renal, penis, balls, female reproductive Flashcards

1
Q

kidney functions
 Structure: filter %
 Excretes what waste?
 Regulates?
 Maintains what balance?
 Endocrine?

A

 Structurally complex - 0.4% of body weight, but filters 25% of blood through glomeruli
 Excretes nitrogenous waste products of metabolism - cleans the blood – turns 1.5 L into urine
 Regulates body water and electrolytes
 Maintains appropriate acid-base balance
 Endocrine organ – secretes hormones
 Renin – blood pressure
 Erythropoietin – proliferative effect on bone marrow to make RBCs

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2
Q

components of the nephron

A

 Glomeruli
 Convoluted tubules
 Collecting ducts

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3
Q

JGA controls? how/components?

A

BP
 Juxtaglomerular cells in wall of afferent arteriole: Sensor for blood pressure
 Macula densa in wall of distal convoluted tubule: Sensor for sodium

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4
Q

Azotemia – Laboratory Findings

A

 Elevation of blood urea nitrogen and creatinine levels

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5
Q

azotemia usually related to what?

A

 Usually related to reduced glomerular filtration rate (GFR)

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6
Q

azotemia can be associated with what disorders?

A

Associated with many primary renal disorders or May also be associated with extra-renal disorders

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7
Q

pre and post renal azotemia

A

 Pre-renal azotemia – hypoperfusion of the kidneys decreases GFR in the absence of parenchymal damage

 Post-renal azotemia – urine flow obstructed below the level of the kidney

both lead to azometia

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8
Q

Uremia – Clinical Findings

A

 Progression of azotemia to produce clinical manifestations and systemic
biochemical abnormalities

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9
Q

causes of uremia

A

failure of excretion or metabolic/endocrine alterations

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10
Q

gastric? nn? pericadium? skin?

uremia secondary involvment of organ systems

A

 Uremic gastroenteritis
 Peripheral neuropathy
 Uremic fibrinous pericarditis
 Uremic stomatitis

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11
Q

possible clinical manifestations of renal dx

A

nephritic
nephrotic
acute failure
chronic failure
UTI
nephrolithsatsis
UT obstructiuon
renal tumors

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12
Q

signs?

nephrotic syndrome

A

Glomerular syndrome
 A non-specific disorder in which the kidneys are damaged, causing them to leak large amounts of protein from the blood into the urine.
 Heavy proteinuria
 Hypoalbuminemia
 Severe edema
 Hyperlipidemia
 Lipiduria

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13
Q

nephritic syndrome
 onset?
 signs?

A

 Glomerular syndrome
 A non-specific disorder in which the kidneys are damaged, causing them to leak protein and red blood cells from the blood into the urine.
 Acute onset
 Grossly-visible hematuria
 Mild-to-moderate proteinuria
 Azotemia
 Edema
 Hypertension

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14
Q

 Glomerulonephritis
 tx?

A

an immune mediated disease of the renal glomeruli
 Treated with steroids

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15
Q

 Pyelonephritis
 Treated with?

A

an infection of the kidney (not the glomerulus) usually caused by bacteria and of retrograde origin
 Treated with antibiotics

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16
Q

Post-Streptococcal Glomerulonephritis
(Postinfectious Glomerulonephtitis)
 onset?
 Type of immune injury

A

 Acute onset of nephritic syndrome in 9-14 days following
Streptococcal infection
 Type III immune injury (Immune complex-mediated inflammation)

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17
Q

Pyelonephritis paths of infection

A

 Hematogenous dissemination – least common
 Ascending infection – most common
 Fecal bacteria from perineal area

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18
Q

tx?

how to test for polynephritis

A

Culture and sensitivity – Bactrim tx

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19
Q

Pyelonephritis is much ______ common than glomerulonephritis

A

Pyelonephritis is much more common than glomerulonephritis

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20
Q

Kidney Stones (Nephrolithiasis)
Urolithiasis
common? may cause?

