Preliminary Examination Study Guide:

I. Cell & Its Functions

a. Organization of Cells
b. Cellular Adaptation
c. Progressive types of Cell Injury and Responses
d. Causes & Mechanisms of Cellular injury
e. Cellular Death-Apoptosis & Necrosis
f. Extracellular Fluid
II. Genes & Genetics
a. Phenotype, Genotype & Carrier
i. Phenotype-the observable/outward appearance of the genetics
of an organism “what they demonstrate”
ii. Genotype- the genetic makeup of an organism “what they have”
1. Pt w/ A blood type could be AA or AO; A is the phenotype
AA or AO is the genotype
b. Transcription & Translation
i. On exam: disorder, manifestation (prob turner, Klinefelter's,
down syndrome)
III. Acid Base Balance
a. Distribution of body fluids
i. Intracellular fluid
ii. Extracellular fluid
iii. Interstitial fluid
iv. Intravascular fluid
v. Lymph, synovial, intestinal, biliary, hepatic, pancreatic, csf,
sweat, urine, pleural, peritoneal, pericardial, intraocular fluids
b. Alterations in Na+, Cl- and water balance (Isotonic, Hypotonic &
Hypertonic)
i. Isotonic
1. Total body water change w/ proportional electrolyte
change
2. Isotonic volume depletion
3. Isotonic volume excess
ii. Hypernatremia
1. Serume dofium >147
2. Related to sodium gain or water loss
iii. Hypertonic
1. Water deficit
a. Dehydration
b. Pure water deficits
c. Renal free water clearance
d. Manifestation:
iv. Hypotonic alterations
c. Hyperkalemia, Hypokalemia, Hypercalcemia & Hypocalcemia,
Hypomagnesemia & Hypermagnesemia
i. Hyperkalemia
1. >5.5
2. Rare due to efficient renal excretion
3. Caused by increase intake, shift if k+ from icf, decreased
renal excretion, insulin deficiency, cell trauma
4. Mild attacks: hyperpolarized membrane, causing
neuromuscular irritability: tingling of lips/fingers,
restlessness, intestinal cramping, diarrhea
5. Severe attacks: cell unable to repolarize: muscle
weakness, loss of muscle tone, flaccid, paralysis, cardiac
arrest
ii. Hypokalemia
1. <3.5
2. Causes: reduced potassium intake, increased potassium
entry, increased potassium loss
3. Manifest: mem hyperpolarization causes a decrease in
neuromuscular excitability, skeletal muscle weakness,
smooth muscle atony, dysrhythmias
iii. Hypercalcemia
1. Increases the block of Na+ into the cell
2. Decreased neuromuscular excitability
3. Muscle weakness
4. Increased bone fx
5. Kidney stones
6. constipation
iv. Hypocalcemia
1. Decrease the block of Na+ into cell
2. Increased neuromuscular excitability (partial
depolarization)
3. Muscle cramps
4. Possible question: Diagnosis given findings given ex: a 71
male yo pt came to clinic due to muscle weakness fatigue
and frequent urination lack of appetite. One of his
problems is constipation. Labs show pt has increased
protein, urinalyses. Diagnosis of hypercalcemia. NP is
aware s/s are
a. A hypercalcemia
b. Hypophosphatemia (no constipation w hypo)
c. A and b
d. None of the above
v. Hypermagnesemia
 1. Skeletal muscle depression
2. Muscle weakness
3. Hypotension
4. Respiratory depression
5. Lethargy, drowsiness
6. bradycardia
vi. Hypomagnesemia
1. Associated with hypocalcemia and hypokalemia
2. Neuromuscular irritability
3. Tetany
4. Convulsions
5. Hyperactive reflexes
d. Acidosis & Alkalosis
i. Respiratory acidosis- elevation of PCO2 due to ventilation
depression
ii. Respiratory alkalosis- depression of PCO2 due to alveolar
hyperventilation
iii. Metabolic acidosis- depression of hco3 or an increase in Non
carbonic acids
iv. Metabolic alkalosis- elevation of hco3 usually due to an
excessive loss of meabolic acids
e. Mechanism of edema formation (ON EXAM)
i. Increase capillary hydrostatic pressure
ii. Decrease capillary oncotic pressure
iii. Increase capillary membrane
iv. Lymphatic obstruction
v. Losses/diminishhed production of plasma albumin
IV. Mechanism of Self defense
a. First line of defense, biochemical barriers, normal bacterial flora, etc.
b. Mast Cells, Phagocytosis, Cytokines
c. Vascular response
d. Systemic manifestations of inflammation
e. Healing process (Reconstruction & Maturation)
f. Adaptive Immunity
g. Active vs. Passive Immunity
h. Secretory (Mucosal) Immune system
i. IgE
j. T & B cell-receptor complex
k. Helper T lymphocytes
l. B cell activation
m. Antibody function (Direct & Indirect)
n. Immune Diseases
o. Hypersensitivity (Type I-IV)
 p. Autoimmunity (HIV1; HIV 2; RNA virus;
q. Progression to AIDS
r. Infection: Countermeasures
V. Immunity I
a. Phagocytosis
i. Can ingest and destroy invading organisms and participate in
tissue reactions that “wall off” infection
ii. Phagocytosis is the ingestion of particles
iii. Must distinguish foreign particles from host tissues
1. Appropriate phagocytic targets:
a. May have rough surfaces
b. Lack protective protein coats
c. May be immunologically marked for phagocytosis
by antibodies or complement components that are
recognized by receptors on the phagocytes, this
marking is called “opsonization”
b. Reticuloendothelial System
i. After entering tissues, macrophages become fixed and be
resident for years
ii. They can break away and move to sites of inflammation if
stimulated appropriately
iii. Circulating monocytes. Mobile macrophages, fixed tissue
macrophages, and some specialized endothelial cells for the
Reticuloendothelial system.
iv. Almost all derived from monocytes, comprising a phagocytic
system located in all tissues
c. Specialized macrophages
i. Skin, subcutaneous (histiocytes)
ii. Lymph nodes
1. Ingest / sample particles arriving through the lymph
iii. Alveolar macrophages
1. Digest or entrap inhaled particles and microorganisms
iv. Kupffer cells
1. Surveillance of the portal circulation
v. Macrophages in the spleen and bone marrow
1. Surveillance of the general circulation
d. Neutrophils, macrophages & inflammation

