POST LAB EXPERIMENT 13,14, 17, 18, 19, 20, 21 Flashcards

1
Q

is prone to progression with involvement of deeper tissues and organs

A

Streptococcus pyogenes

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2
Q

Streptococcal pyogenic exotoxins (SPEs) may be released and produce

A

scarlet fever

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3
Q

Other complications that result from S. pyogenes infections are the

A

poststreptococcal diseases
rheumatic fever
acute glomerulonephritis

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4
Q

is an example of a pathogen that induces the production of several different antibodies.

A

S. pyogenes

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5
Q

contains antigenic structural components and produces antigenic enzymes, each of which may elicit a specific antibody response from the infected host.

A

S. pyogenes

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6
Q

In the course of an infection, the extracellular products act as antigens to which the body responds by producing specific antibodies

A

S. pyogenes

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7
Q

Most infected patients by S. pyogenes demonstrate increased concentration of antibody against

A

SLO

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8
Q

ANTI-STREPTOLYSIN O DETERMINATION

Titer production begins at about [?] after the onset of infection.

A

7 days

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9
Q

ANTI-STREPTOLYSIN O DETERMINATION

The concentration of antibody (titer) begins to rise about 7 days after the onset of infection and reaches a maximum after [?].

A

4 to 6 weeks

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10
Q

ANTI-STREPTOLYSIN O DETERMINATION

A rise in titer of [?] in 1 to 2 weeks is of greater diagnostic significance than a single titer.

A

50 Todd units*

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11
Q

ANTI-STREPTOLYSIN O DETERMINATION

An elevated titer indicates a relatively [?].

A

recent infection

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12
Q

ANTI-STREPTOLYSIN O DETERMINATION

Peak titers are seen at the time of [?] of acute rheumatic fever, but these titers are no longer at their peak during the [?] of acute rheumatic fever.

A

acute polyarthritis

carditis

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13
Q

Virulence factors of Streptococcus pyogenes.

A

M protein

Exoantigens/exotoxins

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14
Q

Major virulence factor

A

M protein

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15
Q

They are proteins excreted by the bacterial cell as they metabolize during the course of streptococcal infections

A

Exoantigens/exotoxins

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16
Q

It is a filamentous molecule consisting of two alpha-helical chains twisted into a ropelike structure that extends out from the cell surface.

A

M protein

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17
Q

There is a net-negative charge at the amino-terminal end that helps to inhibit phagocytosis.

A

M protein

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18
Q

It limits deposition of C3 on the bacterial surface, thereby diminishing complement activation

A

M protein

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19
Q

Immunity to group A streptococci appears to be associated with antibodies to the

A

M protein

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20
Q

Exoantigens/exotoxins examples

A

Pyrogenic exotoxins A, B, and C

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21
Q

are responsible for the rash seen in scarlet fever and also appear to contribute to pathogenicity.

A

Pyrogenic exotoxins A, B, and C

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22
Q

Pyrogenic exotoxins A, B, and C Antibodies are produced to the following exoantigens:

A

SLO
(DNase B)
hyaluronidase
nicotinamide adenine dinucleotidase (NADase)
streptokinase

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23
Q

is a stepwise method involving the use of a series of serum dilutions. ASO titer of serum is determined as the serum dilution that inhibits nearly 50% of SLO-induced hemolysis. Therefore, the method gives stepwise ASO titers for various sera.

A

Rantz-Randall method

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24
Q

Therefore, the method gives stepwise ASO titers for various sera.

A

Rantz-Randall method

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25
Q

[?] FOR DETECTING ANTIBODIES AGAINST Helicobacter pylori

A

ICT RAPID ASSAY

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26
Q

Virulence factors of Helicobacter pylori.

A

CagA

Vacuolating cytotoxin/VacA

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27
Q

-Highly immunogenic

A

CagA

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28
Q

The severity of the disease is related to injection of the [?] protein into the gastric epithelial cells.

A

CagA

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29
Q

CAUSES DUODENAL OR GASTRIC ULCERS-IF UNTREATED IT MAY LEAD TO GASTRIC CARCINOMA

A

CagA

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30
Q

Once the [?] protein is in the epithelial cells, changes occur in the function of the cell’s signal transduction pathways and in the structure of the cytoskeleton.

A

CagA

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31
Q

The [?] gene codes for a toxin precursor.