A

 Common
 May cause obstruction

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21
Q

signs of nephrolithstasis
tx?

A

 Pain
 Hematuria
 Pyuria (pus in urine)
 Lithotripsy= sound waves to break up stones

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22
Q

those with kdney stones are prone to?

A

ascending infections

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23
Q

nephrolithstasis may be associated with?

A

 May be associated with hypercalcemia (for example,
hyperparathyroidism, metastatic skeletal disease, multiple myeloma

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24
Q

tx of kidney stones

A

Extracorporeal Shock
Wave Lithotripsy (ESWL)= break up to smaller pieces

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25
Q

Staghorn Calculus

A

large calculus deposit in the kidney

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26
Q

forms of nephrosclerosis

A

benign and malignant, both often due to hyperBP

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27
Q

malignant nephrosclerosis

A

CM junction is obstrucuted

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28
Q

simple renal cyst

A

common, benign
can be single or many

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29
Q

genetic dx of polycystic kidneys

A

Autosomal Dominant
Polycystic Renal Disease

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30
Q

where are the dialysis tubes

dialysis vessel complication

A

Dialysis Shunt - Arterio-Venous Fistula possible

both tubes in the vv

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31
Q

what changes can occur at kidneys due to dialysis

A

cystic changes

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32
Q

what can result from cystic chnages of the kidneys with dialysis

A

renal cell carcinoma

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33
Q

how can. this be done potentially

End Stage Renal Disease long term tx

A

End Stage Renal Disease - Transplant

can simply add adiitonal kidney-do not remove other two

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34
Q

what is a comoplication of trnasplant for renal failure

A

rejection, tx with immunosupressants

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35
Q

Renal Cell Carcinoma
 Arises from?
 Often present how?
 May grow into?

A

 Arises from renal tubular epithelium
 Often silent, non-specific S/S
 May grow into renal vein

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36
Q

infarcts and renal cell Ca

A

can lead to infarct such as adrenal gland

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37
Q

is metastisis common at kidney

A

no, but possible

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38
Q

Wilm’s Tumor
(Nephroblastoma)
 demo
 presentation
 sign
survival rate?

A

 Children under 5 years
 Abdominal mass
 Chronic low-grade fever
high survival rate (95%)

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39
Q

Wilm’s Tumor
(Nephroblastoma) histo

A

Histopathology consists of several cell
types, some of which resemble abortive
glomeruli and others that resemble skeletal muscle

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40
Q

Urothelial Carcinoma
 Arises from?
 most common site?
 sign?

A

 Arises from the urinary tract lining epithelium (transitional epithelium)
 Bladder most common site
 Painless hematuria

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41
Q

urothelial carcinoma risk factors

A

 Cigarette smoking, industrial solvents
(beta-naphthlylamine), chronic cystitis,
schistosomiasis, drugs (cyclophosphamide)

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42
Q

Urothelial Carcinoma Clinical significance depends on:

A

histologic grade, differentiation and depth of invasion

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43
Q

where else can urothelial Ca occur?

A

Renal Calyces
kidney

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44
Q

Prostate – Three Major Diseases

A

 Prostatitis
 Benign prostatic hyperplasia
 Adenocarcinoma of prostate

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45
Q

Prostate-Specific Antigen - PSA
 WNL ?
 Increased levels may suggest?
 Elevated in?
 Velocity of change?

A

 Protein present in the serum at low levels (nl: < 4 ng/mL)
 Increased levels may suggest the presence of prostate cancer
 Elevated in prostatitis
 Velocity of change significant

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46
Q

PSA physio functions

A

 Liquefy semen, allowing sperm to swim freely
 Dissolution of cervical mucous cap

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47
Q

Prostatitis
tx?

A

 Acute bacterial disease treated with antibiotics

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48
Q

Nodular (Benign)
Prostatic Hyperplasia - BPH can lead to?

