• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

180 Cards in this Set

  • Front
  • Back
(as a pharmacologic agent)
Prevents further damage by suppressing macrophages and other phagocytes (depresses lysosomal enzyme activity)
Accumulates in synovial fluid to slow progression of bone and articular destruction

One of the most effective agents for rapidly progressive rheumatoid arthritis (not used for acute attacks)
Main use is in rheumatoid arthritis that is refractory to other treatments

Contraindications: hepatic or kidney disease, pregnancy
Adverse reactions: dermatitis, nephritis, proteinuria, agranulocytosis, chrysiasis (grey-blue discoloration of skin), aplastic anemia

Rarely used due to severe side effects
Overdose treated with dimercaprol
Currently used agents: auranofin, gold sodium thiomalate
Unknown mechanism
Reduces rheumatoid factor (no longer used for RA - requires chronic use, high risk for serious side effects)
Also used to chelate heavy metals (only acceptable use currently, due to side effects)

Adverse effects:
Aplastic anemia
(for inflammatory disorders)
Folic acid antagonist - inhibits dihydrofolate reductase
Used in low doses to treat rheumatoid arthritis

Adverse effects:
Megaloblastic anemia
Mucosal ulceration
Liver cirrhosis
Acute pneumonia-like syndrome
Anti-Tumor Necrosis Factor Agents
Also called anti-rheumatic immune-modulators, biologic response modifiers

Very powerful - only for severe inflammatory conditions

Reduce TNF effects or TNF levels

Anti-tumor necrosis factor agent
Inhibits production and secretion of TNF

Uses: leprosy, HIV associated skin lesions, multiple myeloma

Extremely teratogenic - cannot be used in women of reproductive age unless negative pregnancy test and oral contraceptive use
Anti-tumor necrosis factor agent
Phosphodiesterase inhibitor - inhibits TNF secretion
Platelet aggregation inhibitor

Use: acute alcoholic hepatitis
Anti-tumor necrosis factor agent
Monoclonal antibody directed against TNF (human-mouse chimera)

IV administration
Uses: rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, moderate to severe ulcerative colitis and Crohn's

Adverse effects:
Can increase risk for acute onset life-threatening sepsis
Increase risk of acquisition and spread of TB
Increase risk of lymphoma and other cancers
Associated with higher incidence of MS, myelitis, opic neuritis
Risk for serum sickness
Abdominal pain
Anti-tumor necrosis factor agent
Recombinant TNF receptor - binds TNF in the bloodstream

Administered subcutaneously
Uses: rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, juvenile rheumatoid arthritis

Adverse effects:
Potential for acute onset life-threatening sepsis
Increased risk of TB acquisition and spread
Associated with higher incidence of developing MS, myelitis, optic neuritis
Anti-tumor necrosis factor agent
Fully human monoclonal antibody directed against TNF

Uses: rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, Crohn's disease
Not approved for use in children

Adverse effects:
Aplastic anemia
Increased incidence of MS, optic neuritis, myelitis
May worsen heart failure (monitor closely)
Metabolic disorder marked by increased amounts of uric acid (either from increased production or decreased excretion)
Urate precipitates in joints and kidneys

Acute attacks often due to high alcohol consumption, high purine diet, kidney disease
Chronic may be due to kidney disease or malignancy
DOC for acute gout attacks (although first attack often treated with NSAID)

Binds tubulin, disrupting cell's ability to migrate to affected area and inhibiting synthesis and release of leukotrienes
Prevents macrophages from moving to affected site - prevents further irritation

Does not prevent progression, but has suppressive effect in decreasing number of future attacks

Contraindicated in pregnancy
Use with caution in hepatic and cardiovascular disease
Used in treatment of gout

Inhibits xanthine oxidase - inhibits uric acid production

Adverse effects:
Hypersensitivity reactions (skin rashes - months to years of chronic use)
Used in treatment of gout

Uricosuric agent - blocks tubular reabsorption of uric acid, causes greater excretion
Requires high doses - low doses compete with urate at renal transporters and make gout worse

Will raise plasma concentration of drugs that compete at renal transporters
What two specific groups of patients may have chronic gout?
Lesch-Nyhan syndrome
Patients being treated for malignancies (overabundance of nucleic acid from dying malignant cells)
Lesch-Nyhan Syndrome
X-linked recessive

Mental retardation
Compulsive biting of lips and fingers (self mutilation)

Due to deficiency in hypoxanthine-guanine phosphoribosyl tranferase (HGPRT)
What NSAID should never be used to treat gout?

