Pathophysiology - Exam 2 Review

7/30/2019 Pathophysiology - Exam 2 Review

1/14

Waqas A. Gil

Pathophysiology Exam 2 - Review

Ch. 6Cell Death

Know the 4 types of injuries to tissueso Adaptation: Change in a cell structure or function in response to changes in the

Environment, meaning the following changes are revertible:i. Physiological: Inc. in size & # of cells (Ex. Uterine changes duringpregnancy)

ii. Pathological: Temporary inc. in size of myocardial (heart) cells (Ex. High BP)o Cell Injury: Caused by any factor that alters cellular structures, like physical injury of the body,

which leads to deprivation ofO2 ornutrients:

Reversible injury (Sub-lethal) & Irreversible injury (Lethal) Classifications: Chemical, Hypoxic (Lack of O2), Free Radical (Oxidative stress or ROS),

Unintentional, Intentional, Infectious agents, Inflammatory

o Ageing: Long-term effects on cells, where general processes, including those that help repair andmaintain the cell, begin to slow down over time.

o Cell Death: Injured cells must repair ordie. The 3 forms of cell-death are:i. Apoptosis:Programmedcell-death (during development)

Cell-shrinkage, budding, Caspases, p53)a. Nuclear: Nuclear/Chromatin margination, non-random DNA cleavageb. Cellular: Shrinkage, apoptotic bodies, membrane-upkeep, buddingc. Biochemical: Caspases/p53/Cyto-C release, ATP upkeep, no inflame

Cytochrome-C is a mitochondrial protein that activates Caspase in thepresence of ATP (which is why Cyto-C is found in Apoptosis, not Necrosis).

ii. Necrosis: Tissue-death (cell/organelle-swelling, loss of membrane integrity) Once Mito function is lost & ATP-levels fall (>30%), the cell will auto-switch from

Apoptosis Necrosis (aka Oncosis).

Na+/K+ pumps will fail, thus causing an imbalance of concentration gradient so thatH2O/Ca

2+will follow Na

+into the cell (cell-swelling).

Swelling of ER/Mito, Blebbing w/out budding, no caspases, high intracellular Ca2+levels (activatesproteases), and has inflammation.

iii. Autophagy: Cellular self-eating (induced by metabolic stress/starvation) Toxicant-dependent: Ca2+ changes, Oxidants, Cisplatin, Cyclosporine Beclin-1: Facilitates formation of autosome by regulating P13K

Measurements: Morph (what it looks like) & Biochemical(how its activated):a. Morphological: Cell-size, Plasma-membrane integrity (wall-strength), and Organelle-

membrane (mitochondria & nucleus) integrity.

b. Biochemical: Leakage of intracellular enzymes & activation of proteins (caspases,p53, proteases).


2/14

Know what cellular adaptation is, different types of cellular adaptation, and examples:o The ability of our cells to adapt to environmental changes to induce

better protection & response to injury & abnormalities.

i. Atrophy: Dec. in cell size (Malnutrition - less ER/Mito, and acidosis) Acidosis: Lactic acid, O2/CO2 imbalance, lysosomal ruptures

ii. Hypertrophy: Inc. in cell size (opposite of, Muscle, kidney, heart) Signals:Mechanical (stretch) & Trophic (growth hormones)

iii. Hyperplasia: Inc. in cell # - Type of dysplasia (Skin/liver calluses) Multi-step processes of inc. cellular division & synthesis

i. Compensatory: Allows healing (Ex. 70% liver-regeneration) Prometheus - Greek myth of eagle eating liver daily.

ii. Hormonal: Physiological in estrogen-dependent organs Ex. Breast-size inc. during pregnancy/puberty

iii. Pathological: Abnormal inc. of cells, receptors, menstruation Ex. Benign prostrate hyperplasia (BPH)

iv. Metaplasia: Reversible replacement of one mature cell by another lessMature/differentiated cell (mixture of cells).