i. Inflammation is driven by chemical mediators and characterized by heat,

redness, swelling, and pain
ii. Physiologically, it involves…
1. Vasodilatation and increased blood flow
2. Increased capillary permeability
3. Coagulation of interstitial fluids
 4. Accumulation of granulocytes and monocytes
5. Swelling of tissue cells
iii. Mediators: histamine, bradykinin, serotonin, prostaglandins, complement
products, clotting components, lymphokines
iv. Tissue macrophages that encounter foreign particles enlarge and become
mobile to provide a first line of defense
v. Within an hour neutrophils migrate to the area in response to
inflammatory cytokines (TNF, IL-1)
vi. Upregulated selectins and ICAM-1 on endothelial cells are bound by
integrins on neutrophils, leading to margination, followed by diapedesis,
and chemotaxis directing neutrophils into the inflamed tissues, to kill
bacteria and scavenge
e. Eosinophils, Basophils

i. •Eosinophils are weak phagocytes and exhibit chemotaxis

1. Particularly important in defense against parasites
2. Can adhere to parasites and release substances that kill them
(hydrolases, reactive oxygen species, major basic protein)
3. Also accumulate in tissues affected by allergies, perhaps in
response to eosinophil chemotactic factor from basophils
(eosinophils may detoxify some products of basophils)
ii. Basophils

