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51 Cards in this Set
- Front
- Back
- 3rd side (hint)
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Define a "neoplasm".
They can be benign or malignant. Either way, what are 4 characteristics of a neoplasm? |
Clonal proliferation beginning in a cell native to a particular site.
Uncoordinated, uncontrolled, autonomous and persistent growth |
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Define each of the following:
Hyperplasia Metaplasia Dysplasia Hamartoma |
Hyperplasia: increase in the number of normal cells
Metaplasia: change from one cell type to another Dysplasia: alteration of a cell to an abnormal or disordered form Hamartoma: proliferation of normal cells forming a mass |
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What is suffix that is used for benign tumors?
What are the 2 suffixes that are used for malignant tumors? |
Benign: "--oma"
Malignant: Epithelial = carcinoma mesenchymal = sarcoma |
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What is the benign and malignant name of each of the following tumor locations"
- squamous epithelium - epithelium of glands & ducts - urothelium |
- squamous epithelium
B: squamous cell papilloma M: squamous cell carcinoma - epithelium of glands & ducts B: Adenoma M: Adenocarcinoma - urothelium B: urothelial papilloma M: urothelial carcinoma |
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For each of the following cancer types, state whether it is benign or malignant and the location:
Lymphoma Melanoma Leukemia |
Lymphoma - malignant tumor of the lymph nodes
Melanoma - malignant tumor of the melanocytes of the skin Leukemia - malignant tumor of bone marrow blood cell precursors |
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Differentiation refers to the extent to which the microscopic appearance of a tumor resembles the tissue/cells of origin. In malignant tumors there is histologic variation in the nucleus and in the cytoplasm. What is the nature of these changes?
(5 in the nucleus, 1 in the cytoplasm) |
Nucleus:
- hyperchromatism - pleomorphism (multiple shapes) - loss of orientation - iregularity of contour - increased size Cytoplasm: absence of normal constituents making it more akin to a stem cell! |
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At what point can a malignant tumor (undifferentiated and ↑'d growth), do no harm? What is it refered to at this stage?
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Prior to invading a tumor can do NO harm despite being undifferentiated and having ↑'d growth.
The cellular changes seem in epithelium before they become invasive are frequently called dysplasia. |
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What does it mean to be a metastatic tumor?
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A metastatic tumor is not in continuity with the site of origin of the tumor, and it is extrinsic to the organ of origin.
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What type cancer most commonly spreads by body cavity seeding?
What is the effect of this? |
Ovarian - the tumors invate the peritoneum and then shed cells that form multiple implants on the surfaces of that cavity. The implants exude fluid causing profound ascites.
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What is the commonest pathway of metastases? (esp. with what type of cancer?)
Where do cancers that start in the following places, spread to, if they use this pathway? Cervical Breast |
Lymphatic: commonest (esp. with carcinomas), follows the normal routes of drainage
Cervical ---> ext & internal illiac and obturators (can impinge on ureters and cause renal damage!) Breast --> axillary nodes |
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What type of cancer is malignant and invasive but cannot metastasize?
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Basal cell carninoma of the skin!
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When does the M & M relate to malignant tumors usually occur?
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The M & M r/t malignant tumors usually only occurs when invasion &/or metastases have taken place
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What is meant by tumor grade?
How is it reported? How clinical useful is it? How is it done? (ie measured) What does the grade relate to? |
the histologic appearance of a tumor, particularly it's differentiation (for most tumors this is translated to a # grading system - lower #'s are better)
Varies from site to site in clinical utility Done via light microscopy Relates to prognosis and treatment |
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What is meant by a tumor stage and how is it determined?
In what types of tumors is it important? While the prognostic relevance of tumor staging varies from site to site, what feature of staging frequently indicates an incurable disease? |
Extent of disease as determined from a variety of mean (P/E, imaging, histology, etc).
Important in virtually all types of tumors Metastases (even when confined to L nodes) frequently indicates that the disease is incurable |
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Is H5N1, the avian flu, a pandemic? Why or why not?
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No it is not because there is no human to human spread. Only the occasional chicken to human spread when that human has ++ close contact with the bird.