A

VacA

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32
Q

Epidemiological studies have shown that if the [?] genes are present in the strain of bacteria infecting the individual, there is a higher risk of developing gastric or peptic ulcers or gastric carcinoma.

A

CagA and VacA

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33
Q

– widely believed that it started in west Africa and the practice of bushmeat trading.

A

1930s

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34
Q

Meat of wild animals were being sold and transported in the market

A

1930s

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35
Q

– The disease is renamed as Acquired Immune Deficiency Syndrome (AIDS), sexual and through blood transfusion transmission were established

A

1982

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36
Q

– discovered that HIV can be passed from mother to child through breastfeeding

A

1986

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37
Q

– 8-10 million (est) with HIV worldwide

A

1990

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38
Q

– 33 million were living with HIV and 14 million have died from AIDS

A

1999

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39
Q
  • continued efforts are being done by global and local organizations, collaboration with pharmaceuticals to reduce
A

2000s

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40
Q

– improved treatment, approval of PrEP

A

2010s

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41
Q

– UNAIDS reported that AIDS-related deaths have fallen 30% since its peak

A

2013

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42
Q

transcribe HIV infection

A

Human Immunodeficiency Virus

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43
Q

Human Immunodeficiency Virus types

A

HIV-1 and HIV-2

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44
Q

– most advanced stage of HIV infection

A

AIDS (acquired immunodeficiency syndrome)

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45
Q

This abbreviation can mean the virus or the infection

A

AIDS (acquired immunodeficiency syndrome)

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46
Q

is responsible for all of the infection worldwide

A

HIV-1

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47
Q

is the responsible for the epidemic

A

HIV-1 group 1 M Strain

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48
Q

endemic to west Africa, less common and less infectious

A

HIV-2

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49
Q

HIV TRANSMISSION

A

Body fluids (◉ Blood ◉ Breast milk ◉ Semen ◉ Pre-seminal fluid ◉ Rectal fluid ◉ Vaginal fluid )
Contact with mucous membrane
Unprotected anal or vaginal sex
Sharing needles
Breastfeeding During pregnancy or birth

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50
Q

Transmission is caused by exposures such as high-risk sexual behaviors and other activities

A

HIV

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51
Q

These body fluids must come in contact with the damaged/wounded mucous membrane in order for transmission to happen

A

HIV

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52
Q

Risky sexual activities and other modes of transmission

A

HIV

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53
Q

During pregnancy, transmission to the child happens because the blood of an infected mother can pass through the placenta and infect the child.

A

HIV

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54
Q

Mother to child transmission is greatest during vaginal delivery when a baby passes through the birth canal and is exposed to the mother’s blood and other fluids

A

HIV

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55
Q

HIV infection cannot be transmitted through the following methods

A
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56
Q

Enumerate and describe the principles and clinically significant results of other serologic tests for diagnosing infection with HIV

A

Screening and Confirmatory tests

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57
Q

can be caused by one of four single-stranded, positive-sense RNA viruses (serotypes virus type 1 to virus type 4) of the Flavivirus genus.

A

Dengue

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58
Q

Dengue

After an incubation period of 3 to 7 days, signs and symptoms start suddenly and follow three phases:

A

o initial febrile phase
o Critical phase
o final recovery phase

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59
Q

Critical phase at about the time that the fever subsides (?) final spontaneous recovery phase

A

defervescence

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60
Q

Most dengue virus infections are [?], with a wide variety of clinical manifestations.

A

asymptomatic

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61
Q

Signs and symptoms range from mild febrile illness to severe and fatal disease.

A

Dengue

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62
Q

[?] after entering in the body invades the local macrophages and multiply there.

A

Dengue

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63
Q

Infected local cells then migrate from site of infection to lymph nodes, where monocytes and macrophages are recruited, which become targets of infection.

A

Dengue

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64
Q

Consequently, infection is amplified and virus is disseminated through the lymphatic system. As a result of this primary viremia, several cells of the mononuclear lineage, including blood-derived monocytes

A

Dengue

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65
Q

Dengue

Viremia develops within [?]. During this period, virus travels throughout the body.

A

24 hours

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66
Q

Bone marrow cells have also been shown to be susceptible to infection with

A

DENV

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67
Q

In severe case, viral load is very high and many vital organs are affected.

