Exam 3 Flashcards

1
Q

What does the word Lentigo mean?

A

small, pigmented spots on the skin with a clearly-defined edge and surrounded by normal-appearing skin

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2
Q

What is meant by the word nevus?

A

Melanocytic nevi are nests of multi-layered melanocytes found in moles.

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3
Q

What characteristics indicate that a nevus may be dysplastic?

A
ABCD
Asymmetric
Borders (irregular)
Color (varied)
Diameter (increasing size)
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4
Q

What can Acanthosis Nigricans be an indication of?

A

Acanthosis nigricans can be indicative of hyperinsulinemia (associated with obesity but rarely with malignancy).

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5
Q

What is the sign of Leser-Trelat?

A

Sign of Leser-Trelat is the sudden development of multiple lesions, possibly accompanying an underlying malignance. Seen in seborrheic keratosis where there is a “stuck-on” appearing of keratin-filled epidermal pseudocysts.

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6
Q

What are the tests called you can use on physical exam to evaluate for Psoriasis and Pemphigus?

A

Psoriasis - Ausptiz Sign - removal of a scale that results in pinpoint bleeding
Pemphigus - Nikolski’s Sign - manual force to break blister indicates pathology (Microscopically, net-like patterns of IgG between epidermal keratinocytes create bullae, disrupting cellular adhesions

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7
Q

What is the relationship between topical steroids and Tenia infections of the skin?

A

Topical steroids are NOT used in conjunction with antifungals
This decreases the efficacy of the antifungal because corticosteroids suppress the immune system; although provides immediate relief of symptoms for the patient.

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8
Q

What is the difference between Erythema Nodosum and Erythema Multiforme?

A

Erythema multiforme is a hypersensitivity skin reaction to infections or drugs. It is characterized by vesicles, bullae, and “targetoid” erythematous lesions (like Lyme). Stevens - Johnson Syndrome is the most severe form, characterized by extensive involvement of skin and mucous membranes. Erythema nodosum causes raised, erythematous, painful nodules of subcutaneous adipose tissue. Sometimes it is associated with granulomatous diseases and strep.

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9
Q

What layers are involved with the following: BCC, SCC, Melanoma

A

Squamous Cell Carcinoma (SCC) is characterized by nests of atypical keratinocytes that invade the dermis. They rarely metastasize and complete excision is usually curative. Rapidly-growing, dome- shaped nodules with a keratin-filled center are indicative of keratoacanthoma.
Basal Cell Carcinoma (BCC) is the most common tumor in the western world. Typically only locally invasive and characterized by a pearly borders and papules; arises from basal cells of hair follicles. Invasive nests of basaloid cells with a palisading growth pattern.

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10
Q

Define pathology.

A

the study of the essential nature and characteristic of disease (S&S, complications, pathogenesis, etc).

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11
Q

Define disease.

A

impairment of the normal states (known from distinguishing S&S, etc).

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12
Q

Define homeostasis.

A

he maintenance of a harmonious environment within the body.

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13
Q

Define morbidity.

A

sequelae/effects of a disease.

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14
Q

Define Comorbidity.

A

property of a disease that gives it a specific virulence/ sequelae.

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15
Q

Define Iatrogenic.

A

doctor-acquired.

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16
Q

Define idiopathic

A

we don’t know the cause.

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17
Q

Define signs and symptoms.

A

Symptoms are subjective and according to what the patient may feel.
Signs are objective and what the doctor observes.

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18
Q

Define subclinical.

A

he immune system is doing its job and taking care of the infection - not clinically detectable.

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19
Q

Define illness.

A

unhealthy condition of the body or mind (sickness/disease).

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20
Q

Define etiology.

A

underlying cause of disease.

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21
Q

Define pathogenesis.

A

course that a disease takes from start to finish.

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22
Q

Define morphology.

A

the presence/conformation of damaged cells and tissues from the infection.

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23
Q

Define functional disease.

A

what happens when we know the disease exists, but have not discovered any gross or microscopic morphologic changes at this time.

