cancer?
Any age
Li-fraumeni syndrome and Beckwith Wiedemann syndrome
91
Describe pheochromocytoma
A neoplasm arising from neuroendocrine cells (**chromaffin cells**) in the paraganglion system (collection of adrenal medulla -like chromafin cells throughout the body).
92
Name and describe the key rule associated with _Pheochromocytomas_
_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
What are the (6) genes potentially associated with the familial version of pheochromocytoma
1. _RET_ gene (MEN II and III)
2. _NF1_ (Type 1 neurofibromatosis)
3. _VHL_
4. Succinate dehydrogenase genes (_SDHB_, _SDHC_, and _SDHD_)
94
Dx of Pheochromocytoma
Urinary elevation of _metanephrine_ and _VMA_
95
_Neuroblastoma_
1. Macro:
2. Micro:
3. Key clinical features (age and presentation)
1. Macro: Large bulky tumor
2. Micro: Homer-wright rossettes or sheets
3. Common childhood neoplasm, often present as large abdominal mass
96
_Multiple Endocrine Neoplasia Syndromes_
What is it?
Name the (5) main characteristics.
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
**_MEN1_**
1. Inheritance
2. Gene affected
3. Name the main organs involved and describe their involvement
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
_MEN2_ (general)
1. Inheritance
2. Key mutation
1. Auto. Dom.
2. Mutation in RET protoncogene (10q11.2)
99
MEN2A vs MEN2B
_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
Prophylactic tx for relatives of ppl with MEN2
They should get genetic testing for RET, and if positive, have a prophylactic thyroidectomy
101
Most common location for an intramural obstruction
Ureteropelvic jxn
102
Metabolic Syndrome
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
Criteria for screening for DM (3)
1. BMI \> 25 w/ 1+ risk factor, **or**
2. 45 y/o with no risk factor, **or**
3. BP\>135/80
104
What (3) exams/screens do DM patients need annually?
What are the tx targets for DM?
1. Pt's require annual retinal exam, microalbuminuria screening, and foot exam
2. _Targets_: A1C
105
Spironolactone MOA
(3) key side effects
1. Androgen-R competitive inhibitor and Aldosterone-R inhibitor
2. SE: GI hemorrhage, aGranulocytosis and Gynecomastia
106
Main bug associated with acute mastitis
Staph aureus (Associated with breast feeding)
107
1. Most common change in the premenopausal breast. What are the (2) types?
2. Presentation?
3. Histo?
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
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
1. No inc. risk (despite metaplasia)
2. 2x risk
3. 5x risk
109
_Intraductal Papilloma_
1. What is it?
2. What characterizes it?
3. How does it present?
4. What must it be distinguished from?
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
_Fibroadenoma_
1. How common and in who?
2. Presentation
3. Relationship to estrogen
4. Prognosis
5. How does histo look?
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
_Phyllodes tumors_
1. Which component is overgrown?
2. Common in what population?
3. Malignant potential?
1. Overgrowth of fibrous component
2. Common in post-menopausal women
3. Sometimes malignant
LOOKS LIKE LEAF
112
Risk factors for Breast cancer are mostly related to...
_Estrogen exposure_
+ Obesity and atypical hyperplasia
113
What are the general classifications of Breast Carcinoma (4)
_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
_Ductal Carcinoma In-situ_
1. What is it?/Dx
2. What dz is related to it?
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
_Invasive Ductal Carcinoma_
1. How common?
2. Presentation
3. What does biopsy show?
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
Although there is some controversy, when do all experts agree women need to be getting mammographies?
Biennially (every 2y, from ages **55-74 y/o**
117
_Inflammatory carcinoma_
1. What umbrella of breast CA is this under
2. Characterized by what?
3. Prognosis
1. Invasive Ductal Carcinoma
2. Characterized by carcinoma in the dermal lymphatics (and thus, peu d'orange)
3. Poor prognosis
118
_Lobular Carcinoma In Situ_ (LCIS)
1. Presentation
2. Characterization
3. Tx
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
How does _Invasive lobular carcinoma_ characteristically grow?
A single-file pattern due to the loss of E-cadherin
120
What type of gene is HER2/neu? (tumor suppressor or protooncogene)
Protooncogene (it is a gene amplifier)
121
After breast conserving surgery is performed to tx breast CA, what is the next tx step?
