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House Pharmacology > ANTIVIRAL AGENTS And Anti-retroviral Agent > Flashcards

ANTIVIRAL AGENTS And Anti-retroviral Agent Flashcards

1
Q

Viruses are the smallest living microorganism measuring ____-___nm (30 x 10-9M)in size and cannot reproduce outside their host cells which are usually larger including ______ and _____ cells.

A

20 – 30

bacteria and human

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2
Q

A _______ is the free-living virus particle outside the host cells.

A

virion

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3
Q

A virion is the free-living virus particle (inside or outside?) the host cells.

A

Outside

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4
Q

Virion consists of nuclear material (RNA or DNA) enclosed in a _____ coat known as _____ which may also be surrounded by an external ________ envelope.

A

protein; capsid

lipoprotein

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5
Q

The capsid together with the RNA/DNA => ___________

A

nucleocapsid

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6
Q

The capsid is made up of (symmetrical or asymmetrical?) repeating structural units called ___________ .

A

symmetrical

capsomeres

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7
Q

Some viruses also contain enzymes that initiate their replication in the host cell.

T/F

A

T

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8
Q

DNA viruses )-

___________ (warts)

________(Shingles, cold sores, glandular fever)

_________ virus (mononucleosis or kissing disease)

_______ virus (chicken pox)

_________(smallpox)

Hepatitis B virus

_________(sore throat, conjunctivitis)

__________(retinitis).

A

Papillomavirus

Herpesviruses

Epstein-Barr

Varicella zoster

Poxviruses

Adenovirus

cytomegalovirus

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9
Q

DNA viruses (PHEVPHAC)-

Papillomavirus (______)

Herpesviruses (_______,_______ , glandular fever)

Epstein-Barr virus (________ or ____ disease)

Varicella zoster virus (_______)

Poxviruses (smallpox)

Hepatitis B virus

Adenovirus (______ ,_______)

cytomegalovirus (_______).

A

warts

Shingles, cold sores

mononucleosis; kissing

chicken pox

sore throat, conjunctivitis

retinitis

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10
Q

RNA viruses (RHOEPARPARC)-

_________ (HIV/AIDS, T- cell leukamia)

Hepatitis C virus

_______(influenza A, B and C)

_______(myocarditis)

_________(measles, mumps, respiratory tract infections)

Arboviruses (Yellow fever)

________(rabies)

_________(poliomyelitis)

_______ (meningitis, lassa fever)

_______(German measles) and Coronaviruses (RTI).

A

Retroviruses; Orthomyxovirus

enterovirus; Paramyxovirus

Rhabdoviruses; Picornaviruses

Arenavirus; Rubella virus

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11
Q

HPV is a (DNA or RNA?) virus which affects human _____ and the _______ that line the body (throat, mouth, feet, fingers, nails, anus and cervix).

A

DNA

skin; moist membranes

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12
Q

HPV

There are over _____ types, of which ____ can affect the genital area.

Transmission: _____________ with infected person.

Symptoms: Asymptomatic or ________

A

100; 40

skin to skin sexual contact

appearance of warts.

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13
Q

HPV

Prevention:_______,_______, condoms, reduction of _______

Treatment: _____,________ ,________.

A

Vaccination, abstinence

sexual partners

cryotherapy, electrodessication, laser surgery

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14
Q

Mention 2 Effective drugs for papilloma virus infection

A

No effective drugs.

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15
Q

Viral REPLICATION

_______->_______->TRANSLATION- >_______ ->__________

A

ENTRY

TRANSCRIPTION; ASSEMBLY

BUDDING/RELEASE

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16
Q

Viral Replication : DNA Viruses

Viral DNA enters the host cell ______,
where transcription into ______ occurs catalyzed by the (host or viral?) cell _________.

A

nucleus; mRNA

host; RNA polymerase

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17
Q

Viral replication: DNA viruses

Translation of the ____ into _____- specific ______ then takes place.

Some of these proteins are enzymes (DNA polymerase) that _____________, as well as proteins comprising the _____ and ______

A

mRNA; virus; proteins

synthesize more viral DNA

viral coat and envelope.

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18
Q

Viral replication: DNA viruses

After assembly of coat proteins around the viral DNA, complete virions are released by ______ or after _________

A

budding

host cell lysis.

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19
Q

Viral replication: RNA viruses

Enzymes (____dependent ____ polymerase) within the (virion or host ?) synthesize its _____ from the ____ RNA
template, or sometimes the viral RNA serves as its own mRNA.