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Is there an H5N1 vaccine?
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Yes! But it has not been used b/c there is concern that it will create a selective pressure on the viral population and create resistance.
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What are the Xtics of an ideal bioterrorism agent?
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1. Stable
2. Sufficient quantity 3. Easily disseminated 4. Readily transmitted person-to-person 5. High mortality rate |
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What are the 3 categories for CDC classes of bioterrorism agents? (classes A, B & C).
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Disseminated
Transmissability Mortality |
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What are 3 examples of category A agents? (for each one name their mode of transmission)
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Bacillus anthracis - cutaneous, inhalational, GI
Yersinia pestis (plague) - inhalational C. Botulinum toxin - descending flaccid paralysis |
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Describe the organism B. anthracis? (G-stain, O2 needs, etc).
Where is it found and where/how do you get naturally occuring infections? What is the mostly likely weaponised form? Incubation period? |
G + bacillus, aerobic, spore-forming
Spores are ubiquitous in the soil, causes anthrax in animals and gets to humans thru contact with these animals. Most likely to made into a powder or aerosolized. Incubates for 1-7days (but can incubate for up to 60) |
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Describe the 3 clinical presentations of Anthrax.
1. Progression from macule/papule to what 3 things? Finally produces what? 2. Sever acute _______. Progresses to what 3 things? 3. NVD --> 3 things |
Cutaneous: macule/papule --> ulcer --> vesicle --> painless eschar --> painful lymphadenopathy
Inhalational: severe, acute febrile respiratory illness, progress to: - hemorrhagic mediastinum & meningitis - thoracic lyphadenitis GI: nausea, vomiting, diarrhea ---> bloody diarrhea, acute abdomen, septic shock |
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What findings on x-ray would suggest anthrax?
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Clear lungs, but a widened mediastinum and lymphadenopathy
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What is the mortality rate for each of the following anthrax infections (with and w/o Abx):
- cutaneous - inhalational - GI |
Cutaneous: 20% w/o Abx, rare if Abx given
Inhalational: 90% w/o Abx or supportive care, 40% with (death on average w/in 3 days) GI: high mortality given the difficulty of an early diagnoses |
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In what 3 ways is Anthrax Dx?
How is it transmitted? |
Skin biopsy
blood culture CSF culture NO human to human transmission! |
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How is anthrax prevented? (2 ways)
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Vaccine is mandatory for all military personnel.
Prophylaxis (Cipro x 60days) post-exposure |
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What causes small pox?
What is the clinical presentation? (5) |
DNA virus
High fever, malaise, h/a, back ache, maculopapular rash |
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Where does the small pox rash start? How does it spread?
When does it change and what does it change into? *hint* |
Starts in the face/mouth then to forearms trunk and legs
Changes from macular/papular to vesicular around 1-2 days later, then pustular. Crusts on day 8-9 |
Rash: M/P --> ______ --> _______ ---> _____ |
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How is small pox transmitted?
What is it's overall mortality? |
Readily transmitted human to human via contact & airborne transmission.
Overall mortality = 30% |
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How is small pox diagnosed (3)?
How is it prevented (2)? |
E-microscopy, nucleic acid amplification, viral culture
Vaccine (last given in the '70's) Can give vaccine after exposure to increase the immune response |
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How can you tell that a genetic defect (causing cancer) is inherited or acquired?
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An inherited gene defect causing cancer --> person will have gene defect in all body cells.
If however, the defect in acquired it will only be present in the tumor cells |
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By what 2 mechanisms can a person have an inherited (cancerous) genetic defect, but have a mutation that is only present in their tumor cells?
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Cancer-associated germline mutations can also undergo acquired mutations in somatic cells, causing sporadic non-inherited cancers with mutations that are present in only the tumor
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By what 2 mechanisms can viruses cause CA?
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By producing sustained and ongoing inflammation that causes constant cell turnover, the virus increase the risk of a mutation
Can also have viral genomes that do the equivalent of what chemical & physical damage does |
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Do inherited factors alone tend to cause CA? Why or why not?