A

 Obstruction to flow
 Urinary frequency
 Ascending infections

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49
Q

with BPH what should be ruled out

A

neoplasia

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50
Q

tx BPH

A

 Pharmacologic treatment
 Surgical treatment (TURP)

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51
Q

Adenocarcinoma of Prostate common?

A

 70% of men develop prostate cancer by 70-80 years of age

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52
Q

clnical behavior?

diagnosis of prostate adeno-Ca

A

 Digital rectal prostate examination
 Biopsy – multiple cores
 Wide variation in clinical behavior

53
Q

grading of prostate cancer scale name

A

 Gleason grading

54
Q

Metastatic Prostatic
Adenocarcinoma can go to?

A

the spine

55
Q

what lesion can be seen on xray with metastic prostate adeno-Ca

A

Osteoblastic Lesion

56
Q

Testes dx’s

A

 Cryptorchidism
 Seminoma
 Infections

57
Q

Cryptorchidism

A

Cryptorchidism
 Absence of one or both testes in the scrotum
 Failure of testis to descend from an abdominal position through the
inguinal canal into the scrotum (“undescended” testes)

58
Q

Cryptorchidism can lead to

A

 Infertility
 Increased risk for neoplasia

59
Q

Cryptorchidism tx

A

orchiopexy

60
Q

Seminoma
 common?
 demo?
 tx?
 treatable and curable?

A

 Most common germ cell tumor of testis
 Young adults (15-34 years)
 Surgery plus radiation therapy and chemotherapy
 One of the most treatable and curable cancers
 Over 95% long-term survival in early stages

61
Q

Infectious Parotitis
(Mumps) and testes

A

 Complications rare in the young and more common in older individuals
 Orchitis can occur

62
Q

Hypospadias

A

 Developmental defect of the urethra in the male
 Abnormally placed urethral meatus
 Urethral meatus opens on the glans penis most commonly (first degree hypospadias)

63
Q

Peyronie’s Disease

A

fibrous cord in the penis causing curve

64
Q

Phimosis

A

 Foreskin cannot be fully retracted from the head of the penis

65
Q

Priapism

A

 Erect penis or clitoris does not return to its flaccid state, despite the
absence of both physical and psychological stimulation, within
four hours
 Medical emergency
 Hematologic diseases are predesposition: Sickle cell disease and Leukemia
 Trauma

66
Q

Erythroplasia of Querat

A

decreased thickness of tissue at head causing ulceration (immature keratinocytes)

67
Q

can SCCa occur at penis

A

yes

68
Q

Uterine Leiomyoma
 B/M? tissue?
 May cause?

A

 Benign smooth muscle neoplasm= “Fibroids”
 May cause irregular bleeding (metrorrhagia) or Painful intercourse (dyspareunia)

69
Q

what can these cause?

Proliferative Lesions of the endometrium

A

Endometrial Hyperplasia and Polyps
Glandular epithelium
Bleeding

70
Q

Two Major Diseases of the Endometrium

A

 Endometriosis
 Adenocarcinoma

71
Q

Endometriosis
 what/where?
 influenced by?
 sign?
 Symptoms depend on? worsen with?

A

 Endometrial tissue outside the uterine cavity
 Ectopic endometrial tissue influenced by hormonal changes
 Recurring pelvic pain
 Symptoms depend on the site involved and worsen with
the menstrual cycle

72
Q

endometriosis can cause what at ovaries

A

ovarian adhesions and choclate cysts

73
Q

Risk Factors for
Endometrial Carcinoma

A

 Age – most common in the 55 to 65 age group
 Obesity – greater synthesis of estrogen in body fat
 Infertility – women who are nulliparous are at increased risk of endometrial carcinoma

74
Q

Cervical
Squamous Cell Carcinoma detection

A

 Exfoliative cytologic screening for early detection
(Papanicolau smear)

75
Q

where does cervical SCCa occur?