Competes with uric acid at renal transporters (less uric acid excreted)
ATP Yields:
FADH2: 2
Acetyl CoA: 12
Pyruvate: 15
Glycolysis (anaerobic): 2
Glycolysis (aerobic): 8
Glucose (complete oxidation): 38
Fatty acid: 129
Gluconeogenesis (from pyruvate): -12
Urea synthesis: -4
Glycerophosphate shuttle: 2 per NADH
Malate shuttle: 3 per NADH


Key enzyme: phosphofructokinase-1

Allosteric inhibitors: ATP, citrate

Allosteric activators: AMP, fructose 2,6-dp

If enzyme is phosphofructokinase-2, phosophorylation inhibits


Key Enzyme: fructosediphosphatase-1

Allosteric inhibitors: AMP, fructose 2,6-dp

Allosteric activators: ATP, citrate

If enzyme is fructosediphosphatase-2, phosphorylation activates


Key enzyme: glycogenphosphorylase

Effect of phosphorylation: activates

Glycogen Synthesis

Key enzyme: glycogen synthetase

Effect of phosphorylation: inhibits

Pentose Phosphate Shunt

Key enzyme: glucose-6-phosphate dehydrogenase

Allosteric inhibitors: NADPH


Key enzyme: carnitine acyltransferase

Allosteric inhibitors: malonyl CoA

Fat Mobilization

Key enzyme: hormone sensitive lipase

Effect of phosphorylation: activates

Lipid Synthesis

Key enzyme: acetyl-CoA carboxylase

Allosteric activators: citrate

Effect of phosphorylation: inhibits

Cholesterol Synthesis

Key enzyme: HMG CoA reductase

Allosteric activators: cholesterol

Effect of phosphorylation: inhibits

Ketone Body Synthesis
Key enzyme: HMG CoA synthase

Purine Synthesis
Key enzyme: amidotransferase

Allosteric inhibitors: AMP, GMP, IMP

Citric Acid Cycle
Key enzyme: pyruvate dehydrogenase 1
Allosteric inhibitors: acteyl CoA, NADH
Effect of phosphorylation: inhibits

Key enzyme: citrate synthase
Allosteric inhibitors: acetyl CoA, ATP, NADH
What are steroid hormones made from?
Steroid Class:

Example: cholesterol

Number of C atoms: 27
Steroid Class:

Bile Acids
Examples: glycocholate, taurocholate

Number of C atoms: 24
Steroid Class:

Example: cortisol

Number of C atoms: 21
Steroid Class:

Example: aldosterone

Number of C atoms: 21
Steroid Class:

Example: progesterone

Number of C atoms: 21
Steroid Class:

Examples: testosterone, androstenedion, DHEA

Number of C atoms: 19
Steroid Class:

Examples: estradiol, estrogen

Number of C atoms: 18
What are the three areas of the adrenal cortex and the steroids produced in each?
Zona glomerulosa - mineralocorticoids

Zona fasciculata - glucocorticoids

Zona reticularis - Androgens
What is caused by 17-alpha-hydroxylase deficiency?
Male: ambiguous genitalia
Female: primary amenorrhea
What is caused by 21-alpha-hydroxylase deficiency?
Most common defect of corticoid synthesis (95%)

Male: precocious puberty
Female: ambiguous genitalia
(both due to increased DHEA)

Salt wasting in 50-60% of patients (lack of aldosterone)
What is caused by 11-beta-hydroxylase?
Male: precocious puberty
Female: ambiguous genitalia
(both due to increased androgens)

Salt retention - leads to hypertension, hypokalemia
What is insulin's effect on:
General anabolic action

Fat (anabolic): synthesis

Sugar (anabolic):
Uptake in muscle, fat
Glycolysis in liver, muscle
Glycogen synthesis in liver, muscle

Protein (anabolic): synthesis
What is glucagon's effect on:
Fat (catabolic): lysis

Sugar (catabolic):
Gluconeogenesis in liver
Glycogenolysis in liver

Protein (catabolic): increases uptake of amino acids in liver for gluconeogenesis
What is GH's effect on:
Promotes synthesis of protein at expense of fat and sugars

Fat (catabolic): lysis

Sugar (catabolic): gluconeogenesis in liver

Protein (anabolic): synthesis
What is cortisol's effect on:
Increases blood sugar levels and build-up of glycogen stores at expense of fat and protein

Fat (catabolic): lysis and redistribution

Sugar (anabolic):
Inhibits uptake in muscle, fat
Gluconeogenesis in liver
Glycogen synthesis in liver

Protein (catabolic): degradation
What is epinephrine's effect on:
Fat (catabolic): lysis

Sugar (catabolic):
Increases uptake in muscle
Glycolysis in muscle
Gluconeogenesis in liver
Glycogenolysis in liver, muscle

Protein: none
What is the difference between nucleosides and nucleotides?
Nucleosides: purines or pyramidines linked to a pentose sugar

Nucleotides: phosphates (mono, di, or tri) of the nucleoside
What are the purines?
What are the pyramidines?

