Pbd - Week 12

Front 1

If a person had intestinal type carcinoma of the intestine what would you expect to see on endoscopy?

What would be your Ddx? (3)

Back 1

- nodules/masses, but often just deeply penetrating gastric ulcers
* need +++ biopsies to r/o peptic ulcers!

Ddx: gastritis, peptic ulcers, pancreatitis

Front 2

What type of gastric CA has no known etiology/predisposers other than genetics?

What is the germline mutation that causes this?

Back 2

Diffuse type gastric CA

E-Cadherin (most will get a prophylactic gastritis even though not everyone with mutation gets CA)

Front 3

How is gastric CA prevented?(2)

Tx for early and late?

Overall prognosis?

Back 3

Eradication of H.pylori and diet

Tx: Early - resect lesions, Late - gastrectomy +- chemo/rad

Prognosis: POOR! 5yr < 15%

Front 4

What 2 Xtics are used to classify/divide colorectal CA's?

Back 4

DIvided by:
architecture - villous, tubular, tub-villo (villous is a villain!)
Grade - degree of differentiation, well = low grade

Front 5

What is the gene involved and the pathogenesis for FAP?

Tx?

Back 5

Gene = APC (a tumor suppressor gene!)

Pgen = get development of 100's of adenomatous polyps and there is +++ risk that one will become a malignancy

Tx: prophylactice colectomy

Front 6

What is the gene involved in HNPCC?

Where do these polyps occur? What do the cells look like (2)

Prognosis?

Back 6

DNA mismatch repair gene

R-sided lesions
Cells are mucinous and high grade

NOT aggressive, this may be d/t the +++ inflammatory response associated with this tumor.

Front 7

Apart from HNPCC and FAP, what is another genetic cause of colorectal CA?

What type of polyp is seen with this defect?

Back 7

Methylation of CPG islands causing silencing of tumor suppressor genes.

Causes serrated adenoma's that can change to carcinoma's w/o developing nuclear atypia

Front 8

Though they look similar, neuroendocrine tumors of the gut behave differently depending on their location.

Which location tends to be locally invasive but benign?(2)

Which tends to metastasize to the liver?(3)

Back 8

Locally invasive but benign: Appendix and rectum

Mets to liver: ileum, colon, stomach

Front 9

There are numerous genes associated with prostate CA, and a strong family Hx increases the risk of a younger presentation.
That said, what is one of the postulated genetic mechanisms of the disease?

Back 9

Hypermethylation of glutathione-S-transferase gene, seen in >90% of the CA's. This gene plays a role in preventing damage from several carcinogens

Front 10

What, apart from CA, are 4 potential causes of increase PSA?

What are the CA and Non-CA ranges for PSA?

Back 10

- recent ejaculation
- prostatitis
- BPH
- recent instrumentation

** there is considerable overlap between CA and Non-CA levels **
PSA > 8 = CA
PSA < 4 = probably benign
PSA 4-8 = ???

Front 11

Define the following:
- PSA density
- PSA velocity
- Free:bound PSA (significance of F vs B?)

Back 11

PSA density: ratio of [PSA] to size of prostate

PSA velocity: change in [PSA] / time

Free:Bound --> the % of free PSA is lower in CA, so if ratio <10% ?CA
>25% free likely benign (high free means you're CA free!)

Front 12

When is measuring PSA actually of value?

Back 12

Serial PSA measurements are of great value in assessing response to therapy
E.g. rising PSA after radical prostatectomy is indicative of residula or met disease

Front 13

What is the precursor lesion to prostate CA?
Type of architecture? (2) Cell feature?
How is this managed?

Back 13

High grade Prostatic Intraepithelial Neoplasia (PIN)
Complex papillary proliferations, glands surrounded by a 2-cell layer of basal cells (1 cell layer in CA)
Nuclear atypia present
= dysplastic but NOT invasive, pt will need serial biopsies

Front 14

In what 4 ways does prostate CA spread, and to where?

Back 14

1. Local extension to seminal vesicles and base of bladder
2. hematogenous spread primarily to bones of axial skeleton
3. Lymphatics to regional nodes
4. perineural

Front 15

What is Thelarche?