Radiation therapy (daily x 6w)
122
Chemo drugs that can be used for tx of Breast CA. What are potential risks (2 main ones)
**_C_**yclophosphamide, **_H_**erceptin (trastuzmab), **_A_**driamycin, **_T_**axanes
(**_CHAT_**ing w/ Breast CA patients)
123
Curing tx for metastatic Breast CA
It is **_incurable._** 2y survival
124
BRCA1 vs BRCA2
1: ch 17, breast and ovary
2: ch. 13, male breast
125
Most common subtype for male breast CA. Presentation?
_Invasive ductal carcinoma_
Presents as subareolar mass in older males.
126
Gynecomastia and male breast CA
It is _NOT_ a risk factor for male breast CA
127
Stage of fracture healing
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
Osteoporosis and mineralization
In osteoporosis there is a dec. in trabecular _bone mass,_ despite normal **bone mineralization**
129
Type I vs Type 2 primary osteoporosis
T1: **Postmenopause** (due to dec. estrogen and subsequent inc. in RANK/RANKL)
T2: **Senile** (age-related calcium deficiency)
130
What Bone densitometry levels correlate with...
1. Normal
2. Osteopenia
3. Osteoporosis
1. _normal_:
2. _osteopenia_: 1-2.5 SD below young adult mean
3. _osteoporosis_ \>2.5 SD below young adult mean
131
_Osteoporosis Tx_ (6)
**BEERR C**up
1. Bisphosphonates
2. Excercise
3. Estrogen replacement
4. Recombinant PTH
5. RANK-L inhibitor (denosumab)
6. Calcium/Vit D
132
Rickets vs Osteomalacia
1. Patient demos
2. Etiology
3. Pathophys
4. Sx
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
The presence of dissecting osteitis is a sign of what dz process? What is another name for this sign?
The presence of hyperparathyroidism. Also known as railroad tracks. The osteoclasts are cutting through the trabeculue
134
Brown Tumors
Lytic lesions (in the setting of excess osteoclast activitiy) that cause hyperparathyroidism.
135
Von Recklinghausen Dz of the Bone
**Osteitis Fibrosa Cystica**
The bone is replaced w/ fibrous tissue and cystic change
136
_Paget's Dz_
1. Path
2. Etiology
3. Dx
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
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?
1. **Osteolytic** (osteoclasts)
2. **Osteolytic-osteoblastic** (mixed)
3. **Osteosclerotic** (osteoblasts)
Cement lines = osteosclerotic
138
_Paget's Dz_
Presentation
**SAM P**ees **I**n **B**ushes
1. **_S_**kull thickening (leonitiasis ossea)
2. **_A**_xial skeleton, _**A_**rthritis
3. **_M_**id-adulthood
4. **_P**_ain, _**P**_roximal femur, _**P_**latybasia (skull base flattening impinging on foramen magnum)
5. **_I_**ncidental finding
6. **_B_**owing of tibia
139
_Paget's Dz_
Potential consequences and Tx
_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
Which type of OI is autosomal dominant? recessive?
Which type is lethal? not lethal, but severely deforming?
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
_Achondroplasia_
1. What is the defect?
2. Inheritance
3. Presentation
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
Osteonecrosis?
What are some predisposing factors to osteonecrosis of the jaw?
Ischemic bone death.
In the jaw, dental disease, dental damage, oral trauma, chemo/corticosteroids all play a role.
(high dose IV bisphosonates)
143
_Osteoma_
1. What is it?
2. Prognosis?
3. Age
4. Assc. with what syndrome?
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
_Osteioid osteoma_
1. Age
2. Where in the bone does it appear
3. Presentation
4. Tx
1. 2. Cortex of long bone
3. Presents as bone pain that resolves w/ aspirion
4. Tx w/ excision
145
_Osteosarcoma_
1. Incidence
2. Tumor presentation
3. Sx (including location and age at presentation)
4. Dx
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
Describe the (3) grades of **Osteosarcoma**
1. _Low_: **Parosteal Osteosarcoma**
2. _Intermediate_: **Periosteal Osteosarcoma**
3. _High_: **Conventional Osteosarcoma (osteoblastic)**
As grades inc., so does sunburst pattern, atypia, and disorganization
147
_Osteochondroma_
Describe the disorder, _osteochondromatosis_
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
_Chondrosarcoma_
1. Sx/presentation
2. Prognosis/ Grading
3. Tx
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
_Ewing/PNET_
1. What is it?
2. Key translocation
3. View on X-ray
4. Histo
5. Sx
6. Ddx
7. Tx
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
_Benign Fibrosseous Lesions_
1. What is it
2. Are cases usually monostotic or polyostotic?
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
_McCune-Albright Syndrome_
1. What is the triad of sx
2. What gene mutation is it assc. with?
1. (1) Polyostotic fibrous dysplasia + (2) endocrinopathies (ex precocious puberty) + (3) cafe-au-lait skin pigmentation
2. GNAS gene mutation
152
_Giant Cell Tumor of Bone_
1. Describe this tumor
2. Presentation
3. DDx
4. Dx
5. Prognosis/ recurrence
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
Other than TSH receptors, what else lines thyroid follicles?