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24
Q

Define syndrome.

A

group of signs and symptoms that occur together and characterize a particular abnormality or condition.

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25
Q

On an H&E stain, what structures turn blue, and which red?

A

Eosin stains the cytoplasm, RBCs, and collagen pink-red. Hematoxylin stains nuclei and bacteria to blue-purple.

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26
Q

Cellular injury can cause necrosis or apoptosis, know the difference between the two.

A

Necrosis is cell death characterized by inflammation and dead tissue
Apoptosis is programmed cell death, regulated by genes, not involving inflammatory response

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27
Q

What are common causes of cellular injury?

A

Hypoxia is the most common cause of cellular injury, resulting in the inability to synthesize sufficient ATP by aerobic oxidation (ie ischemia).
Infections cause injury by direct infection, toxins, and inflammatory responses of the host. Immunologic reactions
congenital disorders
chemical injury
physical injury - anorexia, obesity/excessive caloric intake.

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28
Q

What disease may be caused by vit A deficiency?

A

squamous metaplasia, immune deficiency, night blindness

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29
Q

What disease may be caused by vit C deficiency?

A

scurvy

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30
Q

What disease may be caused by vit D deficiency?

A

rickets and osteomalacia

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31
Q

What disease may be caused by vit K deficiency?

A

bleeding diathesis (used in clotting cascade)

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32
Q

What disease may be caused by vit B12 deficiency?

A

megaloblastic anemia, neuropathy, spinal cord degeneration

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33
Q

What disease may be caused by vit B9 (folate) deficiency?

A

megaloblastic anemia and neural tube defects

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34
Q

What disease may be caused by vit B3 (niacin) deficiency?

A

pellagra (diarrhea, dermatitis, dementia, and death)

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35
Q

When does cloudy swelling occur?

A

Cloudy swelling occurs when intracellular proteins accumulate in the serum; leaking occurs due to hypoxia and other forms of cellular degeneration. AST, ALT, ferritin, AP, GGT with liver; CK-MB, LDH, troponin T in heart. Cellular swelling occurs when cells are incapable of maintaining ionic and fluid homeostasis. There is a decreased ATP concentration and Na-pump activity, causing Na, Ca, and water to accumulate intracellularly.

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36
Q

Where do free radicals come from?

A

Many free radicals are oxygen-derived; processes such as UV light, metabolism, inflammation, smoking, ionizing radiation, and air pollution also create free radicals.

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37
Q

Describe the basic pathway in an injured cell that begins with mitochondrial dysfunction and leads to cellular swelling

A

Mitochondrial dysfunction leads to a decrease in oxidative phosphorylation and decreased in ATP, making the mitochondria highly permeable, releasing cytochrome c, triggering apoptosis. The Na/K ATPase pumps start to fail, causing influxes of Na and water, efflux of K, cellular and ER swelling. Other nuclear changes: pyknosis is the degeneration and condensation of nuclear chromatin; karyorrhexis is nuclear fragmentation; karyolysis is the dissolution of the nucleus

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38
Q

What is the significance of anaplasia, what are the two chief findings of anaplasia?

A

De-differentiation of cells is anaplasia and will show a “brick-like” pattern and a dramatic increase of the nuclear:cytoplasmic ratio.

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39
Q

What is the difference between primary, secondary, and tertiary (delayed closure) intentions

A

Primary - approximate wound edges and close; decreases scarring and heals well.
Secondary - wound edges do not become approximated and become filled with granulous tissue and fibrin.
Tertiary (delayed) - keep open for a period of time in order to prevent infection or edema.

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40
Q

What is the difference between hypoplasia and agenesis?

A

Hypoplasia is a defective formation or incomplete development of a part whereas agenesis is the absence or failure of formation.

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41
Q

What are the different basic types of stem cells, and which basic tissue types are they found in?

