pathophysiology

Denver School of Nursing – ADN & BSN ProgramsNo Laboratory component for this class

BIO 206 & 308 – Day 1 CH1– 3 Alteration to Cellular Bio & Genetic Path

Intro’s – Please Share with us: 1) What is your name?2) What city have you resided in the

longest?3) Who or what event influenced you

most to enter the field of nursing?4) What field of nursing do you want to

work in?

5) What is your favorite pathological condition?

For the first “warm up” day of Patho we are going to cover:

1) Cellular Biology - Ch. 1 2) Genes and Genetics Diseases - Ch. 2 3) Altered Cell / Tissue Bio - Ch. 3

This whole chapter is a brief summary and

review from Anatomy and Physiology

LETS See how much you remember…

LETS See how much Cell Bio you remember…

~ What are the metaphors for the following images????

What cellular structure does this represent?

Source: http://news.parcel2go.com


Source: http://googleimages.com


Source: http://www.itchmo.com

The “Circle of Cellular Life”


Source: http://www.itchmo.com


Source: chipotle.com

LETS See how much you remember…

~ What is the diff between Prokaryotes & Eukaryotes?

~ Membrane composition- Why are Proteins / lipids important?- Endoplasmic reticulum- Ribosomes

- Golgi complex- Lysosomes- Peroxisomes- Mitochondria- Cytoskeleton (microtubules + actin)

Source: Huether, McCance Understanding Pathophysiology 4th Ed. 2008

~ What are the diff types of cellular signaling?

~ What are the diff types of cellular signaling?

1) Autocrine2) Paracrine3) Hormonal4) Neurotransmitter5) Neurohormonal secretion6) Diffusion vs Transport

What are the Different types of cellular signaling?


What are the two types of cellular division?

Source: http://www.accessexcellence.org

Source: Houston Biology Project: http://sites.google.com/site/houstonbiologyproject

Source: Indian River State College, http://faculty.irsc.edu/

Image Source: http://www.gilmerfreepress.net

What does the “universal genetic code” mean?

The “universal genetic code” All living organisms use precisely the

same DNA codes (codons – triplets of bases: A, C, T & G) to specify the production of proteins.

(Only exception being mitochondrial DNA)


Codons and AA

Source: University of Leicester: www.le.ac.uk

Source: http://artedi.ebc.uu.se/course/UGSBR/codonusage1.html

1) Transcription – from DNA to mRNA Waiter writes down the order from the customer

(DNA)

2) Gene Splicing (introns and exons) HnRNA into “functional” mRNA via removal of

introns, thus only exons remain.

3) Translation – from mRNA to AA Chain The chef (ribosome) translates the order into the

meal


Figure 2-5 (p. 40)


Mutations “Any inherited alteration of genetic

material.” A massive diversity of Mutations exist:▪ Polymorphisms▪ Point Mutation▪ Base pair substitution*▪ Deletion▪ Insertion▪ Frameshift mutation*▪ Inversion

*Focused on in text book


Mutations▪ Polymorphisms – “many forms” = changing of

genes▪ Point Mutation = Base pair substitution – 1 base

pair replaces another▪ Frameshift mutation – Insertion or deletion of

base pairs (as long as not a multiple of 3) causing a shift in the “reading frame” thus causing a huge alteration in AA sequence.▪ Inversion – an entire section of DNA is reversed


Mutations

Source: http://www.genetichealth.com

Point MutationA point mutation is a simple change in one base of the gene sequence. This is equivalent to changing one letter in a sentence, such as this example, where we change the 'c' in cat to an 'h':

Original The fat cat ate the wee rat.Point Mutation The fat hat ate the wee rat.

Mutations


Insertion Mutations that result in the addition of extra DNA are called insertions. Insertions can also cause frameshift mutations, and general result in a nonfunctional protein.

Original The fat cat ate the wee rat.Insertion The fat cat xlw ate the wee rat.

Mutations


Deletion Mutations that result in missing DNA are called deletions. These can be small, such as the removal of just one "word," or longer deletions that affect a large number of genes on the chromosome. Deletions can also cause frameshift mutations. In this example, the deletion eliminated the word cat.

Original The fat cat ate the wee rat.Deletion The fat ate the wee rat.

Mutations


Insertion Mutations that result in the addition of extra DNA are called insertions. Insertions can also cause frameshift mutations, and general result in a nonfunctional protein.

Original The fat cat ate the wee rat.Insertion The fat cat xlw ate the wee rat.