A

 Squamo-columnar junction

76
Q

HPV and cervical cancer

A

 High risk HPV sub-types – 16, 18

77
Q

can cervical cancer be prevented

A

yes HPV vax

78
Q

Sequence of Events That
May Follow HPV Infection

A
79
Q

premalignant lesion of cervical cancer

A

Cervical Intraepithelial Neoplasia -
Grades I, II, III
 LSIL (low-grade squamous intraepithelial lesion)
 HSIL (high-grade squamous intraepithelial lesion)
depends on level of epithelial invasion

80
Q

Teratoma
 contains?
 Generally arise in?
 Most commonly seen in?
 app? – B/M? – may contain?

A

 A tumor containing tissues from all three germ layers (Most tumors are derived from one cell layer)
 Generally arise in gonadal tissues
 Most commonly seen in the ovary
 “Dermoid cyst” of the ovary – a benign cystic teratoma – may
contain a variety of tissues including hair, teeth, bone, cartillage,
thyroid, etc.

81
Q

ectopic pregnancy

A

fertilized egg embeds in the tube
potetnial for rupture and massive internal bleeding, must be removed

82
Q

pelvic inflam dx

A

usually inflammatory mass occrung in F tract that can obscure ovary/tubes

83
Q

Gonorrhea and PID
 microbe?
 can lead to?

A

 Neisseria gonorrhea
 “Mother nature’s birth control”
 causes Pelvic inflammatory disease
 can lead to Tubal scarring and Ectopic pregnancy (infertility)

84
Q

Neisseria Gonorrhea in males may cause?

A

Acute Epididymitis –

85
Q

Neisseria Gonorrheae in females can form?

A

Tubo-Ovarian Abscess

86
Q

Accessory Nipples

A

many forms

87
Q

Breast components?

A

 Glandular epithelium
 Ducts
 Lobules
 Interstitial tissue
 Lymphatics

88
Q

Lymphatic Drainage of Breast

A

mainly to axillary LN

89
Q

Physiologic Hyperplasia of Female Breast /
Breast Development

A

based on hormone levels, increased at puberty/preg and lactation

90
Q

Fibrocystic Changes of the breast

A

often occur at breasts and do present as masses but are benign, most common finding at breasts

91
Q

Gynecomastia
causes?
if bi/unilateral?

A

 Enlargement of male breast may occur in response to estrogen
 Hyperestrinism in male
Cirrhosis of liver – inability to metabolize estrogens
Klinefelter syndrome
Estrogen-secreting tumors
Estrogen therapy

 Bilateral – rule-out hormonal
 Unilateral – rule out tumor

92
Q

Fibroadenoma
 common? B/M?
 present as?
 demo?

A

 Most common benign neoplasm of breast
 Discrete, usually solitary, moveable nodule
 Young women (third decade)

93
Q

forms of malignant breast cancer

A

Lobules - lobular carcinoma
* Lobular carcinoma-in-situ
* Invasive lobular carcinoma

Ducts - ductal carcinoma
* Ductal carcinoma-in-situ
* Invasive ductal carcinoma

94
Q

Pathogenesis of Breast Cancer
 Genetic?
 Hormonal?
 Environmental?

A

 Genetic changes
 Hormonal influences
 Environmental variables

95
Q

Risk Factors in Breast Cancer
 Well-established risk factors

 Age?
 Genetics/genes?
 Menstrual history?
 Length of?
 Nulliparous?
 Geographic?

A

 Age – uncommon < 30 y
 Genetics and family history - p53, BRCA1/2 genes
 Menstrual history – early menarche (<12y), late menopause (>55y)
 Length of reproductive life
 Nulliparous – having children is protective
 Geographic variation

96
Q

other risk factors of breast cancer
 Exogenous?
 contrceptives?
 Ionizing radiation?