Parafollicular or "C" cells, which secrete **Calcitonin**
154
What are the (4) main thyroid hormone fxns?
1. Stimulation of protein synthesis
2. Upregulation of carb and lipid catabolism
3. Inc. metabolic rate
4. Brain development for fetus/ neonate
155
_Thyroid storm_
**MEDICAL EMERGENCY**
And abrupt onset of hyperthyroidism, usuallly in patient w/ hx of graves during infxn, surgery
156
Interpret the following radioactive iodine uptake results:
1. diffuse
2. localized
3. reduced
1. diffuse = graves
2. localized = toxic adenoma
3. reduced = thyroiditis
157
_Cretinism_ vs _Myxedema_
_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
Which thyroiditis types cause pain? Are painless?
_Pain_:
1. Infx thyoiditis
2. Subacute granulomatous thyroiditis (De Quervain thryoiditis)
_No Pain_
1. Reidel's thyroiditis
2. Hashimoto's thyroiditis
159
Key antibodies associated with Hashimoto's dz
**Thyroglobulin and Thyroid Peroxidase (TPO)!!!,** TSH receptor, or iodine receptor
160
_Hashimoto's Thyroiditis_
1. Gross?
2. On Histo?
3. Inc. risk for what type of cancer?
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
_Subacute/Granulomatous (De Quervain) Thyroiditis_
1. Age
2. Pathology
3. How common?
4. How is it resolved?
5. Key points about histo.
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
## Footnote
**VAIN, PAIN, VIRAL**
162
_Riedel thyroiditis_
Rare + extensive fibrosis involving thyroid and contiguous neck structures
163
Key triad for Graves dz
Key antibodies assc.
Hyperthyroidism (with goiter) + exopthalmos + pretibial myxedema
_Auto-Antibodies_: TSI, TGI
164
_Multinodular Goiter_ evolves from what?
What is it called if there is a toxic, autonomous nodule?
Evolves from diffuse goiter. Some cells may become autonomous and continue proliferating.
Toxic + autonomous -- **Plummer's syndrome**
165
_Follicular Adenoma_
Where is this neoplasia? Common mutation association.
Key buzzword
How does it look on iodine scan?
Thyroid.
20% show mutation of RAS or PAX8-PPARG
Buzzword: Capsule
Usually cold on the scan
166
What is the most common type of thyroid CA? What etiology is it associated with?
Papillary carcinoma
Assc. w/ radiation exposure
167
Key nuclear features associated with Papillary carcinoma
What's key about histo of the follucular variant?
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
_Medullary Carcinoma_
1. Describe it
2. What does it secrete
3. Inheritance?
4. Tumor markers
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
What is key to histo for medullary carcinoma?
**Presence of Amyloid**
*"Amy played Medussa"*
170
_Anaplastic Carcinoma_
1. Path
2. Mortality
1. p53 inactivation or beta cetenin activation
2. Virtual 100% mortality
171
Thyroglossal duct/cyst
1. What is it?
2. Risk?
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
Main cell in the Parathyroid gland
Chief cell (also oxyphil cells)
173
What is the most common cause of clinically apparent hypercalcemia? Most common cause of incidental hypercalcemia?
_Apparent_: malignancy
_Incidental_: primary hyperparathyroidism
174
What are the possible types of parathyroid lesion (3) and how common is each?
1. parathyroid adenoma (85-95%)
2. hyperplasia (5-10%)
3. parathyroid carcinoma (1%)
175
Familial Hypocalciuric Hypercalcemia
Autosomal dominant mutation in parathyroid calcium-sensing receptor gene (CASR), ch.3q
176
What is the main difference between parathyroid hyperplasia and adenoma in terms of number of glands?