Nucleoside: adenosine

Nucleotide: adenylate (AMP)

Nucleoside: guanosine

Nucleotide: guanylate (GMP)

Nucleoside: uridine

Nucleotide: uridylate (UMP)

Nucleoside: cytidine

Nucleotide: cytidylate (CMP)

Nucleoside: deoxythymidine

Nucleotide: deoxythymidylate (dTMP)
What are the processes by which purines are made?
De novo synthesis (in liver):
Phosphoribosyl pyrophosphate -> IMP -> AMP or GMP -> ADP or GDP

Salvage of purine bases:
Hypoxanthine -> IMP
Guanine -> GMP
Adenine -> AMP
What is the process of degradation of purine bases?
In liver

Adenosine -> Inosine -> Hypoxanthine -> Xanthine
Guanosine -> Guanine -> Xanthine

Xanthine -> Uric Acid
What are the processes by which pyrimidines are made?
De novo (in liver):
Glutamine -> Carbamoylphosphate -> OMP -> UMP
dUMP -> dTMP

Salvage of pyrimidine bases:
Uracil -> UMP
Cytosine -> CMP
What is the process of degradation of pyrimidine bases?
In liver
Pyrimidine rings can be opened and completely degraded

Cytosine -> CO2, NH4+, beta-alanine
Thymine -> CO2, NH4+, beta-amino-isobutyrate
In prokaryotic DNA

Operational unit that is either "on" or "off"
Consists of promoter, operator, and one or more structural genes
In prokaryotic DNA

RNA polymerase binds to promoter
Located on 5'-end of operon ("upstream")
In prokaryotic DNA

Located between promoter and structural genes
Binding site of repressors
If repressor binds to operator, operon is "off" (polymerase can't proceed)
Prokaryotic protein

Regulatory protein that binds to operator and prevents transcription
Regulator Gene
In prokaryotic DNA

Codes for repressor
Eukaryotic Transcription
No operon - each structural gene has its own promoter containing many different response elements (binding sites for regulatory proteins)
Regulatory proteins can bind to several promoters activating a set of structural genes (which may be located on different chromosomes)
Transcription is regulated by various combinations of regulatory proteins
Transcription Factor

Binds to TATA box (part of promoter)
RNA polymerase does not recognize promoter without transcription factor

Bind to nuclear receptor protein
Inducer-receptor complex binds to DNA and activates some genes, inactivates others

Example: steroid hormones

Regulatory DNA sequence
Can be upstream or downstream of promoter
May be located several thousand base pairs from starting point of transcription
Loops in DNA bring enhancers near promoter region
Around what age does fusion of the bones of the innominate occur?
Age 20

Ilium - Ischium - Pubic bone
All fuse at acetabular notch
What are the main ligaments of the pelvis?
Which are accessory ligaments and true ligaments?
Sacrotuberous ligaments
Sacrospinous ligaments
Iliolumbar ligaments

Sacroiliac ligaments
Sacrotuberous Ligaments
Accessory ligaments of pelvis

Connect sacrum to ischial tuberosity
Sacrospinous Ligaments
Accessory ligaments of pelvis

Connect sacrum to ischial spines
Divides greater and lesser sciatic foramen
Iliolumbar Ligaments
Accessory ligaments of pelvis

Attach L4/L5/iliac crests to SI joints (for stability)
Usually first to become tender with lumbosacral dysfunction

3 ligaments: anterior, posterior, interosseous
Ganglion Impar
Site of fusion of left and right sacral sympathetic trunks
Lies just anterior to coccyx
Pelvic Diaphragm
Comprised of (muscles):
Levator ani (puborectalis, pubococcygeus, iliococcygeus)

Supports pelvic viscera and pelvic floor
Aids in raising pelvic floor
Constricts lower rectum and vagina
Origin: inferior anterior sacrum
Insertion: greater trochanter of femur
Innervation: S1, S2

External rotation of thigh
Extension of thigh
Abduction of thigh when hip is flexed
Psoas - T12-L5 vertebrae
Iliacus - iliac crest, iliac fossa, sacral ala, anterior sacroiliac ligaments
Join within true pelvis

Psoas - lesser trochanter of femur
Iliacus - psoas major tendon, body of femur inferior to lesser trochanter

Psoas - L1-L3 (lumbar plexus)
Iliacus - femoral nerve (L2, L3)

Function: flexion of thigh and stabilization of hip joint
What is the difference between the true and false pelvis?
True: funnel shaped area bounded anteriorly by the pubic bones and posteriorly by the sacrum

False: technically part of abdomen - located in area between ilia
What are the signs of a flexion contracture of the iliopsoas?
L1 and/or L2 flexed, sidebent, rotated toward side of contracture
Nerves and Innervations:

Lumbar Plexus
T12 - L4

Muscles innervated:
Adductor group
(abdomen and thigh)

Lower abdomen
Pubic area
Nerves and Innervations:

Sacral Plexus
L4-5, S1-3, portion of S4

Innervation (motor and sensory):
Lower extremity
Parasympathetic innervation (S2-4) to left colon and pelvic organs

Nerve branches:
Superior and inferior gluteal
Sciatic Nerve
Branch of sacral plexus
Originates from L4-S3

Usually runs through greater sciatic notch just below piriformis
Anomalies exist, including nerves that run through piriformis
Inherent Motion of Sacrum
Associated with cranial cycle of flexion/extension

Craniosacral extension: dips forward into sacral flexion (nutation)

Craniosacral flexion: tips backward into sacral extension (counternutation)

Axis of motion: S2 horizontal axis
Respiratory Motion of Sacrum
Inhalation: sacral base moves posteriorly (extension, counternutation)

Exhalation: sacral base moves anteriorly (flexion, nutation)