A
Labile cells (primary stem cells) =  continuously dividing and found in the epidermis, GI tract, etc. Stable cells - low level of replication and can be induced to divide; they are found in hepatocytes, renal tubular epithelia, alveoli, and pancreatic acini.
Permanent cells - do not ever divide and are found in nerve cells, cardiac myocytes, and skeletal muscle.
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42
Q

What are the three stages of fracture healing?

A

Procallous - hematoma that provides anchorage but no structural integrity. Fibrocartilaginous callous - characterized by a fibrous ball around the fracture.
Osseus callous - formation of bone.

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43
Q

What is the difference between a traumatic fracture and a pathologic fracture?

A

Pathologic fracture - caused by disease sequelae, etc, or from trauma that shouldn’t fracture bone
Traumatic fractures - ‘normal’ fractures of bone, including transverse, linear, non-displaced, comminutes, greenstick, spiral, compound, etc, due to some traumatic impact

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44
Q

What is a karyotype and what is an ideogram (remember that mutations have to be larger than 4mb to be seen on a karyotype)

A

Karyotype - the number and visual appearance of the chromosomes in the cell nuclei of an organism or species
Ideogram - schematic representation of chromosomes showing the relative size of the chromosomes and their banding patterns

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45
Q

What are the parts of a chromosome (long arm, short arm, etc.)?

A

Chromosomes are made of DNA with nucleotide base pairs in a long sequence
p (short) arm and q (long) arm are attached by a centromere

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46
Q

How may pairs of autosomes, and how many sex chromosomes do humans have?

A

Humans have 22 pairs of autosomes and 1 pair of sex chromosomes, making 23 pairs total

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47
Q

How does the medical and general usage of the word “gene” differ?

A

Genes used to be called only protein-coding sequences of DNA

Now, any functional unit of a chromosome is a “gene”

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48
Q

What is a locus?

A

Locus is the exact physical location of a gene on a chromosome. It is the same in all people and marked by a p/q-# and usually given acronyms.

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49
Q

What are alleles?

A

Alleles are the term to describe the 2+ variations in a gene within a population.

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50
Q

What is the difference between genotype and phenotype?

A

Genotype - the particular combination of alleles that a person has for a certain locus. We typically will have two copies of a gene, as we have chromosome pairs.
Phenotype - the physical, observable reflection of a genotype; also, the presence or absence of certain traits

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51
Q

What is a SNP?

A

single-nucleotide polymorphisms - DNA sequence variations occurring when a single nucleotide differs between members of a species or paired chromosomes in an individual. Almost all common SNPs only have two alleles. Genomic distribution of SNPs is not homogenous and occurs more frequently in non-coding regions.

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52
Q

What is the difference between imprinting of the X chromosome, and imprinting of the autosomes?

A

Imprinting - a small number of genes are transcriptionally active only when transmitted by one of the two sexes/parents while homologous locus in the other parent is rendered “transcriptionally inactive” and will be maintained in all somatic cells of the offspring (epigenetic modifications of turning on/off genes)
Imprinting of the X Chromosome: in females this is a natural process called “X- inactivation.” Only one of the two X chromosomes will be active within a cell, although two cells may express different X chromosomal traits, etc.
Imprinting of autosomes can lead to pathology (prader-willi and angelman syndromes)

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53
Q

What are the 5 points of control for gene expression? Which is most studied?

A
Chromatin stage (most studied) Transcriptional stage
Translational stage
Post-translational control into cytoplasm Post-translational modification
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54
Q

Why does DNA naturally wrap around histones, and what epigenetic changes can occur to histone tails to encourage or discourage winding/unwinding?

A

DNA naturally wraps around histones due to Van Der Waals attractive forces of opposite charges (negative DNA with positive protein)
Histone Methylation at CpG islands down-regulates transcription
Histone Acetylation up- regulates transcription

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55
Q

What is a promoter region on a gene, and why are promoter regions generally not methylated?

A

Promoter regions are beginning sequences of genes that call polymerase to bind and transcribe
If promoter is methylated, then gene will be silenced - this could be the cause/method of treatment for some cancers

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56
Q

What is the difference between exudates and transudates and which of those cause non-pitting edema?