A

Dengue

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68
Q

Dengue Virus infected macrophages produces a number of signaling proteins such as (?), other mediators which are responsible for many symptoms such as flue like syndrome and pain.

A

interferons, cytokines, chemokines, TNF

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69
Q

These mediators affect hemostatic system of body.

A

Dengue

70
Q

Fluid from blood vessels starts to leak out so that the blood volume decreases resulting in low blood pressure.

A

Dengue

71
Q

Decrease in blood pressure causes insufficient supply of blood and Oxygen to vital organs such as brains.

A

Dengue

72
Q

also infects bone marrow, so that bone marrow cannot produces sufficient platelets.

A

Dengue

73
Q

Since platelets are needed for blood clotting, infection causes blood clotting defect and increase the risk of bleeding.

A

Dengue

74
Q

Dengue

Laboratory diagnostic testing is by detection of viral components in serum or directly by [?].

A

serologic testing

75
Q

DENGUE Diagnostics tests

A

a. Viral Isolation

b. Dengue NS1 test

c. RT-PCR

d. IgM-capture ELISA (MAC-ELISA)

76
Q
  • Gold standard; 6-10 days to replicate viral cell culture
A

a. Viral Isolation

77
Q
  • is a highly conserved glycoprotein essential for virus viability.
A

b. Dengue NS1 test

78
Q

Detects the acute phase infection

A

b. Dengue NS1 test

79
Q
  • Molecular detection of dengue genomic RNA
A

c. RT-PCR

80
Q
  • First detectable IgM only appears 4-5 days
A

d. IgM-capture ELISA (MAC-ELISA)

81
Q

Diagnosis of acute infection

A

b. Dengue NS1 test

d. IgM-capture ELISA (MAC-ELISA)

82
Q

Currently, no effective antiviral agents are available to treat [?].

A

dengue infection

83
Q

Treatment is supportive.

A

dengue infection

84
Q

If patients have severe bleeding, a blood transfusion can be lifesaving.

A

dengue infection

85
Q

There are four types of human malaria:

A

• Plasmodium falciparum
• Plasmodium vivax
• Plasmodium malariae
• Plasmodium ovale

86
Q

are the most common

A

Plasmodium falciparum and Plasmodium vivax

87
Q

is the deadliest

A

P. falciparum

88
Q

In recent years, some human cases of malaria have also occurred caused by [?], a monkey malaria that occurs in certain forested areas of Southeast Asia.

A

Plasmodium knowlesi

89
Q

[?], a bloodborne parasite, is transmitted exclusively through the bite of Anopheles mosquitoes.

A

Malaria

90
Q

Transmission is more intense in areas in which the mosquito lifespan is longer, and where it prefers to bite humans rather than other animals.

A

Malaria

91
Q

This allows the parasite to have time to complete its development inside the mosquito.

A

Malaria

92
Q

The intensity of transmission depends on factors related to the parasite, vector, human host, and environment.

A

Malaria

93
Q

In many areas, transmission is seasonal, with a peak during and just after the rainy season.

A

Malaria

94
Q

All the important vector species of Anopheles bite at night

A

Malaria

95
Q

• The malaria parasite life cycle involves [?] hosts.

A

2

96
Q

During a blood meal, a malaria-infected female Anopheles mosquito inoculates [?] into the human host.

A

sporozoites

97
Q

• infect liver cells.

A

Sporozoites

98
Q

• There, the sporozoites mature into [?].

A

schizonts

99
Q

• The schizonts rupture and release (?). This initial replication in the liver is called the (?)

A

merozoites

exoerythrocytic cycle

100
Q

• [?] infect RBCs. There, the parasite multiplies asexually (called the [?]). The merozoites develop into [?]. Some then mature into [?].

A

Merozoites

erythrocytic cycle

ring-stage trophozoites

schizonts

101
Q

• The schizonts rupture, releasing.

A

merozoites

102
Q

• Some trophozoites differentiate into.

A

gametocytes

103
Q

• During a blood meal, an Anopheles mosquito ingests the male (?) and female (?) gametocytes, beginning the

A

microgametocytes

macrogametocytes

sporogonic cycle

104
Q

• In the mosquito’s stomach, the microgametes penetrate the macrogametes, producing.

A

zygotes

105
Q

• The zygotes become motile and elongated, developing into.

