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Biochemistry Module 8 > Integration > Flashcards

Integration Flashcards

0
Q

Pelvic inflammatory disease caused by

A

Neisseria gonnorhea and

Chlamydia trachomatis

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1
Q

infectious and inflammatory disorder of the upper female genital tract, including the uterus, fallopian tubes, and adjacent pelvic structures

A

Pelvic inflammatory disease

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2
Q

What is the biochemical mechanism of action of the quinolone

A

Inhibits DNA gyrase

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3
Q

Enzymes that assist in formation of superhelicesand regulate the breaking and rejoining of the DNA chain

A

Topoisomerase

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4
Q

interfere with bacterial DNA synthesis

A

Fluoroquinolones

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5
Q

blocks relaxation of supercoiledDNA

A

topoisomeraseII (DNA gyrase) in gram-negative organisms

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6
Q

interferes with the separation of replicated chromosomal DNA during cell division

A

Topoisomerase IV in gram positive

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7
Q

usually bactericidal against susceptible organisms •exhibit postantibioticeffect

A

Fluoroquinolones

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8
Q

1st generation

A

Nalidixicacid,
Cinaxacin,
Rosoxacin

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9
Q

2nd generation

A

Ciprofloxacin,
Ofloxacin,
Norfloxacin

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10
Q

3rd generation

A

Levofloxacin,
Sparfloxacin,
Grepafloxacin

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11
Q

3rd generation

A

Levofloxacin,
Sparfloxacin,
Grepafloxacin

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12
Q

4th generation

A

Moxifloxacin,
Trovafloxacin,
Gemifloxacin,
Gatifloxacin

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13
Q

urinary tract infections

A

1st generation

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14
Q

gram negatives, gonococci, gram positive cocciand Mycoplasma

A

2nd generation

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15
Q

less gram negative and more gram positive activity, streptococci and enterococci

A

3rd generation

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16
Q

broad spectrum, including anaerobes–with increasing generation, increasing gram positive activity

A

4th generation

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17
Q

increasing generation leads to increasing gram negative activity

A

Cephalosporin

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18
Q

Inhibits DNA replication bybinding to DNA gyraseand topoisomerase IV. Bactericidal

A

Ciproploxacin

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19
Q

Ciprofoxacin toxicity

A

Tendinitis and tendon rupture

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20
Q

FloroquinoLONES hurt attachment to your

A

Bones

Cartilage damage

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21
Q

As the two strands of the double helix are separated, a problem is encountered, namely

A

Positive super coils

Supertwist

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22
Q

Theaccumulating positive supercoils interfere with further unwinding of the

A

Double helix

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23
Q

If the cord is twisted in the direction of tightening the coils, the cord will wrap around itself in space to form

A

Positive super coils

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24
Q

If the cord is twisted in the direction of loosening the coils, the cord will wrap around itself in the opposite direction to form

A

Negative supercoils

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25
Q

which are responsible for removing supercoils in the helix

A

DNA topoisomerase

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26
Q

These enzymes reversibly cut one strand of the double helix

A

DNA topoisomerase 1

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27
Q

Nuclease and ligase

A

Strand cutting

Strand resealing

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28
Q

DNA topoisomerase 1 They do not require ATP, but rather appear to store the energy from the

A

Phopodiester bond

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29
Q

Type I topoisomerasesrelax negative supercoils in ________, and both negative and positive supercoils in ____________

A

E. coli

Eukaryotic cell

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30
Q

These enzymes bind tightly to the DNA double helix and make transient breaks in both strands

A

DNAtopoisomearse 2

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31
Q

The enzyme then causes a second stretch of the DNA double helix to pass through the break and, finally, reseals the break

A

DNA topoisomerase 2

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32
Q

Type II DNA topoisomerasesare also required in both prokaryotes and eukaryotes for the separation of interlocked molecules of DNA following

A

Chromosomal replication

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33
Q

a Type II topoisomerase found in bacteria and plants, has the unusual property of being able to introduce negative supercoils into relaxed circular DNA using energy from the hydrolysis of ATP

A

DNA gyrase

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34
Q

Bacterial DNA gyraseis a unique target of a group of antimicrobial agents

A

Quinolones

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35
Q

A typical human cell contains 46 chromosomes, whose total DNA is approximately

A

1m long

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36
Q

interaction of DNA with a large number of proteins, each of which performs a specific function in the ordered packaging of these long molecules of DNA

A

Histones

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37
Q

Eukaryotic DNA is associated with tightly bound basic proteins, called

A

Histones

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38
Q

DNA into basic structural units

A

Nucleosomes

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39
Q

The complex of DNA and protein found inside the nuclei of eukaryotic cells is called