1. Similar to mast cells adjacent to capillaries

a. both cell types release heparin
2. Basophils and mast cells both release histamine, bradykinin, and
serotonin
3. When IgE bound to receptors on their surfaces is cross-linked by
its specific antigen, mast cells and basophils degranulate,
releasing…
a. histamine, bradykinin, serotonin, heparin, leukotrienes, and
several lysosomal enzymes
f. Leukopenia

i. low white blood cell count, is usually the result of reduced production of
cells by the bone marrow
1. can allow clinically severe infections with organisms that are not
usually pathogenic
2. Within two days of bone marrow shutdown mucous membrane
ulcers or respiratory infection may occur
3. Causes: radiation, chemical toxins, some medicines
4. In most cases marrow precursors can reconstitute normal blood
cell counts with proper support
g. Leukemias
 i. Uncontrolled production of abnormal white blood cells due to a genetic
mutation
1. Clonal, lineage-specific, often immature cells
2. Leukemias are…
a. Lymphocytic vs. myelogenous
b. Acute vs. chronic (sometimes up to 10-20 years)
3. Leukemias with partially differentiated cells may be classified as
neutrophilic, eosinophilic, basophilic, or monocytic leukemias
ii.

VI. Immunity II
a. Antibodies
i. Activated cells that specifically target and destroy invading
organisms and toxins
ii. POWERFUL: can neutralize 100,000 x lethal dose of some toxins
iii. 2 types of acquired immunity
b. Antigen
i. Substance that elicits an immune response
ii. Unique to every invading organism
iii. Usually proteins or large polysaccharides
iv. Mostly large and have reoccurring molecular groups on their
surfaces
v. Molecular structures that are specifically recognized in acquired
immunity are called epitones
c. Mechanism of action- Antibodies
i. Aggulutination
ii. Precipitation
iii. Neutralization
iv. Lysis
v. Complement activation (ON EXAM)
d. Allergy and Hypersensitivity
i. T cell mediated (delayed)
1. Poison ivy, nickel allergies
2. Usually cutaneous, can occur in lungs with airborne
antigens
ii. IgE mediated (immediate)
1. Typical allergies
2. A single mast cell/basophil can bind 500,000 IgE
molecules
iii. Anaphylaxis
1. Systemic, potentially fatal
2. Widespread vasodilation
3. capillary permeability, volume loss
4. Leukotrienes ---->bronchospasm and wheezing
 a. Tx: epinepherine and antihistamines
VII. Cancer Epidemiology: Genetics & Epigenetics
a. Environmental & Lifestyle factors
i. Tobacco use
1. Cigarette smoking is carcinogenic and the most important risk
factor for cancer.
2. Is linked to cancers of the lung, mouth, lips, nasal cavity and
sinuses, larynx, pharynx, esophagus, stomach, pancreas, kidney,
bladder, uterus, cervix, colon and rectum, ovaries, and acute
leukemia.
3. Secondhand smoke: Environmental tobacco smoke (ETS)
increases the risk for lung cancer.
4. Increases DNA methylation.
ii. Diet

1. Nutrigenomics: Is the study of nutrition on the phenotypic

variability of individuals, based on genomic differences.
2. Primary dietary potential donors of DNA methylation include:
a. Folate, methionine, Betaine, serine, choline, B vitamins.
3. Dietary factors
a. Alter micro-ribonucleic acid (miRNA): Predisposes an
individual to cancer.
b. Suppress cancer stem cell renewal: Decreases the risk of
cancer.
4. Consuming kiwi fruits, cooked carrots, or supplemental co-enzyme
Q10 improves DNA repair.
a. Decreases the chance of
cancer.
5. Xenobiotic chemicals
a. Toxic, mutagenic, and carcinogenic chemicals in food
b. Activated by phase I activation enzymes
i. Primary substance: Cytochrome P-450 family
c. Defense mechanisms
i. Phase II detoxification enzymes (liver) and
antioxidants
d. Glutathione-S-transferases (GSTs): Enzyme housekeepers
that metabolize environmental carcinogens and reactive
oxygen species (ROS)
i. If GSTs are lacking, then the risk for cancer is
higher
e. Diets high in red meats and processed food: Colorectal
cancer
iii. Obesity
 1. Is associated with endometrial, colorectal, kidney, esophageal,
breast (postmenopausal), and pancreatic cancers.
2. Correlates with the body mass index (BMI) .
3. Energy expenditure involves resting metabolic rate, thermic food
effects, and physical activity.
4. Causes a poorer outcome for some cancers.
5. Energy balance may affect:

a. genomic instability
b. dysregulated growth signaling and cellular energetics
c. inhibition of apoptosis and immune surveillance
d. angiogenesis.
6. Increases insulin resistance–producing hyperinsulinemia.
a. Increases the risk of cancers of the colon, endometrium,
and possibly the kidney and pancreas.
7. Insulin promotes insulin-like growth factor 1.
a. Increases the risk for prostate cancer.
8. Adipose tissue secretes adipokines.
a. Increases inflammation.
9. Circadian disruptions may affect cancer growth.
iv. Alcohol consumption

1. Is classified as a human carcinogen.

2. Increases the risk for oral cavity, pharynx, larynx, esophageal,
liver, colorectal, and breast cancers.
3. A combination of cigarette smoking and alcohol consumption
increases a person’s risk for cancer.
v. Physical activity

1. Decreases the risk of cancer.

a. Decreases insulin and insulin-like growth factors.
b. Decreases obesity.
c. Decreases inflammatory mediators.
d. Improves immune function.
e. Increases gut motility.
2. Reduces the risk for breast, colon, and endometrial cancers,
independent of weight changes.
3. After a cancer diagnosis, physical activity is associated with
improved cancer-specific and overall survival with early-stage
breast, prostate, and colorectal cancers.
vi. Infection: Is an important contributor to cancer.

1. Human papillomavirus (HPV): Cervical cancer

2. Hepatitis B and C together: Liver cancer
3. Helicobacter pylori: Stomach cancers
 4. Epstein-Barr virus (EBV): Cancers of the nasopharynx, Hodgkin
disease, and non-Hodgkin lymphoma
5. Human herpes virus type 8: Kaposi sarcoma
6. Human T-cell lymphotropic virus type 1: Leukemia and lymphoma
vii. Sexual and reproductive behaviors and HPVs

1. HPV is the most common sexually transmitted virus.

2. HPV types 16 and 18 cause the majority of cancers.
a. Are associated with cervical and anal cancers.
b. Cause almost one-half of vaginal, vulvar, and penile
cancers.
c. Are recently associated with cancers of the oropharynx
(soft palate, base of the tongue, tonsils).
3. HPV infects epithelial cells.
a. Mutations lead to cancer.
viii. onizing radiation

1. Is emitted from x-ray machines, radioisotopes, and other

radioactive sources.
2. Is associated with acute leukemias; increased frequencies of
thyroid and breast carcinomas; lung, stomach, colon, esophageal,
and urinary tract cancers, and multiple myeloma.
3. Enters cells and randomly deposits energy in tissues.
a. Oncogene activation
b. Tumor-suppressor genes deactivation
c. Chromosomal aberrations and DNA damage
d. Genomic instability
e. Bystander effects
ix. Ultraviolet radiation

1. Causes basal cell carcinoma, squamous cell carcinoma, and

melanoma.
a. Squamous cell carcinoma: Mutation in the TP53 gene
b. Basal cell carcinoma: Mutation in the patched gene
c. Melanoma: Mutation in the p16 gene
2. Principal source is sunlight.
a. Ultraviolet A (UVA) and ultraviolet B (UVB)
b. Promotes inflammation and ROS.
x. Electromagnetic radiation

1. Is a type of nonionizing, low-frequency radiation that results in an

induced electromagnetic field with associated currents inside
tissue.
a. Microwaves, radar, mobile and cellular telephones, mobile
telephone base stations, appliances, power frequency
 radiation associated with electricity and radio waves,
fluorescent lights, computers, and other electric equipment
2. Question: Is electromagnetic radiation carcinogenic, especially for
brain tumors (gliomas)?
a. Conflicting research exists.
xi. Air pollution