Axis: horizontal S2
Postural Motion of Sacrum
Flexion of torso: sacral base moves posteriorly (extension, counternutation)

Extension of torso: sacral base moves anteriorly (flexion, nutation)

Axis: S3 transverse
Dynamic Motion of Sacrum
Occurs with ambulation

Step forward with left/weight on right: right sacral oblique axis engaged

Step forward with right/weight on left: left sacral oblique axis engages
What are the two rules for L5 dysfunction affecting the sacrum?
1. L5 rotation is opposite of sacral rotation

2. L5 sidebending engages ipsilateral sacral oblique axis
Anterior Innominate Rotation
One innominate rotates anteriorly with respect to the other

ASIS inferior
PSIS superior
Longer leg on ipsilateral side
Positive standing flexion and ASIS compression tests on affected side

Tight quadriceps
Rectus femoris or adductor group dysfunction

Hamstring tightness
Sciatica (due to piriformis dysfunction)
Posterior Innominate Rotation
One innominate rotates posteriorly with respect to the other

ASIS superior
PSIS inferior
Shorter leg ipsilaterally
Positive standing flexion and ASIS compression test on affected side

Etiology: tight hamstrings

Groin pain
Medial knee pain (due to sartorius dysfunction)
Superior Innominate Shear
One innominate more superior than the other

ASIS superior
PSIS superior
Pubic ramus superior
Positive standing flexion and ASIS compression tests on affected side

Fall on or thrust up the ipsilateral gluteal area
Surprise step off curb into a hole

Pelvic pain
Contralateral SI joint pain
Low back pain
Inferior Innominate Shear
One innominate more inferior than the other

ASIS inferior
PSIS inferior
Pubic ramus inferior
Positive standing flexion and ASIS compression tests on affected side

Car accident

Pelvic pain
Contralateral SI joint pain
Superior Pubic Shear
One pubic bone superior to the other

Pubic bone superior
ASIS level or superior
PSIS level or inferior
Positive standing flexion and ASIS compression tests on affected side

Tight rectus abdominis muscle
Unusual trauma
Posterior innominate rotation
Third trimester pregnancy or delivery

Tender inguinal area with or without dysuria or frequency
Inferior Pubic Shear
One pubic bone is inferior to the other

Pubic bone inferior
ASIS level or inferior
PSIS level or superior
Positive standing flexion and ASIS compression tests on affected side

Tight adductor muscles
Unusual trauma
Anterior innominate rotation
Third trimester pregnancy or delivery

Symptoms: pelvic or SI joint pain
Innominate Inflare
Innominate is rotated medially

ASIS more medial
Taut posterior pelvic muscles
Positive standing flexion and ASIS compression tests on affected side

Etiology: trauma

Symptoms: sometimes dysuria and/or frequency
Innominate Outflare
Innominate is rotated laterally

ASIS more lateral
Lax posterior pelvic muscles
Positive standing flexion and ASIS compression tests on affected side

Etiology: trauma

Symptoms: pelvic or SI joint pain
Bilateral Sacral Flexion
Sacral base more anterior (whole base)

Deep superior sulci
Shallow ILAs
Increased lumbar lordosis
Negative spring test
Negative (false negative) seated flexion test

Delivery (VERY common in postpartum women)

Symptoms: low back pain that worsens with backward bending
Bilateral Sacral Extension
Sacral base positioned more posteriorly (whole base)

Shallow superior sulci
Deep ILAs
Decreased lumbar curvature
Positive spring test
Negative (false negative) seated flexion test

Etiology: trauma

Symptoms: low back pain that worsens with forward bending
Unilateral Sacral Flexion
Sacral base anterior unilaterally
Most common type of sacral shear

Deep superior sulcus on affected side
Shallow ILA on affected side
Negative spring test
Positive seated flexion test on affected side
Shorter leg on affected side

Surprise step into hole or off curb
Lumbar dysfunction

Symptoms: low back pain
Unilateral Sacral Extension
Sacral base is posterior unilaterally

Shallow superior sulcus on affected side
Deep ILA on affected side
Positive spring test
Positive seated flexion test on affected side
Longer leg on affected side

Lumbar Dysfunction

Symptoms: low back pain
Forward Sacral Torsion
Rotation in same direction as axis
R-on-R, L-on-L

Deep superior sulcus contralateral to rotation
Shallow ILA ipsilateral to rotation
Lumbar sidebending ipsilateral to oblique axis
Lumbar rotation opposite of sacral rotation
Negative spring test
Positive seated flexion test contralateral to oblique axis

Etiology: trauma, lumbar dysfunction

Symptoms: low back pain with SI, inguinal, or groin pain (exacerbated by backward bending)
Backward Sacral Torsion
Rotation opposite of axis
R-on-L, L-on-R

Shallow superior sulcus ipsilateral to rotation
Deep ILA contralateral to rotation
Lumbar sidebending to ipsilateral side of oblique axis
L5 rotated opposite rotation
Positive spring test
Positive seated flexion test on side contralateral to oblique axis

Etiology: trauma, lumbar dysfunction

Symptoms: low back pain or SI discomfort (exacerbated by bending forward or walking)
What should be treated before treating any sacral dysfunction?
Any L5 dysfunction
Usually spontaneously resolves sacral dysfunction
Endometrial Polyps
Focal thickening of endometrium