A

Transudates - low protein content and lower specific gravity - NON-PITTING EDEMA
Exudates - fluid with high protein content and cells and a higher specific gravity

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57
Q

What is Virchow’s triad?

A

Hypercoaguability
Stasis
Vascular wall injury

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58
Q

What are examples of the diseases/conditions contributing to stasis, vascular injury, and hypercoagulability?

A

Hypercoagulability - clotting disorders, oral contraceptives, malignancy, pregnancy, sepsis, thrombophilia, IBD
Stasis - atrial fibrillation, immobility, venous obstruction, venous insufficiency/varicose veins
Vascular Wall Injury - trauma/surgery, venepuncture, heart valve disease/replacement, atherosclerosis, catheters

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59
Q

What is the difference between an embolism and a thrombus?

A

Thrombus = clot - can be in coronary and cerebral arteries, heart chambers, aortic aneurysms, heart valves, DVTs and can lead to embolism
Embolism - any intravascular mass carried down bloodstream from site of origin, resulting in occlusion of a vessel - can be thromboemboli (most common), atheromatous emboli, fat emboli,
bone marrow emboli, gas emboli, amniotic fluid, tumor

60
Q

What are the features of pulmonary emboli?

A

Found in almost half of all hospital autopsies. 95% arise from DVTs. Diagnosed by a spiral CT. Right side of heart (where most arise from).

61
Q

What is the most common potential outcome of PE?

A

No sequelae – 75% - asymptomatic or transient dyspnea/tachypnea

62
Q

What is the “newspaper test”?

A

The ability to be able to read a newspaper through the fluid would indicate a transudate edematous fluid (vs exudate)

63
Q

Which countries have the highest incidence of HIV?

A

African countries (South Africa and Nigeria, Kenya and Mozambique) as well as India

64
Q

Describe the replication cycle of HIV.

A

HIV infects CD4+ cells and macrophages, attaching by gp120, gp41 to CD4, CCR5, and CXCR4
Integration into host genome via integrase
Reverse transcription via reverse transcriptase
Replication in metabolically active cells via host machinery
Protease to cleave and package viral products
Budding, using our cell membrane for the envelope.

65
Q

Why do 10% of hemophiliacs not progress to AIDS?

A

possible CCR5 deletion

66
Q

What are the phases of HIV infection that lead to AIDS?

A

Acute Phase - infection, reduced CD4 with viremia, seroconversion, mono-like symptoms
Latent Phase - lymphadenopathy, viral replication, low viremia, opportunistic infections, average length of 10 years

67
Q

What 2 neoplasms are most often seen in AIDS?

A

Hairy leukoplakia and Kaposi Sarcoma (also non-Hodgkin lymphoma and cervical cancer))

68
Q

What is the diagnostic criteria of AIDS, and what lab tests are used to test for HIV?

A

CD4 count <200 cells/microliter, viremia re-emergence, AIDS-defining diseases HIV Testing with ELISA and Western blot

69
Q

What lab tests are used to monitor HIV infection?

A

CD4 count

HIV1 RNA viral load by PCR

70
Q

What are mitotic bodies/figures, and what do they tell you about a cancer?

A

Possible sign of neoplasm/malignancy - stain differently histologically than in a normal cell
Nucleus/cytoplasm ratio, cell orientation, and cell/nucleus size are also features of anaplasia

71
Q

In what types of tissues do sarcomas arise, and how do they prefer to spread?

A

Muscles and connective tissue, spread in blood stream - frequent metastasis to lung

72
Q

In what types of tissues do carcinomas arise, and how do they prefer to spread?

A

Most common cancer, arising in epithelium - spread through lymphatic system

73
Q

What are adenocarcinomas?

A

Glandular cancers

74
Q

Which tissues are most sensitive to ionizing radiation, and why?

A

Dividing cells in mitosis (G2) - radiation causes cross linking/chain breaks of nucleic acids

75
Q

Does the ending “-oma” always mean the cancer is benign?

A

NO! –OMA simply means swelling/tumor

76
Q

How does the Ames test work, and for what reasons might it be misleading?

