Title: USMLE Presentation: Pathology of Breasts and Hearts Monday
1USMLE PresentationPathology ofBreasts and
Hearts
- Monday, February 27th, 2006
- Jou Jou Hanna
2Breast Diseases
- A. Fibrocystic Disease
- B. Benign Tumors
- C. Malignant Tumors
- (Risk Factors)
3A. Fibrocystic Disease
- Presents normally with
- - diffuse breast pain
- - multiple lesions, often bilateral
- Four Histologic Types
- Fibrosis (stroma)
- Cystic (fluid)
- Sclerosing (? acini intralobular fibrosis)
- Epithelial Hyperplasia (? risk of carcinoma with
atypical cells)
4Mostly benign and common change within the
breast. May need mammogram or biopsy to rule out
other diseases
5Epithelial Hyperplasia
- Is there risk of carcinoma here?
- YES!!!!!
6B. Benign Tumors
- Fibroadenoma
- -most common tumor lt 25 y/o, usually seen in
pregnancy - -small, moble, firm mass
- -NOT a precursor to breast cancer
- Cystosarcoma Phy LL odes
- -Large, Leaflike projections
- Intraductal Papilloma
- -tumor of lactiferous ducts, presents with
nIpple discharge.
7- usually benign and typically stop growing after
only reaching a few centimeters in diameter
fibroadenomas are often left alone after they are
diagnosed. Even without treatment, approximately
10 fully recede each year .
8Which do you think is cystosarcoma phyllode,
which is intraductal papilloma?
9C. Malignant Tumors (carcinoma)
- Risk Factors?
- -Gender.so it would affect ME, more than Levi!
?
10Risk Factors cont
- Age
- Early 1st menarche (lt 12 y/o)
- Delayed 1st pregnancy (gt 30 y/o)
- Late menopause (gt 50 y/o)
- Fm Hx of 1st-degree relative with breast cancer
at a young age - Is risk ? or ? with fibroadenoma or
nonhyperplastic cysts??? - NOOOOO!!!! Risk is not increased.
11Malignant Tumors cont
- Common Postmenopause
- Arises from mammary duct epithelium or lobular
glands - Overexpression of estrogen/progesterone receptors
or erb-B2 (HER-2, an EGF receptor) - Women have 2 Breasts
12Malignant Tumors cont
- Histologic Types
- Ductal Carcinoma In Situ (DCIS)
- Invasive ductal (MOST COMMON)
- Comedocarcinoma
- Inflammatory
- Invasive lobular
- Medullary
- Pagets Disease of the Breast
- (eczematous patches on nipple,
- not common, usually unilateral)
13II. Cardiovascular Pathology
- A. Hypertension
- B. Arteriosclerosis
- C. Ischemic Heart Disease
- D. Infarcts red vs. pale
14II. Cardiovascular Pathology
- A. Hypertension
- 1. Definition - high blood pressure with
guidelines of gt 140 mmHg systolic gt 90 mmHg
diastolic - Normal??
- lt 120 lt 80 mmHg
- Prehypertensive??
- 120-139/80-89 mmHg
15II. Cardiovascular Pathology
- 2. Risk Factors
- ? age, diabetes, smoking, genetics,
- gt gt
- Blacks gt White
gt Asians
16II. Cardiovascular Pathology
- A. Hypertension
- 3. Features
- 90 of HTN is primary - ? CO or ? TPR
- 10 of HTN is secondary - due to renal disease
- Predisposes to Atherosclerosis, stroke, CHF,
renal failure, retinopathy, and aortic dissection - Malignant HTN is severe, rapidly progresses,
- and causes fibrinoid necrosis
- of small arteries
- ?