A

 Exogenous estrogens -postmenopausal hormone replacement therapy
 Oral contraceptives – newer formulations of balanced, low doses of estrogen and progestin safe
 Ionizing radiation during breast development

97
Q

 Less well-established risk factors of breast cancer

A

 Alcohol consumption
 High fat diet
 Obesity
 Cigarette smoking

98
Q

what is mutated?

 Familial syndromes and breast cancer

A

Li-Fraumeni Syndrome –germ-line mutations in p53
Cowden Syndrome –germ-line mutations in PTEN
Ataxia-telangiectasia gene – DNA repair genes
BRCA1/BRCA2 – germ-line
mutations

99
Q

HER2/NEU proto-oncogene
 normal function?
Amplified in?
Overexpression associated with?
Therapeutic intervention?

A

Epidermal growth factor
receptor
Amplified in 30% of breast
cancers
Overexpression associated with poor
prognosis
Therapeutic intervention –Herceptin (trastuzumab)

100
Q

amplifications of what genes can lead to breast cancer

A

Amplification of RAS and MYC
(proto-oncogenes)

101
Q

mutations to what genes can lead to breast cancer

A

Mutations of Rb and p53 (tumor suppressor genes)

102
Q

 Estrogen receptor positivity indicates what tx?

A

Therapeutic intervention -
Tamoxifen

103
Q

Hormonal Changes – Risk Factors for breast cancer

A

 Increased exposure to estrogen
Long duration of reproductive life (More estrogen)
Nulliparity – having children is protective
Late age at birth of first child

104
Q

estrogen effect on breast tissue

A

Estrogen exposure has a proliferative effect on breast tissue.
Proliferative breast disease found on biopsy indicates an exposure
to increased levels of estrogen. An increased risk of breast cancer
is found in women who have proliferative breast disease

105
Q

The more estrogen the breasts are exposed to over a lifetime, the ____ risk of cancer? when are these levels higher

A

The more estrogen the breasts are exposed to over a lifetime, the
higher the risk of breast cancer. During each monthly menstrual cycle, the breasts are exposed to increased estrogen levels, especially at the time of ovulation.

106
Q

early age of menses and late menopause effect for breast cancer?

A

 Both early age at the start of menstrual cycles (menarche) and
late menopause increase breast cancer risk through increased exposure to estrogen during more menstrual cycles.

107
Q

Late age for menarche and early age for menopause and breast cancer risk?

A

ate age for menarche and early age for menopause decrease
breast cancer risk through fewer menstrual cycles.

108
Q

Birth control pills and hormone replacement therapy _______
breast cancer risk
why?

A

Birth control pills and hormone replacement therapy increase
breast cancer risk through increased exposure to estrogen.

109
Q

Removal of both ovaries before natural menopause ______
breast cancer risk
why?

A

Removal of both ovaries before natural menopause decreases breast cancer risk by decreasing levels of estrogen.

110
Q

how can OH cause breast cancer?

A

Alcohol consumption. The more alcohol consumed, the more impaired the liver becomes in its ability to metabolize estrogen. Therefore, alcohol consumption increases breast cancer.

111
Q

pre and post menopause

obesity and breast cancer

A

dipose tissue produces small amounts of estrogen. After menopause, obesity increases breast cancer risk by increasing the level of estrogen. The more fat, the higher the estrogen level. Premenopausal obesity does not increase breast cancer risk. Before menopause, obesity causes hormonal changes which decrease estrogen production by the ovaries and can even
result in infertility.

112
Q

age at birth of first child and breast cancer

A

There is a change in structure of breast
lobule at pregnancy. Late age at birth of first child increases breast cancer risk. With late age at birth of first child, type 1 and type 2 breast lobules persist longer. They are more sensitive to carcinogens. Therefore, risk increases. During the 3rd trimester of pregnancy (after 32 weeks), the breast lobules mature into Type 3
lobules. Type 4 lobules are formed after childbirth and produce milk. Both Type 3 and Type 4 lobules are resistant to carcinogens.