A

Chromatin

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40
Q

5 classes of histones

A

H1, H2A, H2B, H3, and H4

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41
Q

5 classes of histones These small proteins are positively charged at physiologic pH as a result of their high content of

A

Lysine

Arginine

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42
Q

antibiotics target bacterial DNA gyrase

A

Quinolones

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43
Q

controlled by topoisomerases which later the topology of the circular DNA but not its covalent structure

A

Super coiling

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44
Q

relax DNA from negative supercoils formed

A

Type 1 topoisomerase

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45
Q

change DNA by creating double break strands in DNA

A

Type 2 topoisomerase

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47
Q

abundant proteins associated with eukaryotic DNA and are a family of basic proteins rich in the positvelycharged amino acids lysine and arginine which interact with the negative charges of DNA

A

Histones

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48
Q

RNA is a polymer composed of alternating units of

A

Ribonucleotides

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49
Q

RNA is a polymer composed of alternating units of ribonucleotides connected through a

A

3-5 phospodiesterase bond

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53
Q

Histones, along with positively charged ions such as _________ help neutralize the negatively charged DNA _____________

A

Magnesium

Phosphate group

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54
Q

HIV affects cells of the immune system, called

A

CD4 cells or T cells

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55
Q

most likely was transmitted to humans and mutated into HIV when humans hunted these chimpanzees for meat and came into contact with their infected blood

A

Simian Immunodeficiency Virus, or SIV from chimpanzees in west Africa

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56
Q

HIV family and subfamily?

A

Family Retroviridae-Subfamily Lentivirus

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57
Q

HIV 1

A

chimpanzees; pan troglodytes

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58
Q

HIV2

A

sootey mangabeys, more related to SIV 2

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59
Q

Retroviridaeis a single stranded RNA virus that has______________, which converts singlestranded RNA viral genome into doublestranded viral DNA

A

Reverse transcriptase

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60
Q

This new DNA is then incorporated into the host cell genome by an

A

Integrase enzyme

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61
Q

contains enhancer and promoter regions of HIV

A

LTR or long terminal repeat

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62
Q

encodes structural proteins which help in packaging RNA of the virus to generate new virus particles

A

Gag

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63
Q

encodes reverse transcriptase and integrase

A

Pol gene

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64
Q

codes for envelope proteins, along with the host plasma membrane complete the virus particle that buds off from the cell

A

Env

65
Q

Regulatory proteins

A

Nef(negative factor), Tat(transactivator of transcription) and Rev (regulator of viral gene expressionresponsible for switching early to late HIV gene located in the 3’ end of envgene

66
Q

catalyzes the insertion of viral DNA into the host genome to establish infection

A

Integrase

67
Q

packaged in a capsidand buds out of the plasma membrane

A

Assembly and budding

68
Q

Early stage–Within 2-4 weeks, many experience flu-like symptoms, often described as the “worst flu ever” also known as

A

Acute retroviral syndrome orprimary HIV infection

69
Q

the first FDA-approved test that independently distinguishes results for HIV-1 p24 antigen and HIV antibodies in a single test

A

HIV-1/2 Ag/Ab

70
Q

helpful in closing the window period (the time between HIV infection and appearance of antibodies to HIV

A

HIV antigen-antibody combination assay

71
Q

People who are infected with HIV experience no HIV-related symptoms, or only mild ones

A

Asymptomatic HIV infection” or “Chronic HIV infection

72
Q

Asymptomatic HIV infection” or “Chronic HIV infection

A

Clinical latency stage

73
Q

Terminates elongation process–Zidovudine, didanosine, stavudine, lamivudine, abacavir–Prevent acute infection of susceptible cells

A

Nucleoside reverse transcriptase inhibitors

74
Q

binds to the active site induces conformational change and inhibiting enzyme function–Delaviridine, nevirapine, efavirenz–Easily metabolized by cytoP450 system and prone to drug interaction

A

Non nucleoside inhibitor

75
Q

inhibits HIV protease which activates precursors of gag-pol–binds to the active site of HIV protease and blocks viral maturation–Saquinavir, ritonavir, indinavir, nelfinavir–Side effects: nausea, vomiting, diarrhea

A

Protease inhibitor

76
Q

2 Reverse transcriptase inhibitor, 1 protease inhibitor

A

HAART

Highly active antiretroviral therapy

77
Q

12,241 cases, of which 93 percent—or 11,520—acquired the virus through sexual contact •85 % involved males having sex with other males (MSM) •Age group 15 to 24 was also notable in most new cases •11 patients with full-blown Aids at the time of reporting •Metro Manila accounted for more than half of the new cases (55%) while Calabarzonhad 14% •Other regions cited were: Central Visayas, 7%; Central Luzon, 3% and Davao region, 5

