Risk Factors for Developing Breast Cancer

Type of Risk Individual Risk Factors

Genetic Deleterious BRCA1 or BRCA2 gene mutations
1st degree relatives with breast cancer (mother or sister)
Modifiable Obesity (BMI > 30 kg/m2)
Use of oral contraceptives or hormone replacement therapy
Alcohol use (particularly if excessive)
Nulliparity
Nonmodifiable Age > 70 years
Early menarche < 12 years, late menopause > 55 years
White race

Tumor Benign Conditions Associated With Malignant Conditions Associat

Marker Elevation Elevation
CA-125 Endometriosis, uterine leiomyoma, Endometrial, breast, lung, ovaria
cirrhosis, pelvic inflammatory disease, pancreatic carcinomas
pleural and peritoneal effusions
CA 19-9 Intraductal papillary neoplasm of the Gastric, pancreatic, gallbladder, o
pancreas cholangiocarcinomas
CEA Cirrhosis, cholecystitis, diverticulitis, Colorectal, breast, pancreatic, th
inflammatory bowel disease, pancreatitis lung carcinomas
Beta-hCG Pregnancy, molar pregnancy (complete) Seminoma/dysgerminoma, chorio
embryonal carcinomas
AFP Fetal neural tube defects (in maternal Yolk sac tumor, embryonal carcin
serum) hepatocellular carcinoma, 
hepatoblastoma
LDH Hemolysis, myocardial infarction Seminoma/dysgerminoma,
lymphoma/leukemia

Etiologies of Oligomenorrhea (Menstrual Irregularities)

Condition Clinical features Laboratory finding
PCOS • Mild hyperandrogenism • Increased LH
• Polycystic ovaries • Increased total testosterone
Androgen-secreting • Severe hyperandrogenism Excessively increased total testo
tumor • Virilization levels > 150
Congenital adrenal • Mild to severe • Increased total testosterone
hyperplasia hyperandrogenism • Elevated 17-hydroxyprogester
• Polycystic ovaries
Cushing syndrome • Hirsutism • Increased total testosterone
• Obesity • Elevated urinary or salivary co
• Hypertension
• Purple striae

Symptoms of Hypermagnesemia
Loss of deep tendon reflexes (patellar, most commonly)
Muscle paralysis
Hypotension
Bradycardia or conduction defects
Nausea, vomiting, flushing
Decreased urine output due to renal insufficiency
Respiratory suppression or failure
Somnolence leading to coma

Menstrual Cycle Phases

Phase Characteristics of Phase
Early follicular  • Menses occurs 
• Low estrogen and progesterone from ovary → loss of negative f
GnRH → small increase in release of FSH and LH
• Select group of developing follicles recruited
Midfollicular • Folliculogenesis (growth of follicles)
• Granulosa cells divide and lead to increased serum levels of estr
inhibin A
• Increased estradiol negatively feeds back on the hypothalamus
to suppress FSH And LH release
Late follicular • Follicles continue to grow and release estradiol and inhibin → do
follicle is selected
• FSH induces LH receptors on ovary to prime for LH surge
• Endometrium thickens 
Early luteal/Midcycle • Estradiol levels reach a peak 1 day before ovulation, causing a s
surge positive feedback control on the pituitary → LH surge
• Dominant follicle completes first meiotic division
• Ovulation occurs: oocyte release from follicle 36 hours after LH
• Granulosa cells luteinize and form a corpus luteum
 Late luteal • Corpus luteum secretes progesterone → stops LH surge
• Decreased LH eventually causes decrease in progesterone and e
release if oocyte not fertilized → endometrial sloughing and onset

- Prader-Willi syndrome as a result of a paternal chromosome 15q

deletion. As presented in this question, the physical exam shows a
narrow forehead, thin upper lip and almond-shaped palpebral fissures.
There is a history of poor suck early in life. Later in life patients suffer
from mild mental retardation.

Patients typically have hyperphagia and increased appetite. This has

been associated with persistently elevated levels of ghrelin hormone.
This hormone is produced by P/D1 cells lining the fundus of the
stomach. Ghrelin increases growth hormone, adrenocorticotropic
hormone, cortisol, and prolactin secretion. As a result, the hormone
regulates hunger and meal initiation.

Even if you did not know the association between Prader-Willi

syndrome and increased ghrelin, remember that ghrelin is an
important hormone in the pathophysiology of obesity, leading to an
increased appetite. This patient's history and examination is consistent
with both obesity and increased appetite, which points to increased
ghrelin.

 G cells are located in the antrum of the stomach and release Gastrin, which
is responsible for increasing gastric H+ secretion, growth of gastric mucosa,
and gastric motility. Unlike the scenario, patients with increased activity of G
cells would resemble Zollinger-Ellison syndrome with symptoms of
abdominal pain, diarrhea, and small intestine ulcers.

I cells release the hormone cholecystokinin (CCK), which is responsible for

increasing pancreatic secretion, gallbladder secretion, and decreasing
emptying. This is clinically significant in patients suffering from cholelithiasis;
patients present with worsening pain after a fatty meal due to increased
CCK. These cells are located in the duodenum and jejunum. This patient
does not have discomfort after eating.

K cells are responsible for releasing the hormone glucose-dependent

insulinotropic peptide (GIP), which decreases gastric H+ secretion and
increases insulin release. K cells are stimulated by fatty acids, amino acids,
and oral glucose. These cells are located in the duodenum and jejunum. 
S cells are located in the duodenum and release secretin hormone. This
hormone increases pancreatic bicarbonate ion release and bile secretion. It
also decreases gastric acid secretion