Mutations


InversionIn an inversion mutation, an entire section of DNA is reversed. A small inversion may involve only a few bases within a gene, while longer inversions involve large regions of a chromosome containing several genes.

Original The fat cat ate the wee rat.Insertion The fat tar eew eht eta tac.

Mutation Mutagens – agents that increase the

frequency of mutations. ▪ EX) radiation, nitrogen mustard, vinyl chloride,

alkylating agents, formaldehyde & sodium nitrite.

Spontaneous mutations (mutation in absence of mutagens) are very rare events.


Polyploidy Euploid Cells – cells with multiple of the

normal number of chromosomes (greek eu = good / true)▪ Gametes Euploid = Haploid▪ Somatic Cells = Diploid▪ > Diploid = Polyploid▪ Interestingly, some liver, bronchial and epithelial tissues

are physiologically polyploid.▪ However a zygote that is triploidy or tetraploidy will

spontaneously abort, or rarely be stillborn. (Triploidy 1:10,000 births)

.Source: Huether, McCance Understanding Pathophysiology 4th Ed. 2008

Aneuploidy A cell that does not contain a multiple of 23 chromo’s▪ Trisomic / Trisomy = 3 copies of one chromosome▪ Often survivable (13, 18, 21 / Trisomy 21 causes what disease?

Trisomy 16 leading cause of trisomy abortuses yet incombatable with life thus not seen in live births)

▪ Monosomy = the presence of only one copy of a given chromosome in a diploid cell.▪ Monosomy of ANY chromosome is lethal ( Generally “Loss of genetic

material induces a much greater consequence than duplication of genetic material”)

▪ Usually a consequence of nondisjunction during meiosis (Text book says also in Mitosis – which is FALSE)

.


Aneuploidy Partial trisomy – an extra portion of a

chromosome is present in each cell. (Less severe consequences)

Chromosomal Mosaics – the body has two or more different cell lines (Thus different karyotypes in different cells of the same organism / patient)

.


Examples of Aneuploidy (In Somatic Chromosomes)

Trisomy 13 – Patau Syndrome▪ One in 10,000 live births

Trisomy 18 – Edwards Syndrome▪ One in 3,000 live births (Increases with maternal age)

Trisomy 21 – Down syndrome▪ Women < 30 y/o risk of 1:1,000 = 0.1%▪ Women > 35 y/o risk of 1:1,000 = 0.1%▪ Women > 45 y/o risk of 3% - 5%


Trisomy 13 – Patau Syndrome

Source: Lucina Foundation: http://www.lucinafoundation.org

Some physical characteristics are flattened facial features, malformed and low-set ears, cleft lip and/or palate, prominent heels, and genital malformations. Often there are problems with the nervous system, including forebrain development, spinal cord development, mental retardation, and seizures. Vision and eye problems are common, as well as respiratory and heart defects. Approximately 45% of Patau syndrome babies die within the first month of life, while the number increases to 70% in the first 6 months.

Trisomy 18 – Edward Syndrome


Patients with trisomy 18 can range from mildly to severely affected. Some characteristics of this syndrome are clenched hands, shield chest with short sternum, short neck, and small jaw. Heart defects are typical of trisomy 18, including ventricular septal defects, atrial septal defects, and coarctation of the aorta. Also common are omphaloceles (externalized GI) and renal pathology

Trisomy 21 – Down Syndrome


Down syndrome is a chromosomal disorder which causes physical and intellectual delays in development and occurs when there are 3 chromosome 21's, resulting in 47 total chromosomes instead of the normal 46. The most common clinical features are short neck and flat face, upward slanting eyes, low muscle tone and a single crease across the palm of the hand. Congenital heart defects accompany Down syndrome in about 40% of the cases. Vision and hearing problems are also common.

Examples of Aneuploidy (In Sex Chromosomes)

Trisomy X – Most Common Aneuploidies Effect 0.1% births▪ Triplet of X in all cells. No physical abnormalities. Do have sterility,

menstrual irregularity and sometimes MR. (5 or > X increases MR, and introduction of physical defects)

Monosomy X – Turner Syndrome▪ Results in a total of 45 chromosomes. (45,X) ▪ 15-20% of spontaneous abortions, only 0.5% survive to term. If

survive, short stature with pathoneumonic webbing of the neck, widely spaced nipples, reduced carrying angle, Also aortic coactation is common, usually sterile but with no MR.