113
Q

main breast cancer location

A

upper outer quadrant

114
Q

Classification of Breast
Cancers (Abridged)

A

Noninvasive – have not penetrated the basement membrane
 Ductal carcinoma in situ (DCIS, intraductal carcinoma)
 Lobular carcinoma in situ (LCIS)

Invasive – have penetrated the basement membrane (infiltrating)
 Invasive ductal carcinoma – most common (scirrhous carcinoma)
 Invasive lobular carcinoma

115
Q

precursor to? if it progresses where will it form?

Ductal Carcinoma in Situ

A

 Precursor lesion to invasive carcinoma
 When invasive carcinoma develops in a woman with a previous diagnosis of DCIS, it is usually in the same breast.

116
Q

if estrogen receptor +? post-menopause?

ductal Ca in situ tx

A

surgery and radiation
 Tamoxifen – antiestrogenic if estrogen receptor + (blocks estrogen receptor)
 Aromatase inhibitors – post-menopausal women (blocks estrogen formation)

117
Q

Paget’s Disease of Nipple

 variant of? how?
 app?
 Underlying invasive carcinoma?

A

Clinical variant of DCIS
 Extension of DCIS up to the lactiferous ducts and into the contiguous skin of the nipple
 Crusting exudate over the nipple and areolar skin
 Underlying invasive carcinoma in 50%

118
Q

Lobular Carcinoma in Situ
 proportion developing invasive
carcinoma?
 The invasive carcinoma may arise in?
 LCIS is a marker of?
 prophylactic mastectomy?

A

 One-third of women with LCIS develop invasive carcinoma
 The invasive carcinoma may arise in either breast
 LCIS is a marker of increased risk for developing breast
cancer in either breast
 Bilateral prophylactic mastectomy may be performed

119
Q

Invasive Ductal Carcinoma
 % breast carcinomas
 Term used for? does not imply?
 synonyms for invasive ductal carcinoma?

A

Invasive Ductal Carcinoma
 Most breast carcinomas (70-80%)
 Term used for all carcinomas that cannot be sub-classified into a specific type (not discussed)
 Does not imply that the tumor specifically arises from the duct system
 Carcinoma of “no special type” or “not otherwise specified” (NOS) are synonyms for invasive ductal carcinoma

120
Q

Invasive Ductal Carcinoma
has what response?

A

IDC has a Scirrhous Response (hardening/induration, dense stroma)

121
Q

invasive ductal Ca invades what tissue of the breast?

A

adipose

122
Q

Clinical Features Common to
all Invasive Carcinomas
 Fixation?
 Adherence?
 Lymphatic involvement may cause?

A

 Fixation secondary to adherence to pectoral muscles or deep fascia of chest wall
 Adherence to overlying skin with retraction or dimpling of the skin or nipple
 Lymphatic involvement may cause localized lymphedema with the skin thickened around exaggerated hair follicles (peau d’orange – orange
peel appearance)

123
Q

TNM Staging of Breast Cancer

A

satges 1-4

124
Q

stage 1 breast cancer

A

umor <2 cm, without nodal involvement, no
metastases

125
Q

stage 2 breast cancer

A

tumor <5 cm with <3 nodes and no distant metastases (or more than 5 cm without nodes)

126
Q

stage 3 breast cancer

A

many categories, any cancer infiltration into skin and chest wall, with nodes, without disseminated metastases

127
Q

stage 4 breast cancer

A

any cancer with disseminated metastases

128
Q

Prognostic Factors of breast cancer
 Size of?
 Lymph node?
 Distant?
 Histologic?
 Estrogen or progesterone receptor? tx?
 Proliferative?
 Aneuploidy?
 HER2/NEU? tx?

A

 Size of primary carcinoma
 Lymph node involvement and
number of nodes
 Distant metastases
 Histologic grade
 Histologic type
 Estrogen or progesterone receptor
expression - Tamoxifen
 Proliferative rate
 Aneuploidy
 HER2/NEU overexpression -
Herceptin