17II. Cardiovascular Pathology
- B. Arteriosclerosis ( 3 types)
- 1.) Monckeberg usually benign, calcification
of only the Media in the arteries - esp radial or ulnar
18II. Cardiovascular Pathology
- 2.) Arteriolosclerosis
- Hyaline thickening of small arteries in essential
(primary) HTN - Hyperplastic onion skinning in malignant HTN
- 3.) Atherosclerosis
- - Thickening and hardening of arteries, that
usually affects the intima of large and
medium-sized arteries
19II. Cardiovascular Pathology
- 3. Atherosclerosis cont
- Risk Factors smoking, HTN, diabetes mellitus,
hyperlipidemia, Fm Hx - Progression
-
- ? Proliferative ?
- Plaque
- Fatty Streaks
? Atheroma - Think of your blood vessels as pipes carrying
essential water to your house. The walls of the
pipes over time may become rusty, eventually
leading to the pipe becoming blocked and your
water supply being cut offie eventually the
Atheroma!!
20II. Cardiovascular Pathology
- 3. Atherosclerosis cont
- Symptoms Doesn't produce symptoms
- until the artery is severely restricted
- or obstructed.
- Chest pain, Leg cramps
- Complications Aneurysms, ischemia, thrombus,
emboli, peripheral vascular disease, and infarcts - Location Abdominal Aorta gt Coronary artery gt
Popliteal artery gt Carotid artery (A. C. P. C.)
21II. Cardiovascular Pathology
- C. Ischemic Heart Disease Manifestations
- 1. Angina (CAD narrowing gt 75)
- a.) Stable mostly 2º to atherosclerosis,
episodic retrosternal chest pain with exertion - b.) Unstable thrombosis but no necrosis,
- worsening chest pain, ie. increase in
- frequency (crescendo)
- c.) Prinzsmetals Variant Prinzes are Prissy
- so lazy, even occurs at rest!
22II. Cardiovascular Pathology
- C. Ischemic Heart Disease Manifestations
- 2. Chronic IHD (progressive onset of CHF over
many years due to myocardial damage) - 3. Myocardial Infarction (most often acute
thrombosis due to coronary artery
atherosclerosis) - 4. Sudden Cardiac Death ( death within 1 hour of
onset of symptoms, most commonly due to lethal
arrhythmia)
23II. Cardiovascular Pathology
- D. Infarcts
- Red vs. Pale
- -Color red is seductive - Pale
is a Prude therefore - So, more loose (tissues)
keeps things tight solid - with collaterals
(tissues), ie. those w/Single Blood supply - - Lungs, Liver, Intestines
- Brain, Heart, Kidney, Spleen -
REd REperfusion
24III Evolution of MI
- A. Time Frame Histologic Picture
- B. Diagnosis
- C. Complications
25III Evolution of MI
26III Evolution of MI
Hey, I want to hear a Bandcontraction band
that is!
- Such a long line to
- get intook 4 hours
- before he saw the
- BANDand then he EMIGRATED in!
- ?
- Mr. neutroPHIL
27III Evolution of MI
- Concert lasted 2-4 days.really Woodstock!
- Finally within that time, the rest of his family,
- The Neutrophils were extensively infiltrated
- extensive Coagulative Necrosis
28III Evolution of MI
29III Evolution of MI
- Now 5-10 days after the band concert, and its
time to clean up! - Police Macrophages
- were tired of the Neutrophils
- hangin around, so they attacked!
- (phagocytosis)
30III Evolution of MI
- 7 10 weeks have gone by
- Neutrophils were so badly beaten up by the
police Macrophageshad a lot of SCARS and
Fibrosis
31III Evolution of MI
- B. Diagnosis of MI
- What is the Gold Standard??
- EKG in the 1st 6 hours
- - ST Elevation (Transmural Infarct)
- Vs.
- - ST Depression (SubenDocardial Infarct)
- Cardiac Troponin I rises after 4 hours is
elevated for 7-10 dys - CK-MB is test of choice in 1st 24 hours post-MI
- LDH1 (former test of choice)
- AST are Asses b/c it is nonspecific, so not
helpful b/c can be found in cardiac, liver,
skeletal muscle cells.