Signal-dependent,potentially cancerous, & re-programs cellsv. Dysplasia: Abnormal change in cell size, shape, org. (like hyperplasia)

Usually found in epithelial cells, close to cancer cells. Know the general types of cellular injuries and examples of each

General Mechanisms: Less ATP, reactive O2 species, Ca2+/permeability alterationi. Hypoxia: Lack of O2 (less air/Hb/RBCs, respiratory disease, Mito. Dysfunction, less ATPedema)

Ischemia (Dec. blood flow clots/edema) & Anoxia (No blood flow) Cellular responses:

a) Dec. in ATP Failure of Na+/K+ pumps and Na+/Ca2+- exchangeb) Cellular swelling Inc. osmolarity of cells (pulls in more H2O)c) Reperfusion Injury Oxidative-stress damage caused by the flow of non-

oxygenated blood to tissues, followed by a surge of O2-rich blood.

ii. Infection: Microbial Pathogenicity (virulence) & Disease-producing potential: Invasion/destruction, Toxin-production, & Hypersensitivity reactions.

iii. Chemical: Induced by all chemicals (drugs) which can lead to injury (its all about dosage/time): Toxicology: Exposure to low doses (Autophagy & Apoptosis), high doses (Necrosis) Begins w/ biochemical interaction b/w chemical & membrane (active/passive) which is what

sets it apart fromHypoxia (begins with dec. in ATP levels).

Mechanisms:Direct toxicity (organelles) & Indirect toxicity (free-radicals) Defense: Cyto-P450 Monooxygenase (ERBioactivation & Detoxification) Offense: CCl4CCl3 + O2, where although its not oxidative, CCl3its still a strong radical

that can induce liver damage Dec. pH Auto-digestion.

iv. Genetic factors: Nuclearor structural alterations (Ex. Sickle-cell anemia, DMD)


3/14

v. Free-radical (ROS): Electrically uncharged (group of) atom(s) w/ unpaired electrons Induce Oxidative-stress (Lipid peroxidation, alternation of DNA & proteins) Unpaired e- causes instability, so it is either given away or paired with another

ROS-formation follows: Initiation, Propagation, Termination Common radicals: O2-& ONOO-, OH-

Free radicals are always present, and terminated w/ anti-oxidants. Know the mechanisms by which free radicals induce injury and how they are terminated

-------------------------------------------------------------------------------------------------------------------------------


4/14

Know the differences between apoptosis, autophagy and necrosis, including differences in nuclear,cellular and biochemical characteristics

Apoptosis Necrosis Autophagosis

Can affect single cells Affects multiple cells

Decrease in cell size (shrinkage) Increases in cell size (swelling)

Organelle function maintained late Organelle function lost early

Plasma membrane integrity

maintained until later phases

Plasma membrane integrity lost

early

Organelle membrane integrity

maintained until later phases

Organelle membrane integrity lost

early

Nucleus dissolvesNuclear structure changes

(shrinks)

Blebs form with organelles Blebs form with no organelles

Chromatin margination No chromatin margination

Non-random DNA cleavage Random DNA cleavage

Little loss of intracellular contents Loss of no intracellular contents

No inflammation Inflammation

Phagocytosis No phagocytosis

Caspase activation No caspase activation

PARP cleavage No PARP cleavage

TUNEL staining No TUNEL staining

Know the mechanisms involved in autophagy, apoptosis, and necrosis If the injury is severe enough, cells will die. Theres 3 ways of dying, however, cell-death leads to

tissue-death, which is always calledNecrosis.

1. Autophagy: Auto-digestion caused by the rupture of lysosomes. This mechanism is cell/toxicant-dependent (Ca

2+, oxidants, cisplatin, cyclosporine)

2. Apoptosis: (Initiation) Intrinsic mechanisms are activated by cell injury, like DNA lesions, which activate P53,

leading to minor pores in the mitochondria. These pores allow Ca2+

and Cytochrome-C to


5/14

enter the Cytosol, where it will activate Caspase-9, which will begin to cleave proteins

throughout the cytosol, exponentially.

Extrinsic mechanisms involve an external signal, like TNF, that binds to an extracellularreceptor, and activates intracellular Caspase-8, which progresses to cleave cytosolic proteins.

(Execution & Phagocytosis)

Cleavage of DNA will be induced by a Caspase who activates DNase by removing itsinhibitor. The DNase will cleave DNA at regular intervals of 180 base-pairs.

Cleavage of the cytoskeleton occurs through Caspase-3, which targets actin fibers, thuscausing the cell to lose its structural integrity. Once this happens, the cell can begin blebbing

with budding, where mitochondria and DNA will fall into these apoptotic bodies (vesicles) as

they bud off of the cell, small enough forphagocytes to digest them. This budding process is

completed at a slow but steady rate to avoid inflammation in nearby cells and tissue.

3. Necrosis: The resultant mechanism of death once ATP levels decline over 30%.Generally, thepresence of cell-membrane damage will always lead to Necrosis.