Often asymptomatic
Estrogen sensitive
Possible genetic relationship
Endometrial Hyperplasia
Thickening of all endometrial wall - "stripe thickening"

Stimulated by high estrogen (mainly) or low progesterone stimulation (progesterone inhibits estrogen)

Risk factors:
Age over 40
Estrogen treatment
Early menarche
Late menopause
Granulosa-theca cell tumor
Type II diabetes
Endometrial Carcinoma
Most common invasive cancer of female genital tract

Develops from hyperplasia
What are the disorders of the cervix?
Non-neoplastic: cervicitis, cervical polyps

Pre-cancerous: CIN (cervical intraepithelial neoplasia)

Carcinoma (invasive)
Inflammation of the cervix

Gardnerella vaginalis
Trichomonas vaginalis
Candida albicans
Chlamydia trachomatis
Cervical Polyps
Non-neoplastic (not neoplasms)

Represent proliferation of cervical epithelium in response to inflammation
(Cervical Intraepithelial Neoplasia)
Usually involves squamocolumnar junction
Three grades

Major association with HPV types 16, 18, 30s, 40s, 50s (although HPV is not the only factor)
Disorganized epithelial growth due to HPV's inhibition of tumor suppressors p53 and RB

May spontaneously regress or may develop into invasive carcinoma

Loop electric excision procedure (LEEP)
Cone biopsy (types II and III)
What are the grades of CIN?
Low-grade intraepithelial lesion
Mild dysplasia of upper layer of cervical epithelium

High-grade intraepithelial lesion
More severe dysplasia
Affects various cells throughout entire epithelial thickness

High-grade intraepithelial lesion
Carcinoma in situ
Entire cervical epithelial layer is replaced by neoplastic cells
Demonstrates no invasion beyond underlying basement membrane
Invasive Cervical Carcinoma
Neoplastic development of cervical epithelium with invasion through underlying basement membrane

Stage 0: carcinoma in situ (CIN III)
Stage 1: invasive carcinoma confined to cervix
Stage 2: invasive carcinoma extends beyond cervix but not onto pelvic wall, and if vagina is involved does not spread to lower 1/3
Stage 3: invasive carcinoma has extended to pelvic wall
Stage 4: invasive carcinoma has extended beyond pelvic wall or has involved rectal or bladder mucosa (with or without metastases)
Polycystic Ovarian Syndrome
Also called Stein-Levanthal Syndrome

Chronic anovulation with symptoms of androgen excess along with obesity
Thought to be due to excess LH production by anterior pituitary

Symptoms: infertility, amenorrhea or oligomenorrhea, acne, hirsutism (usually also obesity, potential for type II diabetes)
>2:1 LH:FSH ratio
High androstenedione, testosterone, estrone

Constant high LH stimulates ovarian theca cells to produce androgen (causes acne and hirsutism) - magnified in obese women due to adipose cell conversion of androgen to estrone
Estrone has negative feedback effect on anterior pituitary, reducing FSH production
Decreased FSH results in decreased follicular development in ovary - prevents formation of ovum ready for ovulation, therefore no ovulation = infertility
Many anomalies in ovarian and pituitary hormone production results in amenorrhea or oligomenorrhea
Presence and proliferation of non-neoplastic endometrial tissue outside the uterine cavity
Develop multiple nests of endometrial cells throughout structures in peritoneal cavity (#1 site is ovary, also uterine ligaments, rectovaginal area, pelvic peritoneum)
Bleeding can occur into ectopic endometrial tissue -- if on the ovary, can develop chocolate cysts (collection of old blood)

Uterine Leiomyoma
Fibroid - smooth muscle tumor
Most common uterine tumor and overall most common tumor in women

Estrogen sensitive - grows during reproductive years, regresses during menopause
Characteristic whorled pattern of smooth muscle bundles
More common in blacks

Abnormal menstrual bleeding (most common)
Urinary frequency
Impaired fertility
Increased risk of spontaneous abortion or fetal malpresentation
Increased risk of postpartum hemorrhage
Hydatidiform Mole
Due to abnormal ovum fertilization that ultimately causes excessive trophoblastic development in the form of grape-like cysts

Complete: 2 X chromosome sperm that have fertilized 1 enucleate ovum
Incomplete: fertilization of 1 ovum with 2 or more sperm (yielding triploidy or more)

Cystic swelling of villi (grape like cysts)
Trophoblastic (placental) proliferation
Very high beta-hCG
Uterus larger than expected for gestational age
Frequent and early metastases - diagnosis usually too late for intervention

Malignant neoplasm of trophoblastic cells (placenta)
Initially asymptomatic
Very high beta-hCG
Late findings: irregular spotting of brown blood foul smelling fluid