A

RNA; RNA

Virion; mRNA; viral

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20
Q

Viral replication: RNA viruses

mRNA, is translated by the (host or virion?) cell into various enzymes, including ____ polymerase (which directs the synthesis of more viral RNA), and also into structural proteins of the virion.

A

Host ; RNA

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21
Q

Viral replication: RNA viruses

The viral structural proteins are arranged around the newly formed viral RNA to form new virions which escape by ______ or ______ .

A

budding or cell lysis

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22
Q

The nucleus is usually not involved in RNA viral replication except for ___________.

A

orthomyxoviruses

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23
Q

Viral replication

Retroviruses: contain _____——- enzyme (virus ____-dependent ____ polymerase), which makes a ____ copy of the viral RNA.

This new copy is integrated into the genome of the host cell by ____ enzyme to form a ____virus which is transcribed into both ___________ and ________.

The latter is translated into (active or inactive?) proteins which are broken down by the _______ enzymes into structural proteins followed by assembly.

A

reverse transcriptase

RNA; DNA; DNA

integrase; provirus

new viral RNA & mRNA; inactive

protease

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24
Q

The ability of several viruses to remain dormant and be replicated together with, the host genome is responsible for the _________________ , such as those caused by __________ (cold sores) or the _______ (chickenpox) virus, which recur when _________ is reactivated when the immune system is compromised.

A

periodic nature of some viral diseases

herpes labialis

varicella zoster ; replication

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25
Q

Some RNA retroviruses can transform normal cells into malignant cells

T/F

A

T

Eg T-cell leukamia

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26
Q

herpes labialis

Aka

??

A

Cold sores

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27
Q

Host defenses against viruses

1)______ skin: can not be penetrated by most viruses unlike sites of ______ and _____

A

Intact

wounds and insect bites.

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28
Q

Host defenses against viruses

Innate and adaptive immune response:
____-lymphocytes killed viral infected cells which it recognises by the complex (formed from ______ and ______ ) presented on the surface of the infected cells.

A

T; viral peptide and major histocompatibility complex

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29
Q

Host defenses against viruses

Natural killer cells: kill viruses (which escape the initial _______-lymphocytes effect) using _________ strategy

A

cytotoxic T-

mother Turkey

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30
Q

Host defenses against viruses

Gene silencing: An attempt by the _____ to use the ______’s translational/transcriptional machinery causes the _______ for the _______ to be ________, probably by ___________, thereby interrupting with viral replication.

A

virus; host; gene coding

viral RNA; switched off

DNA phosphorylation

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31
Q

Antiviral drugs are used for treating viral infections. Unlike most antifungals and antibacterial, they ________________ rather than ___________.

A

inhibit the development or reproduction of viruses

destroying them

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32
Q

Antiviral drugs are the same as viricides

T/F

A

F

Antiviral drugs are different from viricides

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33
Q

viricides are chemicals that ____________

They are not ___________.

A

destroy virus particles

medication!

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34
Q

viricides

Examples: ______, sodium _______, ___________ chloride, essential oils (e.g. ________ oil).

A

Lysol

hypochlorite; benzalkonium

eucalyptus

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35
Q

Classification of non-retroviral Antiviral drugs

1)Viral ________ Inhibitors

2) Viral ________ Inhibitors

3) Viral __________ Inhibitors

4) _____________ inhibitors

A

DNA Polymerase

neuraminidase

coat disassembly

NSE protease

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36
Q

Viral DNA polymerase inhibitors

Examples : aci_____, famci______, ganci_____, penci____ valaci_____, valganci_____, ____ ,_______,_______,______

A

clovir x 6

foscarnet, idoxuridine, ribavirin, and cidofovir

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37
Q

Viral DNA polymerase inhibitors

Uses for the treatment of _____ infections.

In addition, cidofovir, valaciclovir, ganciclovir and valganciclovir are also used for the treatment of ______ infections

Ribavirin is used for the treatment of ______,______, and ______

A

herpes

cytomegalovirus

respiratory syncitial infections, lassa fever and hepatitis c

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38
Q

Viral DNA polymerase inhibitors is used for ______ and _______ infections

And ribavirin_____,______, and _______

A

CMV

HERPES

respiratory syncitial infections, lassa fever and hepatitis c

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39
Q

Ribavarin is used to treat _______,______,______

A

respiratory syncitial infections, lassa fever and hepatitis c

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40
Q

Viral DNA polymerase inhibitors

Mechanism of action- they inhibit the viral DNA polymerase in different ways.