Necrosis is characterized by the premature death of cells, thus making it more fatal in mostcases. Biochemically, it is understood as the cell failing to maintain ion homeostasis, usuallydue to lowered levels of O2 and ATP. Loss of ER and mitochondrial function lead to lower

levels of ATP, which lowers Na+/K

+-pump activity as well. This leaves Na

+in the cell, thus

causing an influx of H2O/Ca2+

into the cell due to the increased osmolarity. This influx of

water leads to cellularswelling and membrane rupture.

Increased Ca2+ levels lead to the activation ofProteases, which go on to damage cellmembranes, cytoskeletal components, and nuclear chromatids. As the structural integrity is

lost early on, the cell will begin blebbing, but will not bud. Eventually, after organelles have

been deactivated, the plasma membrane will eventually lyse, releasing all cellular contents

into the cytosol at once, thus leading to inflammation of the cell.

(Control) (Apoptosis) (Necrosis)

(Apoptosis & Necrosis)


6/14

Understand the role of caspases, p53 and Ca2+ in cell deatho Caspases: Family of cysteine proteases crucial to Apoptosis that has 15 members in 3 groups:

Initiator: Caspase-2, 8, 9, 10, 12 (Activate executioner-cascade through: Intrinsicpathway: Mito, ER, or Nuclear-mediated Extrinsicpathway: Receptor mediated

Executioner (downstream): Caspase-3, 6, 7 Cytokine: Caspase-1, 4, 5, 13, 14

o P53:Tumor-suppressor protein that mediates cellular processes (growth, death, cycle) Induce Caspases in response to nuclear damage & regulates apoptosis: Help promote apoptotic cell-death, which is why >50% of human cancers are found to have

mutatedP53 proteins, meaning that Apoptosis is more difficult to undergo in cancerous cells.

o Ca2+: Necrotic death used to be associated with Ca2+-overload, not to mention, several Apoptoticfunctions have been found to be dependent on Ca

2+-signaling.

Know the differences in the types of necrotic tissues discussed and examples of each.i. Coagulative: In response to hypoxia, protein-denaturation (kidney & heart)

ii. Liquefactive necrosis: From ischemia (neural cells), soft, liquefies (E.Coli, Strep)iii.

Caseous necrosis: TB pulmonary infection, combines Coagulative &Liquefactive Dead cells disintegrate, but not digested (soft & granular, likeclumped-cheese)

iv. Fat Necrosis: Abdominal organs appear chalky-white as lipases breakdown triglycerides and releasefatty0-acids, so that the acids may recombine w/ Ca

2+, Mg

2+, and Na

+to formsoaps.

v. Gangrenous Necrosis: Death of tissue fromsevere hypoxia, as a result of arteriosclerosis & arterialobstruction.

Dry Gangrene: Coagulative &Wet Gangrene:Neutrophil-driven Liquefactive necrosis(Coagulative) (Liquefactive) (Caseous)

(Fat) (Gangrenous)


7/14

Ch. 11Biology of Cancer

(Dr. Raj Govindarajan)

What is a tumor? Know the differences between benign and metastasized tumors.o A tumor is essentially a new growth (neoplasm)

i. Malignant: Rapid, non-encapsulated, invasive growth that is poorly differentiated with a high mitoticindex, meaning that it can spread over long distances (metastasize)ii. Benign: Slow, encapsulated, non-invasive growth that is well differentiated with a low mitotic index,

meaning that it cannot spread over long distances (metastasize)

Know tumor nomenclature for both benign and metastasized tumors.o Benign: Named based on the tissues that they come from, ending in oma.

Lipoma (lipids), Hepatoma (Liver), Osteoma (Bones), Myoma (Muscles)o Metastasis: Also named based on the tissues that they come from, but w/ some exceptions

Epithelial (Carcinoma), Connective (Sarcoma), Lymphatic (Lymphoma), Blood (Leukemia Carcinoma in situ (CIS): Pre-invasive epithelial malignant tumors that are still in-place,

meaning they havent broken the basement membrane and spread to other tissues just yet.This is the earliest detectable type of growth, for Dysplasia is mutated, but its too small.