A

Detects mutagenic effects of potential carcinogens on bacterial cells
Used to screen for potential drugs to weed out possible carcinogens (required under pesticide act)
Introduces mutation and then checks to see if cells mutate back

77
Q

Worldwide, which cancer kills the most females, and which kills the most men?

A

MEN - hepatocellular carcinoma

WOMEN - cervical cancer

78
Q

In the first world, at what age range does cancer incidence peak?

A

Peak range: 80-84 years old

79
Q

Know your MEN syndromes!!!

A

MENI: PPP – pituitary adenoma, parathyroid hyperplasia, pancreatic tumors
MENIIA: PPM – parathyroid hyperplasia, pheochromocytoma, medullary thyroid carcinoma
MENIIB: PMMM – mucosal neuromas, marfanoid body habitus, medullary thyroid carcinoma, pheochromocytoma

80
Q

What is the difference between a preneoplastic disorder, and a paraneoplastic syndrome?

A

Preneoplastic disorders - may be acquired pathology that increase the likelihood of cancer (ie HepB and liver cancer)
Paraneoplastic syndromes occur when a neoplasms elaborates a substance that results in an effect that is not directly related to growth, invasion, or metastasis of the tumor itself (hormone-like substances, etc) - may precede the neoplastic diagnosis, serving as a signal (ie cuchings and lung-small cell CA, polycythemia and renal cell carcinoma)

81
Q

What is an initiator, and what is the difference between direct-acting and indirect-acting chemical carcinogens? What are procarcinogens?

A

Direct - mutagens that cause cancer directly by modifying DNA
Indirect (procarcinogens) - require metabolic conversion to form active carcinogen

82
Q

What is the difference between a genotoxic and non-genotoxic mechanism?

A

Genotoxic - employ DNA damage, chromosomal misentegration, etc leading to genomic damage
Non-genotoxic - employ chronic irritation/cell death, ROS, epigenetic silencing, immunosuppression, etc leading to altered signal transduction
*Both can result in cancer

83
Q

What do geneticists look for when they are trying to find promoter regions on genes, and why do you increase the risk of malignancy as you increase the number of methylations at these sites?

A

Promoter regions are typically rich in CpG islands

Methylation at the CpG island ends with complete silencing of a gene.

84
Q

What type of solar radiation is the most carcinogenic?

A

UVB

85
Q

How does UVB cause cancer?

A

Produces pyrimidine dimers in DNA leading to transcriptional errors and mutations of proto-oncogenes and tumor suppressor genes

86
Q

What type of radiation is the hospitals friend? i.e. The radiation oncologists friend? The friend of sterilization?

A

Ionizing radiation (Gamma radiation)

87
Q

Why is neutron radiation not used?

A

Neutron radiation is more powerful, penetrating deeper and potentially causing unintended damage

88
Q

What 3 essential activities are proto-oncogenes involved in?

A

Cell growth/cell cycle
Cell differentiation
Signal proteins (cytoplasmic/nuclear)

89
Q

What is meant by gain-of-function and loss-of-function mutations? How many “hits” to the alleles are needed to produce each?

A

Gain-of-Function - oncogenes; one-hit process; creation of a more active protein and stimulation of the cell cycle
Loss-of-Function: tumor suppressors; two-hit process; creates no active proteins, inhibits cell cycle

90
Q

Why was Mrs. Rous upset with Dr. Rous? – In his garage, what did he find out that would eventually lead to the understanding that 20% of human cancers come from?

A

Viruses

91
Q

How do viruses cause cancer? What is an acutely transforming retrovirus and how does the process work?

A

Infection of retrovirus and integration of proto-oncogene
Infection of cell with retrovirus carrying promoter gene, integrating promoter adjacent to proto-oncogene
Both processes can cause expression of new oncogene leading to cancer

92
Q

Fred and Freda both have grade II Stage IIa adenocarcinoma of the distal esophagus. What is it about the same type of tumor at the same stage, that still may make the prognosis in these two individuals different?