1. Air pollution is linked to lung cancer.

2. Outdoor pollution: Ozone and particle pollution
a. Ozone: Is the principle component of smog.
b. Particle pollution: Causes pulmonary inflammation,
oxidative stress and oxidation of DNA, proliferative
response, tissue remodeling with fibrosis, and tumor
development.
3. Indoor pollution
a. Is considered worse than outdoor pollution.
b. Cigarette smoke, radon: Lung cancer
c. Inorganic arsenic: Bladder, skin, and lung cancers

VIII. Cancer
a. Difference between Benign & malignant Cancer
i.

b. Benign tumor classification and moneclature

i. “oma”
1. Lipoma, giloma, leiomyoma, chondroma
ii. Mailgnant tumors
1. Named according to the tissues from which they arrise
a. Malignant epithelial tumors are referred to as
carcinomas
i. Adenocarcinoma and basal cell carcinoma
 b. Malignant connective tissue tumors are referred to
as sarcomas
i. Chondrosarcoma and osteosarcoma
iii. Cancers of lymphatic tissue are lymphomas
1. Cancers of blood-forming cells are leukemias
2. Carcinoma in situ (CIS)
a. Preinvasive epithelial malignant tumors of glandular or
epithelial origin that have not broken through the basement
membrane or invaded the surrounding stroma
c. Tumor markers

i. Tumor cell markers (biologic markers) are substances produced by cancer cells
or that are found on plasma cell membranes, in the blood, CSF, or urine
1. Hormones
2. Enzymes
3. Genes
4. Antigens
5. Antibodies
ii. Can be increased by noncancerous as well as cancerous conditions
1. Screen and identify individuals at high risk for cancer
2. Diagnose specific types of tumors
3. Observe clinical course of cancer
d. 3 Step theory of invasion

i. Tumor cell attachment

1. Fibronectin and laminin
ii. Degradation or dissolution of the matrix
1. Enzymes
iii. Locomotion into the matrix
1. Invadopodia (pseudopodia)
iv.

e. Staging of tumor
i. Involves the size of the tumor, degree to which it has invaded, and extent of
spread
1. Stage 1-Cancer is confined to its organ of origin
2. Stage 2-Locally invasive
3. Stage 3 Regional structures
4. Stage 4-Distant sites
 ii.

IX. Cancer in Children

a. Incidence and type of cancer

i. Most common childhood cancers are leukemias and brain tumors.
1. Most common: Acute lymphoblastic leukemia
2. Most common types of solid tumors: Central nervous system
tumors
ii. Sarcomas and embryonic tumors
1. Embryonic tumors originate during intrauterine life.
2. Immature embryonic tissue is unable to mature or differentiate into
fully developed cells.
3. Embryonic tumors are commonly named with the suffix, -blast.
iii. Most childhood cancers originate from the mesodermal germ layer.

1. This layer gives rise to connective tissue, bone, cartilage, muscle,

blood, blood vessels, gonads, kidneys, and lymphatic system.
iv. Childhood cancers are often diagnosed during peak times of physical
growth.
v. Childhood cancers are usually fast growing and have metastasized
before a diagnosis is made.
vi. Boys are affected more than girls.
vii. Adolescents and young adults

1. Account for 2% of all invasive cancers.

2. Malignancy rate in 15- to 39-year-olds is three times higher than
that in children younger than 15 years.
3. Most common cancers in 15- to 39-year-olds are:
a. Hodgkin lymphoma, leukemia
b. Germ cell tumors
c. Central nervous system tumors
d. Non-Hodgkin lymphoma
e. Thyroid cancer
f. Sarcoma
g. Breast and cervical cancers
h. Melanoma
i. Liver, thyroid, and colorectal cancers