(Benign differentiated

Cell w/ irregular lumen(Control) & multiple rows of cells)

(Malignant, well (Poorly differentiated

Differentiated tumor malignant tumor, with no

Membrane has been clear basementBroken) membrane)

(Completely undifferentiated, (Benign tumor)

Anaplastic cell, meaning its

Original cell cantbe traced)


8/14

Normal Adult Stem cells vs. Cancer stem cells: Stem-cell Properties:

i. The capacity to self-renew (daughter-cell maturing to main cell in casemain cell dies)

ii. Its unlimited potential to become any terminally differentiated cell. Undifferentiated cells that can be manipulated to mature into a

particular cell.

o All cells have a small percentage of dormant stem-cells in case of cell-injury, inwhich case they will begin to differentiate to regenerate the tissue. Cancerstem-cell are the dormant stem-cells of a cancer-infected cell. We do not knowwhethercancertakes over a cells stem-cells, or if it induces the synthesis of its

own, but what we do know are particular properties related to these cancer-

related stem cells, regardless of where they originated from. They are: Extremely resistant to chemotherapeutic agents, so while the therapy

may potentially kill 99.9% of cancerous cells, these 0.1% of cancer

stem-cells will survive, and over the course of a few months, can

potentially repopulate the entire tumor with fresh cancer cells! This is why targeting these particular cancer stem-cells has become a

key goal in Oncology.

Understand what a tumor cell marker is and how its used. o Biological markers/substances produced by cancer cells & found on cell

membranes, blood, CSF, or urine (Ex. Hormones, enzymes, genes, & antigens).

o These markers are used to identify, diagnose, & observe the course of tumors. Understand what must go wrong in order for a tumor to form (genes, signaling)

o Cancerous tumors are predominantly caused by ageingcells (most cancers are in older generations).o Cancerouspropertiesinclude those that give selective advantages over its neighbors ( Apoptosis).o Gene Mutations: Can occur in an array of areas, such as:

Growth factors To increase their mitotic index (rapid growth) GrowthreceptorsTo keep it in the On position (unregulated growth) Ras Signaling proteinA ProtoOncogene that is mutated to increase triggering cell division Rb//P53 suppressorTumor-suppressors that are mutated to lose their good-guy properties

Unregulated growth, similar to signal amplification Mutations of growth factors, suppressors, etc work together Angiogenesis: Tumor-mechanism to induce Tumor-growth is proportional to the # of mutations present. the growth of new vessels from surrounding Invasive Carcinoma is what we would refer to as the cancer tissues to bum off of their O2& nutrients.


9/14

6 Hallmarks of Cancer: Know these characteristics of what differentiates cancer-cell functions.

Hallmark combination 1: Shows 8 genes, 2 of which are the same, meaning those 2 genes willcombine to help advanceMetastasis. All 8 of these genes work together to exhibit the 6 cancerous

traits depicted in the circular-diagram.

Hallmark combination 5: Shows the opposite possibility, where only 5 genes will exhibit all 6cancerous traits, since 1 of the genes has dual-traits (sustains angiogenesis & evades Apoptosis).

Know the differences in Oncogenes, Tumor Suppressors, and Proto-genes:o Oncogenes: Mutant genes that

Direct protein synthesis & cellular growth in theirnon-mutantstateo Tumor-suppressors: Anti-Oncogenes

Encode proteins that negatively regulate proliferation in theirnormalstateo Proto-Oncogene:

A normal, nonmutant gene that codes for cellular growth

2 sister-chromatids are combinedthrough gene-translocation.

The result of this was C-Myc&ABL proteins.

The C-Myc is now under the controlof another stronggene-promoter

(immunoglobulin)Oncogene (blue)

ABL is fused from 2 proteins:BCR + ABL ProtoOncogene Can now create more Oncogenes

C-Myc: Gene is intact, promoter switched, whereasACL: Fusion of2 genes


10/14

Understand gene mutations:o Mutation of tumor-suppressor genes: P53

Allows unregulated cellular growth since Apoptosis has been suppressed.o Loss of heterozygosity: d

Both chromosome copies of a gene are inactivatedo Gene silencing

Whole regions of chromosomes are shut off in some, but not all genes.1st hit = The 1st mutation, which results in 1 mutated (blue) gene, and anormal sister-chromatid. This mutation is considered a reversible,heterozygous condition, since it can be repaired.