A

Hormone receptivity/sensitivity. (Estrogen-sensitive cancers may grow more rapidly, but also show a greater sensitivity to radiation therapies)

93
Q

What are the 7 fundamental changes in cell physiology that are needed for the tumor to behave in a malignant fashion?

A

Self-sufficiency in growth signals
Insensitivity to growth-inhibitory signals
Evasion of apoptosis
Limitless replicative potential Sustained angiogenesis
Ability to invade and metastasize
Defects in DNA repair

94
Q

What is the guardian of the genome, and what phase does it normally stop the cell from entering if the cell has damaged DNA?

A

P53 - prevents a cell with damaged DNA from entering the S phase in which DNa is supposed to replicate (between G0 and G1 checkpoints, which are both preparatory phases for mitosis).

95
Q

What is Li-Fraumeni syndrome, and what does it cause? What year was it described first in?

A

germ-line rotation of p53 (chromosome 17); high rate of many types of tumors; childhood sarcomas, breast cancer, brain tumors, leukemia
First described in 1969

96
Q

Apoptosis is regulated by which two genes?

A

bcl-2 (inhibits)

p-53 (stimulates)

97
Q

What is FNA (fine needle aspiration), and what does it not give the pathologist?

A

Method of cancer diagnosis - the syringe is coated in cells that allows the pathologist to determine metastatic qualities of the cells, but not the morphologic qualities.

98
Q

How, on an angiogram, can you tell if vessel growth is normal, or has been caused by angiogenesis resulting from a neoplasm?

A

Normal angiogenesis - like tree branching in fractal pattern

Neoplastic angiogenesis - torturous, irregularly shaped vessels

99
Q

Why are mice, and not horses or rabbits, sometimes chosen to produce monoclonal antibodies to human cancers in?

A

Cost effective - high yield offspring

100
Q

What do monoclonal antibodies specifically target in human cancers?

A
Serum tumor markers 
● CEA: colon CA, stomach CA, some breast and ovarian CAs
● AFP: liver CA
● CA 19-9: pancreatic CA
● CA 125: ovarian CA
● Β-HCG: testicular CA
● PSA: prostate CA
● BRCA 1, 2: breast CA
● CA 15-3: some breast CAs
● AFP, HCG: testicular CA
● HER2: TISSUE CA ONLY
101
Q

What is the difference between tumor grading and staging?

A

Grading - specific for each type of tissue and cancer within it; doesn’t indicate prognosis well; more about histology
Staging - clinical estimate of extent of tumor spread - better predictor of prognosis, using TNM
T (size of primary tumor)
N (extent of lymph node spread)
M (presence of metastatic disease – standard for all cancers);

102
Q

What is Grade 4 cancer, and what is Stage 4 cancer?

A

Grade 4 - glands are fused; no intervening stroma

Stage 4 - METASTASIS - bad prognosis

103
Q

In tumor progression, what does genetic instability mean? What does this translate to, for people that have a cancer recurrence, and need chemotherapy again? Is this analogous to antibiotic resistance in bacteria?

A

Malignant cells are more prone to mutate and accumulate additional genetic defects
For those who have cancer recurrence, this would mean that the selective growth advantage of the continued cell lines would give way to malignancy (like antibiotic resistant bacteria, kinda)

104
Q

What is the difference between seeding and transplantation as it relates to metastasis?

A

Seeding is when something is growing on the surface of a cavity and will metastasize to another site/ area within the same cavity/tissue
Transplantation occurs when “clean margins” are not maintained and, for instance, a surgical incision may take the cancerous cells to another site in the body.

105
Q

?Who was Sister Mary Joseph, and what principle of metastasis did she discover?

A

Sister Mary Joseph was a nurse who discovered palpable periumbilical nodes resulting from metastasis of malignant cancer in pelvis, abdomen, in her case, pancreatic cancers.

106
Q

Which 3 cancers tend to metastasize to the brain?