A

ookinetes

106
Q

• The ookinetes invade the (?) of the mosquito where they develop into.

A

midgut wall

oocysts

107
Q

The oocysts grow, rupture, and release [?], which
travel to the mosquito’s [?].

A

sporozoites

salivary glands

108
Q

Inoculation of the [?] into a new human host perpetuates the malaria life cycle.

A

sporozoites

109
Q

for P. vivax

A

• 12 to 17 days

110
Q

for P. falciparum

A

• 9 to 14 days

111
Q

for P. ovale

A

• 16 to 18 days or longer

112
Q

for P. malariae

A

• About 1 month (18 to 40 days) or longer (years)

113
Q

However, some strains of P. vivax in temperate climates may not cause clinical illness for

A

months to > 1 year after infection

114
Q

Manifestations common to all forms of malaria include

A

Fever and rigors—the malarial paroxysm
Anemia
Jaundice
Splenomegaly
Hepatomegaly

115
Q

is caused by hemolysis of infected RBCs, released merozoites and other malaria antigens, and the inflammatory response they elicit.

A

Malarial paroxysm

116
Q

The classic paroxysm starts with malaise, abrupt chills and fever rising to [?], rapid and thready pulse, polyuria, headache, myalgia, and nausea. After [?], fever falls, and profuse sweating occurs for [?], followed by extreme fatigue.

A

39 to 41° C

2 to 6 hours

2 to 3 hours

117
Q

Fever is often hectic at the start of infection.

A

Malarial paroxysm

118
Q

In established infections, malarial paroxysms typically occur every [?] depending on the species

A

2 to 3 days

119
Q

serologic tests for diagnosing malaria:

A

Microscopy - Thick and Thin Smear

Indirect Fluorescent Antibody Test

120
Q

remains the ―gold standard‖ for laboratory confirmation of malaria.

A

Microscopic examination

121
Q

A blood specimen collected from the patient is spread as a thick or thin blood smear, stained with a Romanovsky stain (most often Giemsa), and examined with a 100X oil immersion objective.

A

Thick and Thin Smear

122
Q

Malaria antibody detection is performed using the

A

indirect fluorescent antibody (IFA) test

123
Q

can be used to determine if a patient has been infected with Plasmodium.

A

indirect fluorescent antibody (IFA) test.

124
Q

Because of the time required for development of antibody and also the persistence of antibodies, [?] is not practical for routine diagnosis of acute malaria.

A

serologic testing

125
Q

a chronic systemic inflammatory disease primarily involving the joints

A

rheumatoid arthritis

126
Q

The serum and synovial fluid contain

A

rheumatoid factor

127
Q

Rheumatoid factors are synthesized within

A

lymphoid infiltrates

128
Q
  • immunoglobulin complex activates the complement
A

Rheumatoid factor

129
Q

Pain occurs in small joint and later in large joints

A

rheumatoid arthritis

130
Q

IgM Ab directed against Fc portion

A

IgG

131
Q

3 classes:

A

IgM, IgG and IgA

132
Q

Immune complexes consisting of the rheumatoid factor

A

IgM, IgG and IgA

133
Q

immunoglobulin activate the complement cascade and lead to a number of inflammatory phenomenon’s affecting the joints.

A

IgM, IgG and IgA

134
Q

Initially swelling and pain occur in small joints and later it involves the larger joints.

A

Rheumatoid Arthritis

135
Q

Advance cases –

A

joint deformities

136
Q

Invasive pannus consists of

A

macrophages, mast cells and fibroblasts

137
Q

Synovial fluid contains organized lymphoid tissues (?)

A

CD4+ T cell, B cells and macrophages

138
Q

Increase [?] in synovial fluid

A

neutrophil count

139
Q

In advanced cases (?) occur and the patients are crippled.

A

permanent joint deformities

140
Q

In [?], the synovial membrane is infiltrated with inflammatory cells and forms an invasive pannus consisting of macrophages, mast cells, and fibroblasts.

A

Rheumatoid Arthritis

141
Q

The junction between the [?] is a focus for enzymatic degradation.

A

invasive pannus and the joint cartilage

142
Q

Organized lymphoid tissues (?) are present around the synovial blood vessels.

A

CD4+ T cells, B cells and macrophages

143
Q

The synovial fluid of RA patients contains large numbers of neutrophils (up to ?).

