BHS 116.3- Physiology III
Notetaker: Shruti Patel
Date: 5/1/13
Page: 1
Final Exam Review Continued…
Chemical Carcinogenesis
 2 step process:
o 1st step: Initiation (HAS to be the first step)
o Results from exposure to carcinogenic agent
o Irreversible damage to DNA
o Not sufficient for tumor formation
o 2nd step: Promotion
o Can induce tumors from initiated cells
o Promoters are growth factors that trigger transcription
o Need to have presence of promotion in repeated exposures over a period of time
after initiation
o Not tumorigenic by itself. We need both initiation and promotion for the process to
work.
o Is reversible
Viral Carcinogenesis
 DNA viruses
o More common: Epstein-Barr virus triggers Burkitt lymphoma
 RNA viruses
o Human T-cell Leukemia virus Type 1 (HTLV)
 Involved in the pathogenesis of T-cell leukemia/lymphoma
Host Defense Against Tumors
 Our immune system does a great job of destroying cancer cells from the beginning.
 Number of types of antigens that are recognized by our immune system:
o Overexpressed or Aberrantly expressed antigens (tissues that shouldn’t be expressing a
given antigen all of sudden are expressing that antigen…this is sign of tumor)
o Mutated Self Protein
o Antigens resulting from mutations (oncogenes)
o Viral antigens
Anti-Tumor Mechanisms
 All of the cells of the immune system can get involved in this process.
 CD 8+ T-cells will recognize mutated protein expressed on MHC or cancer antigens expressed on
MHC
 Natural Killer cells can recognize lack of MHC-1 that many tumors will trigger OR If there is an
antibody bound to a tumor antigen on the cell surface, we can have antibody dependent cellular
cytotoxicity
 Macrophages will recognize some of the tumor cells and release cytokines to trigger migration
of leukocytes to that site
 B-cells can produce antibodies against those various tumor antigens
Staging of Tumors
 TNM System
BHS 116.3- Physiology III
Notetaker: Shruti Patel
Date: 5/1/13
Page: 2
o

Describes the size of the tumor, the degree of lymph node involvement, and whether it
has metastasized or not.
AJC System
o Divides into stages 0-IV which incorporates the size of the lesion as well as nodal
involvement and metastases.
Congenital Anomalies
 5 types of errors in morphogenesis
o Malformations
o Disruptions
o Deformations
o Sequence
o Malformation Syndromes
 There are periods in fetal development that are more susceptible to things that will disrupt
normal formation of the fetus.
o Fetal period (first 9 weeks): much more sensitive especially weeks 4-5 when organs are
really starting to develop
o Embryonic period
Prematurity and Fetal Growth Restriction
 PPROM (Preterm rupture of placental membranes)
o Anything that causes rupture of placental membranes will trigger premature birth
 Intrauterine infections
Perinatal Infections
 Transcervical (Ascending) Infections
o Infections that are from the reproductive tract that move up to the fetus and cause
infections in the fetus OR fetus can pick this up during the birthing process
o Bacterial in nature
 Tranplacental (Hematologic) Infections
o Carried through the mother’s blood, cross the placenta, and get into the fetus
o Much more common in transplacental
o TORCH viruses (Toxoplasma, Rubella virus, Cytomegalovirus, Herpesvirus, and a number
of Other microbes
Neonatal Respiratory Distress
 Disease of prematurity
 Decreased production of surfactant because the lungs are underdeveloped
 Collapsing of alveoli hypoxemia and CO2 retention leads to other issues with baby
Immune Hydrops
 Early stages of fetal development
 Usually not going to occur during the 1st pregnancy
Sudden Infant Death Syndrome (SIDS)
 If there is underdevelopment of regions in the brain stem (especially arcuate nucleus), the fetus
will succumb to increased body temperature or increased CO2
BHS 116.3- Physiology III
Notetaker: Shruti Patel
Date: 5/1/13
Page: 3
Benign Tumors
 Found in early childhood
 3 most common:
o Hemangiomas (MOST COMMON)—blood vessel tumors
o Lymphangiomas—lymphatic counterpart of the hemangiomas
o Saccrococcygeal Teratomas
 Most of these resolve on their own without any issues.