A

Skin
Breast
Lung

107
Q

Which cancers tend to metastasize to the bone

A
Breast
Prostate
Kidney
Thyroid
Lung
108
Q

On x-ray , what cancers produce osteoblastic vs. osteolytic lesions?

A

Osteoblastic lesions - from prostatic adenocarcinoma

Osteolytic lesions - from renal cell carcinoma and breast cancer

109
Q

What test can you use on physical exam to test for possible bony metastasis to the spine?

A

Spinous percussion, Rinne tuning fork test (indicates sensorineural loss if louder next to the ear than when placed on mastoid bone)

110
Q

What is induction treatment?

A

Sole treatment used for advanced disease or when no other treatment exists

111
Q

What is a neoadjuvant treatment?

A

(primary treatment) - chemotherapy given 1st, followed by another (secondary) treatment

112
Q

What is adjuvant treatment?

A

Treatment combined with another modality - given after other treatments are used

113
Q

What is salvage treatment?

A

For tumor that fail to respond to initial chemotherapy

114
Q

Which types of tumars are sensitive to XRT (radiation therapy)? Why?

A

Kidneys, lungs, liver, and lymphocytes are most sensitive to XRT (seminomas, lymphomas) because these cells are turning over fast, spending lots of time in M phase where XRT does its work

115
Q

Which types of tumors are radioresistant? Why?

A

Epithelial tumors and sarcomas are resistant to XRT, as well as large tumors - these tumors are not replicating as quickly as seminomas and lymphomas

116
Q

What is NCCN?

A

National Comprehensive Cancer Network - It shows staging and allow you to look up possible therapies or beneficial stories.

117
Q

What toxin is associated with the odor of bitter almonds?

A

Cyanide

118
Q

What toxin is associated with fruity odor?

A

ketoacids, isopropanol

119
Q

What toxin is associated with the odor of garlic?

A

oranophosphates, arsenic, DMSO, selenium

120
Q

What toxin is associated with the odor of mothballs?

A

napthalene, camphor

121
Q

How often do patients with carbon monoxide poisoning turn cherry red?

A

rarely

122
Q

What poisoning often accompanies carbon monoxide poisoning in residential fires, yet was not even know of until very recently? How are each treated?

A

Cyanide poisoning - both present the same clinically
CO poisoning is treated by removing exposure and using hyperbaric oxygen
CN poisoning is treated with antidote kits to convert CN to thiocyanate which can be excreted by kidneys

123
Q

What is generally meant by heavy metals, and what 2 ways are their exposures described in?

A

Heavy metals are metals or metalloids of environmental concern - Lead, chromium, arsenic, mercury, cadmium (denser than iron)

124
Q

What is bioconcentration? How do they get into the air?

A

Biomagnification/bioconcentration is the process of the concentration of toxic substances in living organisms as they move up each step of the food chain. The smoke released contains the radioisotope or its fallout (residual radioactive dust).

125
Q

Does a bottle of wine made in 1924 contain Cesium?

A

No, bottles of wine up until the 1942 won’t have cesium in them

126
Q

How can you increase the toxicity of Hg?

A

Methylation - allows Hg to be more water-soluble and can cross the BBB and placental barrier; consumption of carnivorous fish can cause bioaccumulation.

127
Q

What are the 2 main toxicities caused by Hg?

A

Neurotoxicity and nephrotoxicity

128
Q

Why is arsenic poison? Is it poison to everything on earth?

A

Acute poisoning causes CNS toxicity and hemorrhagic gastroenteritis
Chronic posoning causes malaise, abdominal pain, skin changes, and mees lines
Arsenic serves as a backbone for some species (in place of phosphorous)

129
Q

What is the difference between Mees lines and lead lines?

A

Mees lines are transverse bands on the fingernails seen in arsenic poisoning.
Lead lines are lead depositions at the gingivodental line (also lead lines in bone, at epiphyseal plate).

130
Q

Why is lead poisoning more of an issue with children?

A

Children absorb 4-5x more lead. There are additional complications for children, mainly having to do with CNS toxicity (lethargy, somnolence, cognitive impairment, developmental delay, cerebral edema, and peripheral neuropathy).