A

105/ml

144
Q

LABORATORY DIAGNOSIS OF RA

A

Sheep cell agglutination test/Rose-Waaler test
Latex fixation test (Singer and Plotz)
Sensitized alligator erythrocyte test (Cohen et. Al)
Bentonite flocculation test (Bloch and Bunim)

145
Q

Sheep cell agglutination test/

A

Rose-Waaler test

146
Q

(Singer and Plotz)

A

Latex fixation test

147
Q

(Cohen et. Al)

A

Sensitized alligator erythrocyte test

148
Q

(Bloch and Bunim)

A

Bentonite flocculation test

149
Q

When using RF latex tests, a titer of [?] or greater is generally considered a positive reaction.

A

80

150
Q

A titer of [?] is considered a weakly positive reaction.

A

20 to 40

151
Q

If there is no agglutination at [?], the specimen should be considered negative for RF, even is subsequent dilution shows agglutination.

A

1:20

152
Q

used to describe a proliferation of cells that produces a mass rather than a reaction or inflammatory condition

A

neoplasms

153
Q

are neoplasms and are described as benign or malignant.

A

Tumors

154
Q

Most tumors are of

A

epithelial origin (ectoderm, endoderm, or mesoderm)

155
Q

forms in the skin or tissue cells that line the body’s internal organs, such as the kidneys and liver

A

carcinoma

156
Q

grows in the body’s connective tissue cells, which include fat, blood vessels, nerves, bones, muscles, deep skin tissues and cartilage.

A

sarcoma

157
Q

The remaining tumors are of

A

connective tissue origin

158
Q

Malignant neoplasms arising from tissue embryologically derived from ectoderm or endoderm are usually.

A

carcinomas

159
Q

carcinomas Examples include:

A

• Squamous cell carcinoma of cervix
• Adenocarcinoma of stomach
• Hepatocellular carcinoma
• Renal cell carcinoma

160
Q

Malignancies arising from mesoderm (connective tissues) are usually [?]. sarcomas Examples include:

A

• Leiomyosarcoma
• Chondrosarcoma
• Osteosarcoma
• Liposarcoma

161
Q

The key distinction between benign and malignant tumors is the ability of [?] to invade normal tissue and metastasize to other secondary sites.

A

malignant tumors

162
Q

Tumor Risk Factors:

A

• Smoking is responsible for one third of cancers.
• Other risk factors include a high-fat, low-fiber diet, obesity, and a sedentary lifestyle.
• Risk factors are important in specific cancers.

163
Q

CAUSATIVE FACTORS IN HUMAN CANCER

A

• Environmental Factors
• Infectious diseases
• Cancer predisposing genes

164
Q

Specific Tumor Markers

A
  1. Alpha-fetoprotein
  2. CA 125
  3. Human epididymis protein 4
  4. Thyroglobulin
  5. Prostate-specific antigen (PSA)
  6. Carcinoembryonic antigen
  7. CA 19-9
  8. CA 15-3
  9. CA 27.29
  10. HER2/neu
165
Q

Other markers include the

A

beta subunit of human chorionic gonadotropin

166
Q

Ten protein cancer biomarkers have been FDA-approved for clinical use:

A

Human Epididymis Protein 4

CA 27.29: Breast Carcinoma–Associated Antigen

HER2/neu

167
Q

is recommended for monitoring patients for recurring epithelial ovarian cancer.

A

Human Epididymis Protein 4

168
Q

Carcinoma of the breast often produces mucinous antigens

A

CA 27.29: Breast Carcinoma–Associated Antigen

169
Q

is encoded by an oncogene and is over expressed in 15% to 20% of invasive breast cancers.

A

HER2/neu

170
Q

• have the potential to uncover signature gene expression patterns for specific cancers and ultimately assist in the staging of tumors, prognosis, and treatment.

A

DNA microarray technology

171
Q

• Three aspects of importance in Next Generation Sequencing (NGS) are:

  1. Identification of
  2. Detection of low levels of
  3. Improved management of
A

somatic mutations

genomic alterations

cancer treatment

172
Q

• The ability to isolate and characterize rare circulating tumor cells (CTCs) may provide critical insights into primary tumors, the process of metastasis, and monitor disease progression

A

Continuous Field-Flow Assisted Dielectropheresis (DEP)