Klinefelter Syndrome (47,XXy) ▪ Moderate MR, Have general male appearance but usually sterile,

with gynecomastia and incomplete secondary male maturation. Long limbs also common. 1:1,000 male births, Increased freq q Materal age.


Mode of Inheritance – the pattern in which a genetic disease is inherited through generations. Usually studied via pedigree charts.

1) Autosomal Recessive

2) Autosomal Dominant

3) X – Linked Recessive

4) X – Linked Dominant

.



1) Autosomal Recessive ▪ A genetic mutation (or allele) present on one of the 23 autosomes▪ If one mutation then - genotype = ?

- phenotype = ?

▪ If two mutations then - genotype = ?- phenotype = ?

2) Autosomal Dominant▪ A genetic mutation (or allele) present on one of the 23 autosomes▪ If one mutation then - genotype = ?

- phenotype = ?

▪ If two mutations then - genotype = ?- phenotype = ?



1) Autosomal Recessive ▪ A genetic mutation (or allele) present on one of the 23 autosomes▪ If one mutation then the genotype would be rN – phenotype =

normal + silent “carrier”▪ If two mutations then genotype would be rr – phenotype =

presentation

2) Autosomal Dominant▪ A genetic mutation (or allele) present on one of the 23 autosomes▪ If one mutation then genotype would be Dn – phenotype =

presentation thus NO “carrier”▪ If two mutations then genotype would be DD – phenotype =

presentation



3) X – Linked Recessive ▪ A genetic mutation (or allele) present on the X chromosome▪ If Female + one mutation: -genotype/ phenotype = ??▪ If Female + two mutations: -genotype/ phenotype = ??▪ If Male one mutation -genotype/ phenotype = ??

4) X – Linked Dominant▪ A genetic mutation (or allele) present on the X chromosome▪ If Female + one mutation: -genotype/ phenotype = ??▪ If Female + two mutations: -genotype/ phenotype = ??▪ If Male one mutation -genotype/ phenotype = ??



3) X – Linked Recessive ▪ A genetic mutation (or allele) present on the X chromosome▪ If Female + one mutation results in genotype Xx, phenotype “carrier.“▪ If Female + two mutations results in genotype xx, phenotype of disease▪ If Male one mutation = genotype xY + phenotype presentation▪ Male could not have two X chromosomal mutations

(unless what disease is present?)

4) X – Linked Dominant▪ A genetic mutation (or allele) present on the X chromosome▪ If Female + one mutation results in genotype Xx, thus phenotype of

disease▪ If Female + two mutations results in genotype XX, also phenotype of

disease▪ If Male one mutation = genotype XY + phenotype presentation


Of Course, in reality it is much more complicated:

Polygenic Traits▪ Phenotypic traits that result from the genotype of multiple genes all

acting together to produce a complex cumulative effect.

Multifactorial Inheritance▪ When environmental factors influence the expression of the trait.

Most traits are multifactorial. The textbook sites height and IQ as more complicated phenotypes that are determined and influenced by genotype and the infleuence of environment as well.

Empirical Risks▪ Is the probability of disease not based on punnet squares and

calculations but instead is the probability of disease based on direct observation of patient samples over time.


Source: http://www.answersingenesis.org

Source: http://googleimages.com

Review of Terms: Atrophy Hypertrophy Hyperplasia Metaplasia Dysplasia Hypoxia

▪ Which of these above are physiologic vs pathologic??


Source: Cervical Cancer Study by http://www.colposcopy.org.uk

Source: Fetal and Neonatal Journal - http://fn.bmj.com

Source: http://basicpathology-histopathology.com

Table 3-1: Adaptation – atrophy, hypertrophy, hyperplasia &

metaplasia

Active Cell Injury – Immediate response of the entire cell.▪ a) Reversible – Loss of ATP, cellular swelling, detachment of

ribosomes, autophagy of lysosomes.▪ b) Irreversible – “Point of no return” structurally when severe

vacuolization of the mitochondria occurs and calcium moves into the cell.

▪ c) Necrosis – common type of cells death with severe cell swelling and breakdown of roganelles

Apoptosis – “Programmed Cell Death” physiologic cellular self destruction for elimination of unwanted cell populations.

When there is a problem or lack of apoptosis what disease develops?