131
Q

What is Pica?

A

Pica is the desire to eat dirt (as well as ice, etc). It is a genetic condition seen in children - can lead to lead poisoning

132
Q

What is basophilic stippling

A

Basophilic stippling is seen in conjunction with microcytic anemia in lead poisoning. The ribosomes of the cells are spread throughout the cell, showing small dots at the periphery.

133
Q

Why do people that start smoking at age 30 or 40 usually not get COPD?

A

People usually have a lesser chance of getting COPD because epithelial transition ends beginning around age 20. When you start smoking later, the cumulative effects take longer to appear.

134
Q

Why is 20 pack years a notable number in lung cancer?

A

It was the old belief that if you had not had 20 pack years of smoking, then you would not get cancer. It will show significant enough tissue damage/change to cause a larger effect on the body.

135
Q

What are the 3 main illness in children that second hand smoke seems to increase the risk of getting?

A

SIDS, otitis media, asthma/URIs

136
Q

what photochemical is smog? How does it differs from smog when it was first described in 1905?

A

Smog in 1905 was “pea soup fog” caused by burning large amounts of coal in a city; it contained soot particles, sulfur dioxide, etc.
Photochemical smog is the reaction of sunlight, NO, and volatile organic compounds in the atmosphere leading to airborne particles and ground-level ozone (aldehydes, NO2, tropospheric ozone, VOCs)

137
Q

What are VOC’s and how are they made? Through what chemical reaction are we making Ozone? Where does the ozone go if there is an air inversion?

A

VOCs = volatile organic compounds, coming from photochemical reactions in the atmosphere
Ozone is formed from VOCs
With air inversion, pollution is trapped close to the ground, for humans to breathe

138
Q

Why is silicosis the most common pneumoconiosis?

A

Silica is an abundant mineral on earth that can be breathed in (dust/smog)

139
Q

What is silicosiderosis?

A

Silicosiderosis is the disease caused by inhaling mixed dust particles containing silica & iron.

140
Q

What is Caplans syndrome?

A

Caplan’s syndrome is pneumoconiosis in combination with multiple pulmonary rheumatoid nodules found in RA patients.

141
Q

What is the difference between silicates, silicon, and silicone?

A

Silicates - addition of other atoms onto silica to make minerals.
Silicon - chemical element, but almost always in combination with oxygen.
Silicone - synthetic polymer of silicone with carbon and oxygen; found as solid, liquid, or gel.

142
Q

What are the two meanings of “pathognomonic”?

A

1) a symptom/sign that is characteristic of a disease

2) this will – without a doubt – tell you that it is one disease and not another - TRUE MEANING

143
Q

In what disease are eggshell calcifications seen on CXR? Are they pathognomonic in both definitions for this disease?

A

Eggshell calcifications indicate silicosis. YES it is pathognomonic in both definitions.

144
Q

How do inhaled particles of silicates, asbestosis, and many other things cause fibrosis in the lungs?

A

Macrophage ingestion of the asbestos fibers triggers a fibrogenic response via the release of growth factors, promoting collagen deposition by fibroblasts.

145
Q

Where in the lungs do the fibers of asbestosis localize? What are these fibers called, and what type of lung cancer do they cause? Where is this lung cancer localized? Why?

A
The fibrosis will appear as brown nodules in the septum of the alveolus and in the distal lung and may have a rod/dumbbell shape with multiple segmentations. Asbestos tends to like the outer linings of the lungs.
Causes mesothelioma (1000-fold more common with asbestos exposure) that involves the lower lobes and pleura. The issues can begin as fibrotic plaques.
146
Q

How many fold does a person’s risk of getting lung cancer increase if they are exposed to asbestosis? With smoking? What does this relationship tell us about the nature of environmental toxins?

A

abestosis - 5-fold
with smoking - 55-fold
This is a demonstration of the additive effect (“the whole is greater than the sum of its parts”) because it exponentially increases your risk of developing the cancer.