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No b/c it is a multi-step process. CA cells have multiply changes in functioning and thus require multiple mutations to develop, including both hereditary and acquired
(thus is all the cells in the body already have 1 defect (from inheritance) there is ↑ risk of getting a second acquired mutation that will cause CA) |
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Does prostatic hyperplasia increase the risk of prostate CA? Why or why not?
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No - b/c the mechanism isn't ↑ cell turnover but rather the hyperplasia is accomplished by blocking apoptosis.
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Which is more common a carcinoma or a sarcoma? Why?
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Tissues that normally are rapidly dividing will be common sites of cancer (e.g. skin) as opposed to sites of slow or no growth (e.g. the heart). Thus, Cancinomas (epithelial tumors) are far more common than sarcomas.
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What is the general trend in the incidence of cervical and prostate CA. Why is this?
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Cervical CA is declining b/c the screening for this CA identifies pre-cancerous lesions and is able to provide effective Tx.
Conversely, prostate screening cannot ID pre-cancerous ppl but rather early (pre-invasive) CA. It is also ID a CA lesion that may have never developed into a symptomatic CA (thus screening may be artificially ↑ing incidence) |
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What are the 3 causes of altered gene function in cancer (broadly speaking)?
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- environment
- inherited factors - chance ** the gene alteration begins in a single cell and all progeny will have the malignant phenotype |
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What are the 4 causes of alteration in gene function?
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1. Inherited or acquired mutations
2. Gain or loss of genetic material 3. disordered regulation of gene expression 4. Viral alteration of gene function |
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Define an oncogene?
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Oncogene: cenes promoting cell proliferation whose gain of function is associated with cancer
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Define a "tumor-suppressor gene"
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TSG: genes inhibiting cell proliferation whose loss of function is associated with cancer
(Rb, Cyclin DK-inhibitors, APC, PTEN, TGF-B) |
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In what type of cellulitis would you give IV Abx? Why? What type (3 C's)?
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Must give abx IV in head/neck cellulitis d/t risk of brain infection.
Give Cefazolin, cloxacillin or ceftriaxone |
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What Abx can you give only if a person is healthy and not on other meds? Why?
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Probenicid 1g - b/c it decreases renal clearnace of drugs
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What are the 4 risk factors for Nec Fas?
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DM
Obesity Drug use Immunosuppression |
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What are the 5 signs/symptoms of Necrotizing fasciits?
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1. Tense edema
2. Disproportionate pain 3. Bullae 4. Crepitus 5. SQ gas (gas gangere d/t clostridium |
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What causes type 1 and type 2 necrotizin fasciitis?
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Type 1: Polymicrobial (DM, PVD, post-op)
Type 2: GAS (pyogenes). ** must consider MRSA! ** |
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What non-specific lab findings would you see in someone with necrotizing fasciitis? (3 things)
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1. High WBC
2. Coagulopathy 3. High CK, lactate and CR |
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What is the treatment for Necrotizing Fasciitis?
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Treatment:
- early and complete Sx debridement PLUS - Abx therapy |
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What tests do you do for malaria and how often?
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Malaria = thick & thin films Q16h x 3.
D/c pt if negative, admit if +ve Fluids, analgesia, O2, antipyretics |
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When a person has Dengue fever what do you need to watch for?
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Dengue hemorrhagic fever where they get heme concentration and die of shock!
(mosquitos that cause this bite during the day in urban centres) |
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Compare Marasmus (M) to Kwashiokor (K) in the following ways:
- liver steatosis - Sm bowel mucosal atrophy - B marrow HoPlasia - Cerebral atrophy |
- liver steatosis
M = No K = Yes! - Sm bowel mucosal atrophy M = No K = Yes! - B marrow HoPlasia M & K = YES! - Cerebral atrophy M & K = ? possibly |
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What 2 things regulate 1,25-OH-vitD?
1. how is a-1-OH-lase slowed down? 2. sped up? |
1. Elevated 1,25-OH-vitD will down-regulate the a-1-OHlase enxymes in the kidneys
2. PTH & HypoPhosphatemia activated a-1-OH-lase |
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