2nd

hit = The 2nd

mutation, which results in the loss of an entire gene-

pair. ThisLoss of Heterozygosity (LOH) is bad, because you irreversiblylose the function of that gene.

o Exposure to Mutagens: Somatic cells =Non-reproductive cell (22of the 23 chromosomal-pairs are somatic)

May cause tumors in host-organism, but will not pass to next generation. Germline cells = Sex chromosome cells (sperm + oocytes) Vertical transmission

Can transmit mutations to the next generation through meiosis. Know that viruses can lead to cancer:

o Hep-B/C, Epstein-Barr (EBV), Kaposi sarcoma herpes (KSHV), T-cell Leukemia (HTLV)o HPV Horizontal, sexual transmission of Human Papillomavirus from one person to another

Bacterially induced cancers:o Helicobacter Pylori (H. pylori): Chronic infections

associated with: Peptic ulcers, stomach carcinoma, and Lymphoma

of the mucosal region

Gene vs. Environmental factors affecting Cancer progression:o Factors leading to the emergence of cancer are dependent

on location, environment, and gene history.

Understand the role of inflammation in cancer.o Inflammation can lead to the release of cytokines & growth-hormones that will stimulate cell-

proliferation, along with radical-formation.o These mechanisms, although beneficial under normal conditions, will aid the cancerous growth in

metastasizing even further.

Understand risk factors and the cancer types given: The best way to reduce risk is physical activity.o Tobacco: Multipotent carcinogenic mixture linked to cancers of the lung, lower urinary tract, aerodigestive

tract, liver, kidney, pancreas, cervix, uteri, and myeloid leukemia.

The nicotine gets absorbed into the blood, forcing organs like the kidneys and liver to work harderand become exposed, increasing those organs chances for developing cancer.

o Radiation: X-rays, radioisotopes, Gamma-rays Exposure to these emissions has commonly caused cell-death & mutations in the past. Alter gap-junction intracellular communication, leading to depressed info exchange.


11/14

o UV-radiation: Caused basal-cell carcinoma, squamous-cell, and melanoma UV-A: shorter frequency/longer wavelength (Much more invasive and dangerous) UV-B: longer frequency/shorter wavelength (Much less invasive & easy to fix)

o Alcohol consumption: Converted to Acetyl-Aldehydes (acidic) in the body Create RoSs, and increase the chances for oral, throat, and liver cancers.

o Occupational hazards: Carcinogenic agents Asbestos, dyes, rubber, paint (lead), explosives, heavy metals, air-pollution, Radon

o Diet: Xenobiotics Toxic, mutagenic, and carcinogenic chemicals that we obtain from cooking fat, meat, & proteins. Activation: Phase-I activation enzymes ; Defense: Phase-II detox enzymes

o Obesity: Correlates with our BMI, and can lead toHyperinsulinemia, which is a condition where theincreased free-floating fatty-acids cause give rise to the amount of insulin the body Imbalance of proteins

This can give way to colon, breast, pancreatic, & endometrial cancers.

Depicts the interconnectedness of environmental factors and their effects on the body and its internal mechanisms.


12/14

Ch. 12Metastasis & Tumor Spread

(Dr. Raj Govindarajan)

Know what invasion/tumor spread is and its mechanisms. o Direct: Known as local spread of contiguous organs

Local Spread of malignant neoplasms that enter thethin-walled Lymph vessels (easy) + blood vessels.

This process may lead to the spread of metastatic tumorsin several organs (liver, lungs) but not kidneys, due tothe lack of CXCL12 receptors (some preference there).

3Step Theory i. Tumor-cell attachment:

a. Fibronectin/Laminin: Substances thathelp break down the basement membrane

ii. Degradation of the Matrix:Lytic enzymesa. Enzymes: Help create pores to exit from

iii. Locomotion into the Matrix:a. Invadopodia: Foot-like projections

o Metastasis:Spread of cancer cells to adjacent and distant sitesthrough the lymph and blood supply. Implantation:A very rare form of metastatic spread

induced by cross-contamination of other tissues duringsurgical procedures or biopsies.

Phases of Tumor spread:i. Transformation: The process by which a cell is converted into a tumor-cell.

ii. Growth: The progression of a single-cell becoming a clinically detectable mass This growth takes about 30 doublings to become a detectable 1 gram cell.

iii. Local invasion: Proliferation of genetically unstable cells as they accumulaterapid/random mutations and invade local or adjacent cells. iv. Distant metastasis: Tumor growth of heterogeneous cells along with metastasis.

o Anoikis: A specialized form of Apoptosis, where cell-death is dueto the loss of attachment.

When normal cells are detached, they usually die byAnoikis, but cancer-cells evade this process, just like they

evade Apoptosis.