32III Evolution of MI
- C. MI Complications
- Cardiac Arrythmias
- LV failure Pulmonary Edema
- Thromboembolism
- Cardiogenic Shock
- Rupture of Ventricular free wall, papillary mm,
interventricular septum, cardiac tamponade - Fibrinous Pericarditis friction rub
- Dresslers Syndrome autoimmune resulting in
Fibrinous Percarditis
33IV Cardiomyopathies
- A. Dilated
- -Large, globulated
- -Most common (90)
- -Systolic Dysfunction
- -Etiologies
- Alcohol abuse Looks like a
- Beriberi Balloon on Chest X-ray
- C? Coxsackie, Chronic Cocaine, Chagas ?
- Doxorubicin toxicity
- pEripartum
- Hemochromatosis
34IV Cardiomyopathies
- B. Hypertrophic
- -LV walls are thickened
- -Often Asymmetric involves
- intraventricular septum ?
- -50 familial A.Dominant
- - Hyper High Jump therefore,
- cause of sudden death in athletes
- -Diastolic Dysfunction
-
- Chamber becomes
- Banana Shaped on Echo ?
35IV Cardiomyopathies
- C. Restrictive/obliterative
- -heart is restricted in its ability to contract
because the inner lining of the heart becomes
stiff - -does not expand properly when filling
- -Major Causes Restrictive APE²S
- Amyloidosis
- Postradiation fibrosis
- Endocardial fibroelastosis
- Endomyocardial fibrosis (Lofflers)
- Sarcoidosis
-
36IV Cardiomyopathies
- A. Dilated - fundamental defect is INEFFECTIVE
CONTRACTION (smaller ejection fractions) - B. Hypertrophic - fundamental defect is
INABILITY to FILL a hypertrophic LV during
DIASTOLE. Ejection is forceful here, but
ineffective b/c amt. of blood is ?. - C. Restrictive fundamental defect is a STIFF
Inelastic ventricle that can be filled ONLY with
GREAT EFFORT
37Practice Questions
- 1.) 52 y/o woman noticed a lump in her left
breast 3 months ago, after extensive work-up
decides to undergo surgery. A surgical specimen
is sent to a pathologist. Their report states,
small, glandular structures, lined by poorly
differentiated cells. Based on the hx, path
report, and incidence of different types of
breast cancers, which is the following carcinomas
does this px most likely have? - Colloid (mucous)
- Invasive ductal
- Invasive lobular
- Medullary
- Metastatic bronchogenic
38Practice Questions
- Answer
- B. Invasive Ductal Carcinoma
- Its the most common 75-80
- Develops from epithelial cells of the terminal
duct - Histo presentation is same
- Most common mode of presentation is a palpable
mass in the breast
39Practice Questions
- 2.) 17 y/o MALE develops a painless, firm mass
beneath the nipple of his left breast. Right
breast is normal upon examination. Which of the
following is conditions does this mass most
likely represent? - Fibrocystic changes
- Gynecomastia
- Intraductal papilloma
- Invasive duct carcinoma
- Invasive lobular carcinoma
40Practice Questions
- Answer
- B. Gynecomastia
- Most common breast mass in men, esp. under 25
yrs/o - Benign proliferation of ductal stromal elements
of the breast - Generally idiopathic, may be due to hormonal
changes
41Practice Questions
- 3.) 53 y/o man complains of progressive weakness
and inability to exercise. Its been getting
worse over the last 2 years. He also notes his
ankles have been getting bigger. He DENIES any
episodes of chest pain, arm pain, or jaw pain
either at rest or when exercising. Hes not
diabetic, but admits to having high cholesterol.
What is the most likely etiology of his
progressive symptoms? - Chronic Ischemic Heart Disease
- Myocardial Infarction
- Prinzmetal Angina
- Stable Angina
- Unstable Angina
42Practice Questions
- Answer
- A. Chronic Ischemic Heart Disease
- Atherosclerosis of coronary arteries is the
underlying pathologic change in the majority of
ischemic heart disease - States that it is progressive
43THE END!!!!
- Thank you very much
- Any questions?????