Table 3-1: …continued…

Chronic cell injury – subcellular alterations▪ Persistent stimuli response may involve only specific

organelles or cytoskeleton (ex-phagocytosis of bacteria)

Accumulations or Infiltrations▪ Water, pigments, lipids, glycogen, proteins

Pathologic Calcification▪ Dystrophic and metastatic calcification

.Source: Huether, McCance Understanding Pathophysiology 4th Ed. 2008

Apoptosis: is the active process of “programmed cell death”

An average adult will produce 10 BILLION new cells – and also kill off 10 billion cells, to be recycled and renewed.

Apoptosis – Occurs from embryologic development through old age, to regulate and provide physiologic homeostasis.▪ Physiologic Apoptosis Responsible for local deletion of cells during

tissue turnover and normalembryonic development. Also seen in normal endocrine regulated atrophy.

▪ Pathologic Apoptosis is the result of intracellular events or adverse exogenous stimuli.

Examples:▪ Viral Hepatitis C will cause massive portions of the liver to undergo apoptosis.▪ Apoptosis in hemopoietic cells is linked to the production of free radicals and can

spontaneously occur in some malignant turmors as well as what occurs id cells that undergo ionizing radiation and chemotherapy


Source: http://www.microbiologybytes.com

Apoptosis: is the active process of “programmed cell death”

Source: http://ghr.nlm.nih.gov

Absence of apoptosis will cause serious pathologic change.

A mutation in a gene (Example bcl-2) that promotes apoptosis, will then allow the cell to proliferate uncontrollably = cancer.

Know the difference between: (Muy importante mis amigos…)▪ Tumor suppressor genes▪ Onchogenes

Apoptosis – is often performed from initial signal to termination of a cell in only a few minutes. Thus it can be difficult to quantify or visualize rate of apoptosis occurring.▪ Karyohexis = fragmentation and destruction of the nucleus▪ Karyohexis is the primary marker for apoptosis


Day 2 of Patho will focus on Oncology

CH 9 – Biology of Cancer and Tumor Spread

CH 10 – Cancer Epidemiology, Manifestations & TX

Lets start with our baseline knowledge…

What do you know about cancer?

Who does it primarily effect?

Why?

Critical Terminology:1) Tumor

2) Neoplasm

3) Benign

4) Malignant

5) Metastasis

Critical Terminology: Definitions from Huether, Understanding Patho.

1) Tumor – originally defined swelling now refers to new growth

2) Neoplasm – new growth

3) Benign – usually well encapsulated and well differentiated, retain some normal tissue structure and do not invade or spread to distant locations.

4) Malignant – rapid growth rates and specific microscopic alterations, including loss of differentiation; absence of normal tissue organization; lack of capsule; invasion into blood vessels,

lymphatics, and surrounding structures; and distant spread.

5) Metastasis – distant spread of malignant tumor

Critical Terminology: Definitions from Robin’s, Patho of Basic Disease.

1) Tumor – new growth of tissue from genetic changes that allow excessive and unregulated proliferation thus becoming autonomous.

2) Neoplasm – is an abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of the normal tissues and persists in the same excessive manner after cessation of the stimuli which evoked the change

3) Benign – microscopic and gross characteristics are considered “relatively innocent,” implying that it will remain localized, is generally amenable to local surgical removal, and patients generally survive.

4) Malignant – implies that the lesion can invade and destroy adjacent structures and spread to distant sites (metastasis) and cause death.

Pathologically all tumors have two basic components:

1) Parenchyma – constituted from the clonal neoplastic cells

2) Stroma – the reactive supporting tissue for the parenchyma (CT, vasculature, and variable macrophages and lymphocytes)

Source: Robins Pathologic Basis of Disease 8th Ed. 2010

Benign Tumors – designated with suffix – omaexamples: fibroma

chondromameningiomalipoma

Note – nomenclature for benign epithelial tumors is more complicated

Malignant TumorsFrom Germ layer Origin are called carcinomas

ex) Squamous cell carcinoma, adenocarcinomaFrom Mesenchymal tissue are called sarcomas

ex) fibrosarchoma, chondrosarchoma, rhabdomyosarcoma


Malignant TumorsA majority of the time it is clear that benign and malignant neoplasms within the parenchymal cells were derived from a single cell and thus bear a close resemblance to each other.

Important exceptions:

1) Mixed Tumors

2) Teratomas


Malignant Tumors

Important exceptions:1) Mixed Tumors – divergent differentiation of a single neoplastic clone along two lineages will create a “Pleomorphic adenoma”

2) Teratomas – neoplasm containing recognizable mature or immature cells / tissues representative of more than one germ cell layer and sometimes all three. Origination from totipotential cells (usually ovarian or testicular), yet sometimes present from “embryonic rests.” Teratomas have the capacity to differentiate into any of the cell types found in the adult body. Benign and Malignant teratomas exist based on differentiation.