Aciclovir, valaciclovir and penciclovir are __________ that are first converted to the ________ by viral ________ more rapidly by the (viral or host?) enzyme but this can also be done by the (viral or host?) enzyme.

A

guanosine analogue; monophosphate

thymidine kinase
Viral; host

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41
Q

Viral DNA polymerase inhibitors

Mechanism of action-

After Aciclovir, valaciclovir and penciclovir are converted to the mono phosphates , They are then converted by the (viral or host?) kinases to their _____ which _____________________ for ________________ by the enzyme viral DNA polymerase.

This leads to chain _________ and _________ of viral DNA replication.

A

Host; triphosphates

compete with host natural guanosine triphosphate

incorporation into viral DNA chain

termination and suppression

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42
Q

Ribavirin is a synthetic (nucleoside or non-nucleoside ?) analogue that is thought to act by altering the ______________ or by interfering with the _________

A

nucleoside

viral nucleotide pool

synthesis of viral mRNA.

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43
Q

Foscarnet is a (nucleoside or non nucleoside?) analogue of ______ which inhibit viral DNA polymerase by binding to the _________ binding site.

A

Non-nucleoside; pyrophosphate

pyrophosphate

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44
Q

Inhibitors of viral neuraminidase

Examples: oselta ______, zana_______, lanina_____ & pera_____.
n protein

A

mivir x4

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45
Q

Inhibitors of viral neuraminidase

Uses: are for treament of _____ and ________ infections and they are only effective in the ______ stage of the infections.

A

influenza A and influenza B viral

early

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46
Q

Inhibitors of viral neuraminidase

Mechanism of action: the neuraminidase inhibitors prevent the ____________________________________ by inhibiting the viral neuraminidase which is an protein enzyme on the surface of the virion that is responsible for __________________________

A

escape of the newly replicated viruses

severing the bond between the viral coat and the host sialic acid (neuraminic acid).

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47
Q

Neuraminidase is responsible for ______________ between the _________ and ____________

A

severing the bond

viral coat and the host sialic acid

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48
Q

sialic acid

Aka

??

A

neuraminic acid

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49
Q

Inhibitors of viral neuraminidase

Side effects: GIT symptoms such as nausea, vomiting, _______ and diarrhoea.

A

dyspepsia

50
Q

Inhibitors of viral coat disassembly

Examples: Amantadine & rimantadine Uses: only for the treatment of influenza A
•
viral infection. No action on influenza B virus.
•
Mechanism of action: (i) Amantadine acts by blocking the M2 ion channel which is another protein through which an influx of H+ occurs

A
51
Q

Inhibitors of viral coat disassembly

Examples: Aman______ & riman______

A

tadine

tadine

52
Q

Inhibitors of viral coat disassembly

Uses: only for the treatment of __________ infection. No action on _________

A

influenza A viral

influenza B virus.

53
Q

Inhibitors of viral coat disassembly

Mechanism of action: (i) Amantadine acts by blocking the ___________ which is another protein through which an influx of _____ occurs to _____ the viral particle in the host cell cytoplasm thereby —————— so that the viral RNA genome can be released into __________ for ________

A

M2 ion channel

H+; acidify

enhancing its dissassembly

the host cell for replication.

54
Q

Inhibitors of viral coat disassembly

Side effects: most common:> dizziness, _________ and _______

A

slurred speech and insomnia.

55
Q

NS3 protease inhibitors

Examples: Asuna______, boce________, grazo_____, parita______, sime_____ and tela_______

A

previr

previr

previr

previr

previr

previr

PaST BaGrA

56
Q

NS3 protease inhibitors

Uses:to treat _______

A

Hepatitis C

57
Q

NS3 protease inhibitors

Mechanism of action: Inhibits viral NSE protease enzyme which converts _____________ to ________________

A

large inactive protein/polypetide (formed after translation from mRNA)

smaller active functional and structural protein.

58
Q

________ and _______ can be used to treat hepatitis C

A

Viral DNA polymerase inhibitors (ribavirin)

NS3 protease inhibitor(asunaprevir)

59
Q

Antiretroviral agents: drugs for the treatment of infection caused by ________.

A

retroviruses

60
Q

A retrovirus is an RNA virus which possesses _________ enzyme with which it produces _____ copy of its _____ genome.