A

Nice to know

78
Q

Timothy Brown also known as the “Berlin patient” •Diagnosed with HIV in 1995 •After controlling the virus for many years with antiretroviral therapy, Brown was diagnosed with acute myeloid leukemia (AML) and in 2007, destruction of his immune system and a stem cell transplantionwas done from a donor with a rare genetic mutation (homozygous CCR5∆32) that resists HIV infection •Nearly four years after his transplant, Brown remains free of both his cancer and readily detectable HIV

A

Nice to know

79
Q

Lyme disease

A

spirocheteBorrelia burgdorferi

80
Q

Three shape of spirochete

A

cocci(spheres)–bacilli(rods)–spirochetes(spirals

81
Q

Weakly staining, gramnegative spirochetes largest medically important bacteria Stains well with aniline dyes (Giemsaor Wright

A

Borreliaburgdorferi

82
Q

Borreliaburgdorferi curtured on

A

BarbourStoenner-Kelly medium

83
Q

Transmission of lyme disease

A

bite from deer tick Ixodes scapularis

84
Q

Once in the skin, the spirochete can:–Be eliminated by host defense mechanisms–Remain viable and localized in the skin where it

A

Erythema migrans

85
Q

Characteristic expanding rash (target lesion) at the site of the tick bite 7-14 days after the tick is removed

A

Erythema migrans

86
Q

Erythemamigrans is an example of

A

Erythema mutiforme

87
Q

Dark center of small papule, vesicle, or bulla •Pale intermediate zone •Peripheral rim of erythema

A

Erythema mutiforme

88
Q

Atrophy and skin as thin as cigarette paper

A

Acrodermatitischronicumatrophicans

89
Q

Occurs within 30 days of Erythema migrans Fatigue, myalgias , bite arthralgias , headache, fever, chills, and neck stiffness

A

Early lyme disease

90
Q

Occurrs weeks to months after the bite. Musculoskeletal and neurologic symptoms are the most common Cardiac and dermatologic

A

Early disseminated lyme disease

91
Q

Months to years after infection Musculoskeletal (mainly joints) and neurologic systems are most commonly affected

A

Later or chronic lyme disease

92
Q

A tetracycline drug that inhibits bacterial protein synthesis by binding to and interfering with ribosomes

A

Doxycycline

93
Q

Cell wall inhibitors

A

Penicillin

Cephalosphorin

94
Q

DNA synthesis inhibitors

A

Quinolones

95
Q

Metabolic inhibitors

A

Folate inhibitor

96
Q

50 + 30 = 70

A

Prokaryotic ribosomes

97
Q

Protein synthesis inhibitor

A

Aminoglycosides Tetracylcines Macrolides Lincosamides Chlolamphenicol Linezolid

98
Q

act on the ribosomesto inhibit translation

A

Protein synthesis inhibitor

99
Q

Cell wall

A

Peptidoglycans

100
Q

Unit

A

-10 to the minus 30

101
Q

60+40=80

A

Eukaryotes ribosomes

102
Q

bind to 30 s, preventing the binding of amiono acyl tRNAto heriosomes.

A

Tetracyclines

103
Q

work against 30Ssub unit, stored the structure in iniation of protein synthesis stop.

  • a suicide antibioticor bomb shell antibiotics, stop initiation of translation, incorporation of, prematurely termination of translation.
  • example, gentamycin, streptomycin
A

Aminoglycosides

104
Q

inhibit the formation of initiation complex of 30s and 50 s.

-last resort antibiotic, cause its very expensive

A

Linezolid

105
Q

anti 50 S drugs, inhibits translocation

A

Macrolides

106
Q

the most common, arise in epithelial cells

A

Carcinoma

107
Q

from connective tissue (e.g. bone, cartilage

A

Sarcomas

108
Q

from white blood cells

A

Lukemia and lymphomas

109
Q

The sequence of events that occurs in the proliferation of individual cells is known as the

A

Cell cycle

110
Q

which controls progression through the cycle so that, once the cell passes G1, it is committed to divide

A

G1

111
Q

DNA is synthesized and the original DNA duplicated

A

S phase

112
Q

the chromosomes separate and move to the two ends of the cell

A

G2

113
Q

the cell divides to produce two daughter cells

A

M phase

114
Q

the tissue contains cells that proliferate continually to replace those that die or are lost (e.g. the skin, intestine, bone marrow). These cells are known as stem cells

A

Continual renewing

115
Q

the tissue contains cells (stem cells) that can be stimulated to proliferate in response to an appropriate signal (e.g. liver after injury, lymphocytes during an infection

A

Conditionally renewing

116
Q

the cells in the tissue never proliferate (e.g. nerve, muscle) Most primary tumours arise in continually renewing tissues (often epithelium