A = AsymmetryNormal moles or freckles are completely symmetrical. If you were to

draw a line through a normal spot, you would have two symmetrical halves. In cases of skin cancer, spots will not look the same on both sides.

B = BoarderA mole or spot with blurry and/or jagged edges.

C = ColorA mole that is more than one hue is suspicious and needs to be

evaluated by a doctor. Normal spots are usually one color. This can include lightening or darkening of the mole.

D = DiameterIf it is larger than a pencil eraser (~1/4in or 6mm), it needs to be

examined by a doctor. This includes areas that do not have other abnormalities.

E = ElevationIf mole is raised above the surface of the skin or if it has an uneven

surface.

What is the most important parameter of all oncology screening???

What is the most important parameter of all oncology screening.

Relative Change within a single patient

Oncogenes “Are mutant genes that in their normal

nonmutant state direct synthesis of proteins that positively regulate (accelerate) proliferation.”

Tumor-Supressor Genes“Encode proteins that in their normal

state negatively regulate (put the brakes on) proliferation.”

Oncogenes ex) MYC protooncogene on chromo 8Normally turned on in proliferating

lymphocytes and turned off in mature lymphocytes.

Translocation of myc t(8;14) Ig gene has high levels of translation in mature lymphoctes, thus the Ig promotor is now regulates and increases myc production, thus causing Burkitt lymphoma.

(N-myc – gene detected in human neuroblastoma cells)

Tumor-Supressor Genesex) Retinoblastoma (Rb) gene, normally

strongly inhibits the cell division cycle. When it is inactivated, the cell division cycle can proceed unchecked. Rb is mutated in retinoblastoma (obviously) but also in many lung, breast and bone cancers.

p53 = The “Guardian of the Human Genome”

The p53 protein is a tumor suppressor encoded by a gene whose disruption is associated with approximately 50 to 55 percent of human cancers. The p53 protein acts as a checkpoint in the cell cycle, either preventing or initiating programmed cell death. Since cancer is the unchecked proliferation of cells, p53's role is critical

p53 = The “Guardian of the Human Genome”The p53 molecule can be inactivated in several ways. In some human families, for example, p53 mutations are inherited, and family members have a high incidence of cancer. More often, the molecule is inactivated by an outside source. DNA tumor viruses, such as the human adenovirus and the human papilloma virus, can bind to and inactivate the p53 protein function, altering cells and initiating tumor growth. In addition, some sarcomas amplify another gene, called mdm-2, which produces a protein that binds to p53 and inactivates it, much the way the DNA tumor viruses do.

Source: Genentech Bio-oncology http://www.biooncology.com


NRP1 is a growth factor receptor that is important for promoting vascular growth and maturation. Anti-NRP1 is a monoclonal antibody designed to target NRP1 and inhibit angiogenesis and the subsequent vascular maturation that is necessary to form the functional vasculature that supports tumor growth


Net decrease in vascular maturation and vessel sprouting with combination TX of Anti-VEGF, Anti-NRP1, Anti-EGFL7


Another mechanisms of oncogenesis is the permanent activation of telomerase which inhibits natural cell death via programed loss of the telomere in each mitotic division. (Fig 9.11)

CH 10 – Cancer Epidemiology, Manifestations & TX

Source: Cancer Statistics, 2008. CA Cancer Journal Clinical Medicine 58:2, 2008

Females Males 26% - Breast 25% - Prostate 14% - Lung 15% - Lung10% - Colon & Rectum 10% - Colon & Rectum6% - Uterine 7% - Urinary & Bladder4% - Melanoma of Skin 5% - Non-Hodgkin lymphoma4% - Thyroid 5% - Melanoma of skin23% - Other 20% - Other


Females Males 26% - Lung 31% - Lung15% - Breast 10% - Prostate9% - Colon & Rectum 8% - Colon & Rectum6% - Pancreatic 6% - Pancreatic6% - Ovarian 4% - Esophageal3% - Leukemia 4% - Liver2% - Brain 4% - Leukemia25% - Other 24% - Other


Female Incidence Female Death26% - Breast 26% - Lung

14% - Lung 15% - Breast

10% - Colon & Rectum 9% - Colon & Rectum6% - Uterine 6% - Pancreatic

4% - Melanoma of Skin 6% - Ovarian

4% - Thyroid 3% - Leukemia23% - Other 25% - Other


Male Incidence Males Deaths25% - Prostate 31% - Lung15% - Lung 10% - Prostate9% - Colon & Rectum 8% - Colon & Rectum7% - Urinary & Bladder 6% - Pancreatic5% - Non-Hodgkin lymphoma 4% - Esophageal5% - Melanoma of skin 4% - Liver4% - Kidney 4% - Leukemia25% - Other 24% - Other


Mutations or chromosomal aberrations are shown as filled circles and apparently normal cells as open circles.