Adenoma is single gland enlargement; hypertrophy is mullti
177
Potential PTH Sx
"Painful bones, Renal Stones, Abdominal groans, and Psychic Moans"
178
_Metformin_
1. Key AE
2. Key contraindications (3)
1. _AE_: Lactic Acidosis
2. _Contra_: Hx of Renal Failure, MI, or CHF
179
_Sulfonylureas_
1. Key AE
2. Key Contraindications
1. _AE:_ Inc. Hypoglycemic risk
2. _Contra_: Renal/Liver disease
180
_Thiazolidinediones_
1. Key AEs
2. Key Contraindications
1. _AE_: Weight gain (sub q); fluid retention; inc. HF risk; inc. bone fracture in women
2. _Contra:_ Liver dz, CHF, CVD
181
_Ureteritis/ Cystitis Cystica_
1. What is it?
2. Histo?
3. Gross?
1. Metaplasia of urothelium
2. Gross: translucent, pearly-yellow cysts
3. Histo: von Brunn's nests (circular infiltrate w/ central degeneration)
182
_Non-bacterial Cystitis_
1. Who is affected
2. What is this dz associated with?
3. Sx?
4. Dx?
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
_Malakoplakia_
1. What is it?
2. Sx
3. Histo
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
_Leukoplakia_
1. Gross/ Path
2. Risk factor for what?
1. Gray-white areas of squamous metaplasia which are the result of long-term irritation or chronic infxn
2. Risk of SCC
185
_Bladder Cancer_
1. Sx (3)
2. What is the most common etiology
3. What is the primary pathology?
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
Tx for CIS-high grade bladder cancer
Intravesical immnotherapy (BCG); beyond that, must do cystectomy. Good prognosis (if low grade)
187
_Prostate Cancer_
1. What type of cancer is it usually?
2. What genetic changes increase susceptibility? (4)
3. Key biomarkers
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
_Prostate CA treatment_
If organ confined?
If advanced/metastasized?
1. Confined: radical prostatectomy or radiation
2. Advanced: Androgen deprivation
189
_Prostatic Intraepithelial neoplasia (PIN)_
1. What is it?
2. Relation to prostate CA?
1. Proliferation of neoplastic cells w/in large ducts
2. Very high assc. w/ prostate CA but not causative
190
Hypospadia vs Epispadia
_Hypo_: Urethral opening on the ventral surface
_Epi_ (get an epidural into your back): Urethral opening on the dorsal surface
191
Phimosis vs Paraphimosis
_Phimosis_- prepuce annot be retracted
_Paraphimosis_- forcible retraction of phimotic prepuce leading to damage
192
What is the cause of Molluscum Contagiousm?
Which cause is most prevalent? Which is sexually transmitted?
Caused by DNA poxvirus, (MCV)
MCV1 = most prevelant
MCV2= sexually transmitted
193
Risk factors for SCC of the penis (4)
1. Poor hygiene phimosis
2. Acumulation of smegma
3. Hx of genital warts
4. HPV types 16/18
194
Cryptorchidism is sometimes associated with what genetic defect?
Trisomy 13
195
For a pt with epidymitis, which bugs do you expect if he is...
\>35 y/o
\> 35 y/o: e. coli, pseudomonas
196
_Seminoma_
1. How common
2. Tx
3. Markers
4. When do they usually present?
1. Most common germ cell tumor
2. Extremely **radiosensitive**
3. bHCG
4. Presents at stage I
197
What neoplasia is a risk factor for Testicular Tumors?
Intratubular Germ Cell Neoplasia (ITGCN)
Large, atypical, fried-egg like cells
198
_Nonseminomatous tumors_
(general facts)
1. Aggression?
2. Presentation?
3. Tx?
1. Much more aggressive than seminomatous
2. Usually present at stage II/III
3. **_Radioresistant_** but 90% cure rate w/ aggressive chemo
199
90% of invasive testicular tumors have what chromosome defect?
Isochromosome of the short arm of chromosome 12
200
_Embryonal Carcinoma (male)_
1. Age
2. Gross
3. Histo
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
_Yolk sac tumor (male)_
Most common testicular tumor in who?
Infants up to 3Y
202
_Leydig Cell Tumor (male)_
1. How common?
2. Key micro finding?
3. What do they produce?
1. Most common sex-cord stromal tumor
2. _Histo_: Crystalloids of Reinke
3. Produce androgen so can lead to precocious puberty or gynecomastia
203
_Teratoma_ (male)
Benign or malignant?
ALWAYS MALIGNANT IN MALES!!!
204
Most common testicular neoplasm for men \>60?
Lymphoma (poor prognosis) -- and also the most common bilateral testicular tumor overall!
205
Which are more common in the testis? Mixed tumors or pure histologic types?
Mixed