A

reverse transcriptase

DNA

RNA

61
Q

A retrovirus

Examples:______________ (HIV),___________ and _____________ (HTLV-1

A

Human immune deficiency virus

Simian immunodeficiency virus (SIV)

Human T-cell lymphotropic virus type 1

62
Q

Structure of HIV-1

HIV-1:

(Small or large?) in size (~___ nm).

Consists of 2 single stranded RNA (___ genes) tightly bound to the viral enzymes (______,_____,_______, and ________) and surrounded by a protein coat (capsid).

A

Small

120; 9

Reverse transcriptase , integrase, protease, & ribonuclease

63
Q

Structure of HIV-1

HIV-1:

Capsid made of repeated units (______) and surrounded by _____ of viral proteins which in turn is surrounded by a ________ envelope

A

capsomere; matrix

lipoproprotein

64
Q

Structure of HIV-1

HIV-1:

a lipoproprotein envelope made of mainly _____ & protein from _______ and also few copies of viral protein [gp _____ (___) + gp ____ (___)].

A

lipid bilayer; human host

120; cap

41; stem

65
Q

Structure of HIV-1

HIV-1:

The stem are of ____ molecules

A

3

66
Q

In HIV

gp 120 is the ________

gp 41 is the ______

A

cap

Stem

67
Q

Life cycle of HIV
Step 1: Binding-

the virus binds to molecules on the surface of the _____ cell: first a ____ receptor and then either a ______ or ______ coreceptor.

A

CD4

CD4

CCR5 or CXCR4

68
Q

Life cycle of HIV
Step 1: Binding-

the virus binds to molecules on the surface of the ______ cell: first a ____ receptor and then either a ______ or _____ coreceptor.

A

CD4

CD4

CCR5 or CXCR4

69
Q

Life cycle of HIV

Step 2: Fusion-

HIV _________ fuses with the
CD4 ___________ which allows HIV to enter the CD4 cell and releases HIV RNA & HIV enzymes into the cell.

A

Viral envelope

cell membrane

70
Q

Life cycle of HIV

Step 3: Reverse transcription-

HIV releases and uses __________ to convert its genetic material—HIV _____—into HIV _____ which allows HIV to enter the CD4 ___________

A

reverse transcriptase

RNA; DNA

cell nucleus

71
Q

Life cycle of HIV

Step 4: Integration-

Once inside the host CD4 cell nucleus, HIV releases ______ enzyme. HIV uses HIV this enzyme to _____________________________________ to form a ______

A

integrase

insert its viral DNA into the DNA of the host cell

Provirus

72
Q

Life cycle of HIV

Step 5: Replication-

After integration. The _______ DNA is transcribed into _____________________. The latter is translated into ———

A

provirus

both new viral genome RNA as well as mRNA

inactive proteins.

73
Q

Life cycle of HIV

Step 7: Assembly-

new HIV RNA and HIV proteins made by the host CD4 cell move to the _____ of the cell and assemble into (mature or immature?) (infectious or noninfectious?) new virions.

A

surface

Immature

noninfectious

74
Q

Life cycle of HIV

Step 8: Budding-

immature virions ((can or can’t?) infect another CD4 cell) pushes themselves out of the host CD4 cell.

Once outside the CD4 cell, the new HIV releases HIV ______ enzyme which break up the (short or long?) (active or inactive?) protein chains to form (smaller or larger?) HIV active proteins that combine to form (mature or immature?) , (non-infectious or infectious ?) HIV.

A

Can’t ; protease

Long; inactive

Smaller

Mature ; infectious

75
Q

Classification of Antiretroviral agents

1.___________ inhibitors (NRTIs)
2. ___________ inhibitors
3. ___________ inhibitors
4. _________ inhibitors
5. ________/______ inhibitors
6. ________ inhibitors
7. ________ inhibitors

A

Nucleoside/nucleotide reverse transcriptase

Non-nucleoside reverse transcriptase

Protease

Fusion; Entry/CCR5

Integrase; Maturation

76
Q

(1)Nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs):

Examples: ______ (ABC), _______ (TDF) [nucleotide], ______ (DDC), _________ (FTC), _________, ________ (3TC), ______ (D4T) & ___________ (AZT).

A

abacavir; tenofovir; didanosine

emtricitabine; zalcitabine

lamivudine; stavudine

zidovudine

77
Q

(1)Nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs):

Mechanism of action:

initial _________ of the NRTI’S by the ____ cell enzymes (kinase) to their ___________ derivatives.

These then compete with their corresponding _________ and act as __________ to the viral reverse transcriptase enzyme in the synthesis of the proviral DNA.

The incorporation of the ________ into the growing viral DNA chain eventually results in chain _________.