Risk factors:
Retained GTN
Retained placenta after delivery or abortion
May develop spontaneously in ovary as type of grem cell tumor
Fibrocystic Change of Breast
Multiple bilateral nodules
"Lumpy bumpy" breast
Fluctuate in size and tenderness with menstrual cycle
Breast Cancer
Typically one solitary nodule
Usually unilateral
Often non-tender in early stages
Does not fluctuate with menstrual cycle
Fibroadenoma of Breast
Fibrous and glandular tissue - stromal tumor
Single sharply circumscribed mass - mobile, marble shaped and sized
Usually <30 years of age
Mildly increased risk of subsequently developing breast cancer
Phylloides Tumor of Breast
Benign (if becomes malignant, called cystosarcoma phylloides tumor)
Stromal tumor

Usually occurs >60 years of age
Grows quickly
Rapidly becomes huge log-shaped tumor
Intraductal Papilloma
Epithelial tumor

Tumor comprised of ductal epithelial cells
Nipple discharge frequently bloody or serous
Ductal Carcinoma In Situ

Non-invasive carcinoma (cells do not cross basement membrane)
Neoplasm of ductal epithelial cells

5 types:
Comedocarcinoma - solid sheets of malignant cells with central areas of necrosis that become calcified (microcalcifications)
Invasive Ductal Carcinoma
Neoplasm of ductal epithelium
Most common breast cancer

Often scirrhous (hard)
May see peau d'orange, nipple retraction, dimpling
May palpate fixed mass
Lobular Carcinoma In Situ

Tumor of lobules, terminal ducts, ductules (acini)
Never forms calcifications or masses
Tend to be bilateral
Signet ring cells common
Invasive Lobular Carcinoma

Diffusely invasive through breast (makes detection difficult)
Tend to be bilateral (high risk of recurrence in opposite breast - recommend bilateral removal)
High metastasis rate (CSF, ovary, bone marrow, uterus)
Confers rubbery consistency to breast
Signet ring cells common
Single file arrangment of neoplastic cells
Paget's Disease of the Nipple

Form of DCIS that extends from nipple ducts into contiguous nipple skin and areola (involvement of epidermis by malignant cells called Paget cells)
Palpable mass usually present in breast - represents invasive ductal carcinoma that started as DCIS
Nipple may be fissured, ulcerated, oozing, hyperemic, edematous
Medullary Carcinoma of Breast
Young women
Often associated with BRCA1 gene mutation
Soft fleshy consistency
Colloid (Mucinous) Carcinoma of Breast
Older women
Gelatinous consistency
Usually receptor positive
Tubular Carcinoma of Breast
10% of mammographically identified tumors
Conspicuously spiculated
Late 40s age range
Multifocal and unilateral OR bilateral
Usually receptor positive
Excellent prognosis
Sarcoma of Breast
Stromal tumor
Usually very bulky and palpable

Mammographic Findings of Breast Tumors
Invasive ductal or tubular: spiculated density with irregular infiltration of surrounding tissue

Cyst or fibroadenoma: well circumscribed density with smooth borders

Medullary or mucinous carcinoma: well circumscribed with smooth border

Lobular carcinoma: distortion of breast without discrete density

Malignant lesion (ex, DCIS): small irregular numerous and clustered or linear and branching calcifications
What are the most common metastatic sites for breast cancer?
What is the role of estrogen and progesterone receptors in breast cancer?
Found in 50-85% of breast tumors
More common in post menopausal patients
Yield slightly better prognosis
If present, allow almost 3/4 of receptor positive tumors to regress with hormonal manipulations
What are the oncogenes and tumor suppressor genes associated with breast cancer?
Oncogenes: c-erb-B2 (HER-2, neu)

Tumor suppressor: BRCA-1, BRCA-2, p53
Inflammation of tongue

Associated with vitamin B2 (riboflavin) or B12 (cobalamin) deficiency
Drying and scaling of lips with fissuring at corners of mouth

Associated with vitamin B2 (riboflavin) deficiency
Smooth Beefy-Red Tongue
Atrophy of papillae and mucosa to expose underlying vasculature

Associated with advanced vitamin B12 (cobalamin) deficiency
Strawberry Tongue
White coated tongue through which hyperemic papillae poke, giving appearance like bumps on a strawberry

Associated with scarlet fever
Koplik's Spots
Ulcerations on buccal mucosa

First sign of measles
What is the terminology used for esophageal diverticula?
Termed for location:
Zenker's - above upper esophageal sphincter
Traction - midpoint of esophagus
Epiphrenic - above lower esophageal sphincter

Termed for number of layers involved:
Pulsion - herniation of mucosa only (false diverticulum)
True - all layers
Acute Erosive Gastritis
Focal inflammation/damage of gastric mucosa

Risk factors:
Cancer drugs
Chronic Type A Gastritis
Glandular destruction and mucosal atrophy
Affects fundus

Autoimmune - antibodies against gastric glands, parietal cells, intrinsic factor
Usually associated with Hashimoto's, Addison's, or vitiligo

Pernicious anemia (due to loss of intrinsic factor)
Achlorhydria (no HCl due to parietal cell loss)
Chronic Type B Gastritis
Chronic irritation due to H. pylori
Affects antrum

Chronic irritation leads to eventual mucosal atrophy and metaplasia, eventual carcinoma
Menetrier's Disease
Mucosal hyperplasia due to inflammation of gastric mucosa