Know the mechanisms how neoplastic cells survive during metastasis.o Neoplastic/Tumor cells mutated P53 proteins not only allow them to avoid Apoptosis and Anoikis,but the mutations that it obtains over time are geared towards adapting to Hypoxic environments, so

even though tumors will eventuallyAngiogenerate their way to nutrition, they are designed to thrive

in uninhabitable conditions, thus aiding in their survival during metastasis.

o They release certain lytic enzymes that help them get into the lymph and blood vessels, so that theycan journey to almost any part of the body and find more suitable conditions.

.


13/14

Know tumor staging nomenclature.o Involves the size of the tumor, degree to which it has invaded, and the extent to which it has spread

i. Stage 1: Cancer is confined to its organ-of-originii. Stage 2: Locally invasive

iii. Stage 3: Regional structuresiv. Stage 4: Distant sites

Know the clinical symptoms of cancer.o Pain:Not associated with early stages of cancer, which is why its harder to detect.

Influences: Fear, anxiety, sleep-loss, fatigue, and muscle loss. Causes: Pressure, obstruction, invasion, stretching, tissue-destruction, inflammation.

o Fatigue: Tiredness, weakness, inability to concentrate, lack of motivation Causes: Sleep disturbance, cytokines, nutrition, environment, level of activity

o Cachexia: Most severe form of malnutrition, present in 80% of cancer patients at death. Includes: Anorexia, anemia, asthenia, taste alterations, altered bodily metabolism.

o Anemia: A decrease in blood-Hb (hemoglobin) levels Mechanism: Chronic bleeding (Fe2+-deficiency), malnutrition, & malignancy in organs.

o Leukopenia & Thrombocytopenia: Direct tumor-invasion to the bone-marrow Causes: Leukopenia/Thrombocytopenia, & worse because chemotherapy is toxic to marrow.

o Paraneoplastic Syndrome: Headaches, migraines, etc (non-definitive symptoms) Symptom-complexes that cannot be explained by local/distant spread of the tumor or by the

effects of hormones released by the tissue from which the tumor arose

o Infection: Risk increases as Neutrophil and Lymphocyte (WBCs) counts drop. Know the different types of general treatments for cancer and their targets.

o Chemotherapy: The use ofnon-selective cytotoxic drugs that are used to target both cancer-cells andnormal cells metabolic pathways, cell-growth, and replication. Goal:To kill enough tumor cells, so that the bodys immune-system can take care of the rest. Compartments:

1. Mitosis & Cytokinesis: Usually takes a day, but happens quicker when cancerouso Targeting tubulin formation would be one way of inhibiting mitosis.

2. Cells enter G1 phase:


14/14

3. Non-dividing cells: Highly specialized, differentiatedcell that will die a natural death Mechanism: Initial exposure to Chemo usually quickly kills the bulk of cancerous cells, but

small % of resistant cells will survive..

Problems: The small percentage of surviving resistant cancer cells has the potential torepopulate the entire tumor.

Types of Chemotherapy:i. Single-agent chemotherapy: Will usually have the largest impact, initially

ii. Combination chemotherapy: Helps with countering resistance development.iii. Principle of dose intensity: Toxicity is an important factor to consider.iv. Therapeutic index:Narrow range of maximal effectiveness vs.minimal toxicityv. Neoadjuvant chemotherapy: Primary chemo used before surgery to help reduce the

bulk to make the surgical removal of tissue easier.

o Ionizing radiation: Aids in damaging the cancer cells DNA Goals: Eliminate cancer w/out excessive toxicity & avoid damage to normal structures.

o Surgery: Biopsy & Lymph-node sampling (sentinel nodes__ ) Debulking or Palliative surgery

o Hormone-therapy: Interferes w/ cell-growth and signaling Through the activation or inhibition of

certain receptors.

o Immunotherapy: In theory, the best way toeradicate tumors Anti-tumor responses are made to

selectively kill cancer cells, while sparing

normal cells.

Meaning you haveselectivity, butnot as much efficacy, which can be

a bad trade-off. Immune-memory is long lived, which is

not that useful in cancer treatments, sincecancers are rarely the same when you

come back for the 2nd

round of treatment.

Numerous immunologic mechanisms arecapable of rejecting different types ofcancer

Biologic response modifiers (BRMs)

o Cancer Side Effects: (Combination Chemotherapy) Gastrointestinal tract Bone marrow Hair and skin Reproductive tract

Documents

Pathophysiology - Exam 2 Review