Back 15

Thelarche = sustained period of mammary gland growth in adolescent girls. Abberations in mammary development include extra nipples and breast tissue

Front 16

Lymphatic drainage of the breasts is to where?

Back 16

Lymphatic drainage of the breast is to ipsilateral axillary nodes

Front 17

What causes fibrocystic breast changes? How is it treated? What does it do to your breast CA risk?

Back 17

Fibrocystic Breast changes:
-caused by a normal, but exagerrated response to hormonal fluctuations
- Tx is hormone manipulations (e.g. the pill) to relieve symptoms. Sx only done to obtain definitive Dx
- NO increase in CA risk!

Front 18

Describe the histological changes seen in Proliferative breast changes
- w/o atypia
- w/atypia
What is there respective impacts on breast CA risk?

Back 18

W/o atypia - normal ductal Hplasia (risk 1.5-2x higher)
w/atypia - atypiccal ductal and lobular Hplasia (risk 5x higher)

Front 19

Phyllodes Tumor (benign form) of the breast is similar to fibroadenoma but has what 3 things? *hint*

Back 19

Phyllodes tumor:
- increasing cellular prolif
- atypia in the stroma
- glandular overgrowth

Hint 19

increasing ____
____ in stroma
_______ __growth

Front 20

A fully malignant Phyllodes tumor is what type of cancer? What is it composed of?

Back 20

A fully malignant Phyllodes tumor is a sarcoma and is composed of stromal tissue only

Front 21

What are the 2 pathological risk factors for breast CA?
For the second one list 2 histological features (no..... & intact.....)
What is the # for increased risk?

Back 21

1. Proliferative breast disease +- atypia
2. Preinvasive (in-situ) disease
- Ductal CIS or Lobular CIS
- no evidence of invasion and Myoepithelial layer remains intact
10x increased risk!

Front 22

What does Paget's disease of the nipple look like?
Histological apperance? (just read the answer!)

Back 22

Paget's disease: crusted, red, eczematous lesion

Hito = malignant glandular epithelium w/in squamous epidermins

Front 23

What is Paget's disease of the nipple invariably associate with? (2)

Back 23

Invariable associated with Ductal CIS or breast CA
- malignant cells have extended up terminal lactif ducts to the surface of the nipple

Front 24

A malignant breast lesion will have what 3 features on mammogram.
What are 2 other features that will be seen in the mammogram of a malignancy?

Back 24

solid
poorly circumscribed
irregular, spiculated borders

invasion & distortion of surrounding tissues
calcifications

Front 25

What is HER2-neu? What does it do/regulate in the cell?

What type of mutation in this gene is seen in 10-30% of ovarian and breast CA's?

What is the implication for Tx?
(ie what drug do we have and how does drug work?)

Back 25

A transmembrane tyrosine-kinase receptor. Controls cellular proliferation, motility and survival

Mutation: amplification or overexpression

Now have monoclonal Ab to HER2-neu receptor = Herceptin. Drug increases overall disease-free survival

Front 26

What are 4 causes of Cushing's Syndrome?

Back 26

Cushing's Syndrome = ↑ [cortisol]
1. Pituitary adenoma (aka Cushing's disease) that secretes ACTH.... will cause bilateral cortical Hplasia
2. Adrenal cortex neoplasms - usually benign the high cortisol causes adjacent & contralateral atrophy by suppressing ACTH from the pituitary
3. Ectopic ACTH - lung mass, causes more Hplasia that pituitary adenoma
4. Iatrogenic

Front 27

What are 2 causes of Conn's Syndrome?

Back 27

1. Benign Adenoma
2. Hyperplasia of the Zona Glomerulosa

Front 28

What ALWAYS causes increase sex steroids in adults?

Back 28

Adrenal Cortical Carcinomas!!

Front 29

What are the 5 clinical features of Addison's?

Back 29

1. fatigue/weakness
2. HoNa+
3. Hyper K+
4. low [glucose]
5. Hyperpigmentation

** risk of going into shock if stressed b/c can't compensate with cortisol

Front 30

What are the 2 main causes of Addison's?