A

Non renewing

117
Q

TUMOR SUPPRESSION GENE

A

P 53

118
Q

The protein p21 can be induced by p53independent factors, including drugs known as

A

Statins

119
Q

Statins are used to lower blood cholesterol by inhibition of its synthesis, via the enzyme

A

HMG CoA reductase

120
Q

sequences of six-nucleotide repeats found at the ends of the chromosomal DNA strands

A

Telomeres

121
Q

These are present at the ends of the strands to overcome a problem posed by the semiconservative mechanism of DNA replication, known as

A

The end replication problem

122
Q

present at the end of the 3′ strand

A

TTAGGG

123
Q

at the end of the 5′ strand

A

AATCCC

124
Q

Replication of the ends of the chromosomes presents particular difficulties, since DNA polymerase can only elongate a pre-existing DNA strand (it cannot initiate DNA synthesis) and can only polymerise DNA in one direction (5′ to 3

A

Need to know

125
Q

Since there is no complementary strand from which to synthesise primers at the ends of the DNA molecule, up to 200 base pairs of DNA

A

Would be lost

126
Q

Problem in cancer

A

no complementary strand

127
Q

Tom maintain the length of the telomeres

A

enzyme, telomerase, which adds on repetitive nucleotides

128
Q

In a normal cell, telomere length is gradually lost during cell replication and, when it is completely lost and then coding sequences are lost, the cell dies via

A

Apoptosis

129
Q

Tumour cells, however, have an enhanced activity of telomerase which maintains the length of the telomeres which contributes to their

A

Evasion of normal apoptotic mechanism

130
Q

compound that is foreign to the body

A

Xenobiotic

131
Q

It may include drugs, chemical carcinogens, and various other compounds •The xenobiotic may be excreted unchanged, or it may me metabolized by the body’s enzymes to other compounds

A

Xenobiotic

132
Q

2 phases of xenobiotic metabolism

A
  1. Hydroxylation / Biotransformation

2. Conjugation

133
Q

Attachment of new functional groups,

A

Phase 1 biotransformation

134
Q

Masking of an existing functional group

A

Conjugation

135
Q

Catalyzed by cytochromeP450, a monooxygenase

A

Hydroxylation

136
Q

Approximately 50% of the drugs humans ingest are metabolized by isoformsof

A

CYTOCHROME P 450

137
Q

The reaction catalyzed by a monooxygenaseis as follows

A

RH + O2 +NADPH + H+→ R-OH + H2O + NADP

138
Q

It is sometimes referred to as a Mixed Function Oxidase

A

Cytochrome P -450

139
Q

Compounds produced in phase 1 are converted by specific enzymes to various polar metabolites by conjugation with glucuronic acid, sulfate, acetate, glutathione, or certain amino acids, or by methylation

A

Conjugation

140
Q

UDP-glucuronic acid is the glucuronyl donor, and glucuronosyltransferases
•This is the most frequent conjugation reaction

A

Glucuronidation

141
Q

Sulfate donor is adenosine 3-phosphate5-phosphosulfate (PAPS), called “active sulfate

A

Sulfation

142
Q

tripeptideconsisting of glutamicacid, cysteine, and glycine

A

Glutathione

143
Q

are conjugated to the nucleophilic GSH: R+GSH→R—S—G

A

Electrophilic xenobiotic

144
Q

R+GSH→R—S—G •The enzymes catalyzing these reactions are called

A

Glutathione S transferase

145
Q

X+Acetyl-CoA→Acetyl-X + CoA •Catalyzed by__________ present in the cytosol of various tissues, particularly the liver

A

acetyltransferases

146
Q

used in the treatment of tuberculosis, is subject to acetylation

A

Isoniazid

147
Q

Polymorphic types of acetyltransferases exist, resulting in individuals who are classified as slow or fast acetylators •Slow acetylators are more subject to certain •toxic effects of isoniazid because the drug persists longer in these individuals

A

Acetylation

148
Q

Xenobiotic may be converted from an inactive to a biologically active compound

A

prodrug or procarcinogen

149
Q

conjugation may increase the biologic activity of a xenobiotic

A

Very few cases

150
Q

it is the conjugation reactions that convert the active products of phase 1 reactions to less active or inactive species, which are subsequently excreted in the urine or bile

A

Other cases

151
Q

PROPERTIES OF HUMAN CYTOCHROME P450

A

Hemoproteins
Broad substrate specificity
Liver and other tissues
Mitochondria or ER enzyme

152
Q

Warfarin

A

Cytochrome

Phenobarbital

153
Q

The preferred lipid in cytochrome P 450 is

A

phosphatidylcholine

Biochemistry Module 8 (9 decks)

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