A, If a cell faithfully repairs DNA damage, then its clonal descendents will appear normal.

B, If a cell is directly mutated by radiation, then all its descendents will express the same mutation.


C, Radiation-induced genomic instability is characterized by nonclonal effects in descendant cells.

Source: National Cancer Institute http://www.cancer.gov

Primary CA TX options:1)Chemotherapy – Chemical destruction of cellular proliferation (8 major types)2)Radiation Therapy (In 2009 1.47 Million Americans were diagnosed with CA and 60-75% received radiation therapy)

a. Proton Therapyb. Brachytherapy (Internal Radiation Therapy)

3)Surgerya. Excisionb. Cryosurgery

4)Immunotherapy (Hematopoietic GF, INF’s, IL’s, Mono’s, Ovarian CA Vac)5)Angiogenesis Inhibitors6)Bone Marrow Transplantation7)Gene Therapy8)Laser Treatments

a. Gama Radiationb. Photodynamic Therapyc. Hyperthermia (Tissue destroyed via raising temp to 113F)

Source: National Cancer Institute http://www.cancer.gov

Vaccine for Ovarian CA:1)In 2008, Dr. Sybilann Williams, a gynecologic oncologist and surgeon of CTCA, began a research study with Dr. David Berd of National Director of Immunotherapy, to develop and evaluate the efficacy of personalized ovarian cancer vaccines for women with Chemo Resistant, advanced-stage disease.

2)First exploratory surgery is performed (sometimes called “debulking surgery”) during which a cancerous tissue sample is obtained then a patient specific “vaccine” is created to develop and then delivery antibodies against the individual tissue specific ovarian CA.

3)Chemotherapy is halted and vaccine is delivered via IM injection over 8 week period of time during which the patient is closely monitored via PE, CT, and blood work for any progression of the CA, which if is detected the vaccine is DCed and Chemo is resumed.

Source: Cancer Treatment Centers of America http://www.cancercenter.com

Chemotherapy:1)Chemoembolization - Chemoembolization allows high doses of chemotherapy drugs to be targeted directly to the cancerous tissue for a longer period of time, without exposing the entire body to the effect of the drugs.

*Primarily for Hepatic tx. Secondarily: Prostate, Breast, Colorectal

1)Chronotherapy - drug-specific research to track a variety of symptoms and discover when tumor tissues may be most sensitive to the chemotherapy drugs. Time sensitive delivery based on specific patient and CA type.

* No specified type of CA

2)HIPEC – Hyperthermic Intraperitoneal Chemo, surgical oncologist removes as much cancerous tissue as possible, then a chemotherapy solution circulates through the abdomen for approximately 90 minutes.

* Colorectal or Ovarian CA

•IAC – Intra-Arterial Chemo, angiogram guided percutaneous delivery of Chemo.

* Hepatic or Pancreatic CA

Source: Cancer Treatment Centers of America http://www.cancercenter.com

Chemotherapy:5) Intraperitoneal Chemo - directly targets cancer cells in the abdomen, minimizing drug exposure to healthy tissues. *Primarily for Ovarian CA

6) Intrathecal Chemo – spinal tap, or intracranial delievery of tx directly into the CSF* CA of the CNS, Leukemis, or lymphoma

7) Intratumoral Chemo – delivery of tx into the lung tissue*Non small cell lung CA

8) Metronomic Chemo – designed for patients that cannot tolerate full dose chemo, thus they receive titrated partial dose treatments.*Not CA type specific

… of Pathopysiology!!

Remember to…

KEEP UP WITH YOUR:

1) Text READING2) Powerpoint Review3) Study Guide / Evolve Prep

pathophysiology

Documents

cellular biology

comwhat cellular structure

diff types of cellular

different types of cellular

types of cellular division

eduimage source

university of leicester

cell bio