Mucosa becomes thickened with concomitant atrophy of glands
What are the major types of intestinal polyps?
Hyperplastic Polyps of Intestine
Most common colonic polyp (90%)
Most common in 50s and 60s

Due to to decreased epithelial cell turnover in bowel, resulting in accumulation of mature cells on surface
Little to no risk for malignant transformation
Hamartomatous Polyps of Intestine
Represent malformations of glands and stroma of epithelium, causing overgrowth of mature tissue natural to area
Little to no risk for malignant transformation
Can occur sporadically or in association with Peutz-Jeghers Syndrome
Inflammatory Polyps of Intestine
Also called pseudopolyps

Represent inflamed regenerating tissue surrounded by ulceration
Most associated with inflammatory bowel disease
Lymphoid Polyps of Intestine
Large but normal variants of intramucosal lymphoid tissue
Adenomatous Polyps of Intestine
Also called adenomas
Neoplastic - pre-malignant

Arise from proliferative dysplasia of epithelial cells lining the colon

3 subtypes:
Tubular adenoma - comprised of tubular epithelial glands
Villous adenoma - villous (finger like) projections - highest risk for malignant transformation if >4cm in diameter - most common to rectum and rectosigmoid colon, usually cause gross rectal bleeding, hyperkalemia, hypoproteinemia
Tubulovillous adenoma - both villous and tubular features
Peutz-Jeghers Syndrome
Inherited autosomal dominant hamartomatous polyp disorder that is a familial polyposis syndrome of the entire bowel

Hamartomatous polyps
Spotted melanin hyperpigmentation of lips, palms, soles

Low cancer potential in polyps, but increases risk of cancer (colon and others) unrelated to polyps
Familial Adenomatous Polyposis
Due to loss of tumor suppressor gene APC
Once polyps develop, near 100% chance of colon cancer development

Develop 500-2500 polyps that carpet the colon
All polyps are adenomatous
Gardner's Syndrome
Form of familial adenomatous polyposis

Classic FAP polyps
Benign mandible and skull tumors
Epidermal cysts
High risk for abnormal dentition

Nearly 100% chance of polyps developing into colon cancer

Autosomal dominant
Turcot's Syndrome
Form of familial adenomatous polyposis

Classic FAP polyps
Malignant brain tumors

High risk (not quite 100%) of polyps becoming colon cancer

Autosomal dominant
Hereditary Nonpolyposis Colorectal Cancer Syndrome
Also called Lynch Syndrome
Autosomal dominant

Due to defective DNA mismatch repair genes
Associated with microsatellites
Increased risk of colon and other cancers (stomach, liver, brain, prostate, skin, biliary ducts, small intestine, especially endometrium and ovary)
Cancer development does not usually aris from polyps
Colonic malignancies occur in multiple sites, not usually formed within or in association with adenomas
Colon Cancer
Usually occurs sporadically
Most arise from adenomas (adenomatous polyps)

Mechanism: AP tumor suppressor gene becomes inactivated, k-RAS (oncogene) mutated and p53 (tumor suppressor) becomes inactivated

Risk factors:
Excessive dietary calorie intake
High refined carbohydrate diet
Intake of red meat
Reduced consumption of dietary fiber

Asymptomatic until late in course
Iron deficiency anemia (right sided cancers)
Positive hemoccult, change in bowel habit, crampy left lower quadrant discomfort (left sided cancers)

Use of NSAIDs and aspirin may be protective
Any over 50 with iron deficiency anemia must be worked up
Liver and lungs are preferred metastatic sites
Diverticular Disease
Chronic or recurrent elevated intraluminal pressures in colon cause small areas of colon wall to form outpouchings

Most common in sigmoid colon
Most common in areas where blood vessels penetrate entire bowel wall (weakened areas)

2 types:
Diverticuli present
Blood vessels at sites of diverticuli are more exposed - often yields positive hemoccult and sometimes gross bleeding
Diagnosed with barium enema and Xray or colonoscopy
Inflammation (due to infection) of diverticuli - complication of diverticulosis
Due to seeds, nuts, or other small objects lodging in diverticulum orifice, causing bacteria to be trapped and cause infection

Lower left quadrant pain
Elevated neutrophils
Often diarrhea (but hemoccult negative - blood vessels are blocked off)

Can cause abscess formation, bowel perforation, sepsis - potentially life threatening

Diagnosed with CT scan
TX: ciprofloxacin and metronidazole
Irritable Bowel Syndrome
Recurrent unpredictable bowel habits (diarrhea and/or constipation) with abdominal cramping
Exacerbated by emotional stress

Thought to be due to dysregulation of enteric nervous system
Crohn's Disease
Inflammatory bowel disease

Rectum usually spared
Ileum usually most involved
"Skip lesions"
Non-caseating granulomas and aphthous ulcers
Crypt abscesses
Strictures, fissures, fistulas
Positive string sign (thin stream of barium on Xray through diseased sections)

More common in whites, Jews have highest risk
Smoking is strong risk factor
Moderate colon cancer risk