Malignant Tumors
 3 main systems affected:
o Blood
o Nervous system
o Soft tissues like the muscle
Neuroblastoma
 Most common malignant tumors
 Develop most frequently in the adrenal medulla
Acute Inflammatory Dermatoses
 Urticaria (hives)
o IgE dependent reaction
o Allergic reaction (Type I hypersensitivity)
 Acute Eczematous Dermatitis (Eczema)
o Most common: Allergic contact dermatitis---goes through same mechanism as delayed
type hypersensitivity reaction
Chronic Inflammatory Dermatoses
 Psoriasis
o Type IV Hypersensitivity Reaction (T-cell mediated)
o Overproduction of keratinocytes gives rise to silver-white scales
Blistering (Bullous) Diseases
 Occur primarily due to blisters forming at one of three levels:
o Subcorneal layer
 Fluid buildup beneath the corneal layer
o Suprabasal layer
 Right above the basal layer
o Subepidermal layer
 Right below the basal layer beneath the epidermis and dermis
 Pemphigous Vulgaris
o Suprabasal (fluid accumulation above the basal cell layer)
o Triggered as an autoimmune disease with antibodies produced against Desmoglein-1
and Desmoglein-3. These proteins play a role in binding cells to each other—adherens
junctions between cells. When antibodies bind to them, that disrupts the attachments
and we get fluid buildup at that level
 Bullous Pemphigoid
BHS 116.3- Physiology III
Notetaker: Shruti Patel
o
o
o
o
Date: 5/1/13
Page: 4
Another autoimmune disease
Subepidermal (below the basal cell layer—tighter/stronger blisters)
Antibodies produced against bullous pemphigoid antigens 1 and 2.
Type II Hypersensitivity Reaction
Malignant Epidermal Tumors
 Basal Cell Carcinoma
o #1 tumor associated with sun exposure
o Rarely metastasize to distant tissues
o Malignant forms are more nodular in nature.
 Squamous Cell Carcinoma
o #2 most common skin cancer related to sun exposure
o Well- defined, red, scaling plaques
o NOT the smooth,red, pearly like we see in basal cell
o Malignant tumors are much more nodular in nature and can cause ulcerations
Tumor and Tumor-like Lesions of Melanocytes
 Nevocellular (melanocytic) Nevus (pigmented mole)
o Tan to brown in color, half a centimeter in size, can be flat or dome shaped with welldefined, rounded borders
o Very uniform in color and shape
o 2 main types
 Junctional type: flat
 Compound Type: dome-shaped (raised) uniform in color, rounded appearance
o Dysplastic Nevi
 Combination of the junctional and compound type
 Have additional lamellar fibrosis that develops histologically
 Have target like appearance—darker center (which can be raised) with a lighter
periphery
Malignant Melanoma
 Very irregularly shaped
 Multicolored
 Can have a combo of raised and flat appearance
 Most of them will be greater than a cm (larger than other types of nevi)
2 stages
o 1st stage: radial growth
o Horizontal growth
o Tumor will NOT be metastatic
nd
o 2 stage: vertical growth
o Growth of the tumor deeper into the dermis
o The further below granular cell layer, the greater the metastatic capability of that tumor
Melanoma of the Eye
o Usually occurs in the uvea
o Two cell types
BHS 116.3- Physiology III
Notetaker: Shruti Patel
o
o
Date: 5/1/13
Page: 5
o Epithelioid
o Spindle
Spindle cell dominant lesions are less aggressive and do not tend to metastasize
Epithelioid dominant lesions are much more aggressive and they tend to metastasize later in
their development