Back 30

1. Autoimmune (Ab's to enzymes or ACTH)
2. Infectious (TB, fungal)

Front 31

Why is it important to distinguish between the 2 possible causes of primary hyperparathyroid?

Back 31

It is important b/c this distinction will determine the extent of the PTH-ectomy that needs to be preformed.
Adenoma = 1 PTH gland out
Hplasia = 3.5 glands out

Front 32

What are the 4 possible causes of PID?

Back 32

Gonorrhea
Chlamydia
Trichomonas
Bacterial Vaginitis

Front 33

For what 3 STI's must you also Tx partners? (2 vaginitis causers and 1 cervicitis)

Back 33

Gonorrhea, Chlamydia (cervical)
Trichomonal (vaginal)

Front 34

What are 2 examples of STI's that you would only Tx if the person was symptomatic?

Back 34

- Yeast & Bacterial Vaginitis

Front 35

Match the following things:
Microbial causes:
-HSV
- Treponema Pallidum
- Chlamydia Trachomatis
- Haemophilus Ducreyi

Pathology:
- Lympho-granuloma Venereum
- Chancroid
- Herpes
- primary syphillus

Back 35

- HSV --> Herpes

- Treponema Pallidum ---> primary syphillus

- Chlamydia Trachomatis ---> Lympho-granuloma Venereum

- Haemophilus Ducreyi ---> Chancroid

Front 36

Under what 4 conditions should you consider rare causes for genital ulcers?

Back 36

1. Travel
2. Systemic Disease
3. I-compromised (HIV +)
4. MSM

Front 37

Do ppl with herpes know they have it? When is it contagious?

Back 37

Most ppl (~60%) who have HSV don't know they have HSV

Contagious even when there are no lesions present (asymptomatic shedding)

** May have a vaccine in 5-10yrs **

Front 38

What is the Tx/management of HSV?

What are the implications for labour & delivery?

Back 38

No cure but anti-virals can decrease symptoms & shorten the course, if taken ongoing can decrease transmission to partners.

Does not necessitate a C-section, unless you have an active breakout at the time of delivery

Front 39

What are the 2 possible genetic causes of Renal cell CA?
* hint *

Back 39

Von Hippel Lindau
- this gene codes for a protein that controls the response to decrease O2 (ie increasing VEGF to increase vascularity). When mutated get +++ angiogenesis

MET - gene
- a proto-oncogene that controls a tyrosine Kinase receptor for H-cyte GFactor --> mutation = constant activation of receptor = increase proliferation, motility and invasion

Hint 39

Von Hippel Lindau

MET - gene

Front 40

75% of pt's with urothelial CA of the bladder have what type?

What are the imlications of this?
propensity to.....
risk that....

Back 40

Papillary, low grade, non-invasive

Propensity to develop new tumors

Risk that recurrences will be higher grade than original

Front 41

What are 2 ways of preventing urothelial CA of the bladder?

In what 3 ways are ppl with a Hx of this CA followed? (ie 3 tests)

Back 41

Tx schisto
don't smoke

Urine cytology, cystoscopy, biopsies

Front 42

What type of imaging is used to Dx prostate CA?

If a person has elevates PSA +- abnormal DRE, what imaging modality would you use to assess:
-local disease
- nodal disease
- mets?

Back 42

Trans-rectal USS to guide the needle for biopsy.

- local = MRI
- nodal = CT
- mets = bone scan

Front 43

What are 2 causes of cervicitis?

What are 3 causes of Vaginitis?

Back 43

Chlamydia & Gonorrhea

Bacterial vaginitis, trichomonas, yeast

Front 44

What causes urethritis (2)?

What are the 2 causes of epididymitis in men <35? >35?

Back 44

Gonorrhea & Chlamydia

< 35yrs = Chlamydia (40%), GH (20%)
> 35yrs = coliforms or pseudomonas

Front 45

What causes a strawberry cervix? How would you treat this?

For which STI would you give Penicillin IM?

Back 45

Trichomonas! Give 1 stat dose of Flagyl

Syphilis