More pain, less bleeding

TX: sulfasalazine or 5-ASA, vitamin B12, metronidazole, corticosteroids, immunosuppressives
Ulcerative Colitis
Inflammatory bowel disease

Begins at rectum and progresses proximally
Can progress through colon to ileocecal junction
Continuous lesions
Mucosa and submucosa only
Nongranulomatous lesions (mucosal ulcers)
Crypt abscesses
Lead pipe colon

More common in whites and Jews, females with highest risk
Smoking has protective effect
High risk of colon cancer and toxic megacolon

More bleeding, less pain

TX: bowel rest, sulfasalazine or 5-ASA, immunosuppressives
What is the most common symptom of malabsorption?
Steatorrhea (may or may not be diarrhea)
What labs should be run for suspected malabsorption?
Stool fat analysis
Sudan III stool stain
D-xylose absorption test
Schilling test
Sudan III Stool Stain
Qualitatively determines if stool fat is increased
Rapid and inexpensive, but limited to screening only
Stool Fat Analysis
Measures quantitatively amount of fat in stool after being fed a measured quantity
High amounts of fat indicates malabsorption

Gold standard test for fat malabsorption
D-Xylose Absorption Test
Patient is fed d-xylose (non-digestible sugar) and it is later measured in urine
D-xylose should be absorbed from gut, enter bloodstream, and be excreted in urine
In malabsorption, only small quantities will be recovered in urine
Schilling Test
Used to identify cause of vitamin B12 deficiency

Patient ingests radioactive cobalt-labeled vitamin B12 and collects urine for 24 hours
Test is repeated on another day with also ingesting intrinsic factor
Failure to have vitamin B12 recovery in urine in first test confirms B12 deficiency
Ability to recover B12 in second test is indicative of pernicious anemia, failure indicates chronic pancreatitis, bacterial overgrowth, or disease of ileum

Rarely done in US because of cost and unavailability of radio-labeled cobalamin
Celiac Sprue
Affects small intestine
Malabsorption of gluten

Biopsy findings: flat villi in duodenum
Labs: anti-gliadin, anti-gluten, anti-endomysial Ab, anti-reticulum

Weight loss
Diarrhea and bloating after wheat, rye, barley, oat ingestion
Some develop dermatitis herpetiformis (papulovesicular skin lesions - treated with dapsone)

Highest risk in whites
Causes increased risk for development of MALT lymphoma
Tropical Sprue
Malabsorption disorder

Probable infectious etiology
Almost exclusively found in natives or former natives of tropical regions (especially Caribbean)

Chronic diarrhea
Weight loss
Whipple's Disease
Malabsorption disorder
Affects any organ, but primarily intestine, CNS, joints
Etiologic agent: Tropheryma whippelii (type of Actinomyces) - gram positive

Biopsy: PAS positive macrophages in mucosa of small intestine

TX: many acceptable antibiotic regimens
Sulfamethoxazole/trimethoprim (first line)
Penicillin OR ampicillin OR tetracycline (second line)
Any antibiotic therapy has to be administered for at least 4-6 months (preferably for one year)

Cholesterol Stone
Due to high cholesterol that ultimately saturates the bile
Excess cholesterol precipitates out in the biliary system (usually the gallbladder)

Most common type of stone in US
Highest risk is fat, female, over 40, fertile

Mixed Stones
Combination of cholesterol and bilirubin precipitant

Most common type of stone worldwide

Pigment Stones
Stones formed from excess bilirubin
Each stone represents an accumulation of bilirubin, specifically insoluble calcium salts of bilirubin and inorganic calcium

Excess bilirubin is a feature of hemolysis
Gallstones in the gallbladder

Usually asymptomatic
All labs normal
Must be treated surgically in those with porcelain gallbladder or Native Americans (due to increased risk of gallbladder cancer)
Gallbladder infection

RUQ pain
Murphy's sign
Elevated neutrophils and alkaline phosphatase
Ultrasound findings: gallbladder wall thickening, pericholecystic fluid, gallstones
Obstruction of common bile duct

RUQ pain
Clay colored stool
Tea colored urine
Elevated alkaline phosphatase and conjugated bilirubin
Ultrasound finding: dilated common bile duct
Ascending Cholangitis
Infection of common bile duct
Complication of choledocholithiasis

RUQ pain
Clay colored stool
Tea colored urine
Elevated alkaline phosphatase and conjugated bilirubin
Elevated neutrophils

Can quickly ascend to liver and cause life threatening sepsis
Charcot's Triad
For ascending cholangitis

RUQ pain
Primary Sclerosing Cholangitis
Non-infectious inflammation and sclerosis of bile ducts with eventual obliteration of all biliary ducts

RUQ pain
Cirrhosis (later in course)
Elevated conjugated bilirubin and alkaline phosphatase

Highest risk: patients with IBD (especially ulcerative colitis)
Unknown cause
Primary Biliary Cirrhosis
Autoimmune destruction of intrahepatic bile ducts

Positive AMA
Elevated alkaline phosphatase and GGT
Elevated bilirubin (later in course)
Anti-mitochondrial antibody

More common in those with CREST, Sjogren's, type I diabetes
Most patients are women age 35-60