A

phosphorylation; host

5’ triphosphate; host cellular triphosphates

false substrate ; 5’-triphospate

termination

78
Q

(1)Nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs):

Mechanism of action:

The mammalian ________ –DNA polymerase is (susceptible or resistant?) to the effect of the NRTI’s.

However the ______-DNA polymerase in their host cell _______ is fairly (sensitive or resistant ?) and this may account for the ____________

A

alpha

relatively resistant

gamma; mitochondria; sensitive

unwanted effects of the NRTI’s.

79
Q

Nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs):

Uses: mainly for _____ with other ARVs.

But Lamivudine, adefovir and tenofovir are also used for ___________

A

HIV

hepatitis B.

80
Q

Nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs):

Uses: ________,________, and _______ are also used for hepatitis B.

A

Lamivudine ,adefovir and tenofovir

81
Q

Nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs):

Adverse effects:

Class adverse effects: ______ which involves the building up of _____ in the blood due to _________ which results in production of ______ as a bye product of energy formation.

A

Lactic acidosis ; lactic acid

mitochondria toxicity; lactic acid

82
Q

Nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs):

Adverse effects:

______ adverse effects

_______ adverse effects

A

Class

Specific

83
Q

Nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs):

Adverse effects:

Specific adverse effects:

Zidovudine ( ________ )

Stavudine (_________ and ________ )

Abacavir (———- reaction)

tenofovir alafenamide (TAF) or tenofovir disoproxil fumarate (TDF).

A

anaemia

peripheral neuropathy & lipodystrophy

allergic

84
Q

Nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs):

Adverse effects:

Specific adverse effects:

________ (anaemia)

_________ (peripheral neuropathy & lipodystrophy)

________ (allergic reaction)

tenofovir alafenamide (TAF) or tenofovir disoproxil fumarate (TDF).

A

Zidovudine

Stavudine

Abacavir

85
Q

Nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs):

tenofovir alafenamide (TAF) or tenofovir disoproxil fumarate (TDF)

Specific adverse effects:

(TAF or TDF?) has better effects on bones and kidney and is preferable in patients with underlying bone or kidney disease than (TAF or TDF?) . However the latter also have better _________ effects .

A

TAF; TDF

lipid lowering

86
Q

Why is TDF better than TAF in lowering lipids levels

A

This is because TDF produce higher level of tenofovir which lowers lipid.

87
Q

Non-nucleoside reverse transcriptase inhibitors (NNRTIs)

Examples

1st generation: _______,________,_______

2nd generation: ———,——-,———-

A

efavirenz (EFV), nevirapine (NVP) & delavirdine

daravirine, etravirine and rilpivirine

88
Q

Non-nucleoside reverse transcriptase inhibitors (NNRTIs)

Uses: for _____ in combination with other ARVs.

________ (resistant case in tmt exp pt only), ______ (tmt naïve pt)

A

HIV

Etravirine

Rilpivirine

89
Q

Non-nucleoside reverse transcriptase inhibitors (NNRTIs)

Mechanism of action: NNRTIs bind to the ————— near its ______ site and _____ it.

A

reverse transcriptase enzyme

catalytic; denature

90
Q

Non-nucleoside reverse transcriptase inhibitors (NNRTIs)

Class adverse effects: ______

Specific adverse effects:

Efavirenz: _____ toxicity

Nevirapine: ______toxicity

Etravirine: _____ reaction

Delavirdine: ______ reaction, fever, _____ vision,stuffy nose.

A

rash

CNS

hepa

allergic ; allergic; blurred

91
Q

Non-nucleoside reverse transcriptase inhibitors (NNRTIs)

Class adverse effects: rash

Specific adverse effects:

__________: CNS toxicity

___________: hepatoxicity

__________: allergic reaction

__________: allergic reaction, fever, blurred vision, stuffy nose.

A

Efavirenz

Nevirapine

Etravirine

Delavirdine

92
Q

HIV PROTEASE INHIBITORS

Ends with??

A

Navir

93
Q

HIV PROTEASE INHIBITORS

Mechanism of action:- protease inhibitors bind to the site where _____ normally occur.

This prevent the viral specific protease from ____________________________ into various viral structural and functional proteins

A

cleavage

breaking down the inert polyproteins at the appropriate cleavage positions

94
Q

HIV PROTEASE INHIBITORS

Uses: for ______ infection in combination with other antiretroviral drugs of different classes

A

HIV

95
Q

HIV PROTEASE INHIBITORS

Class adverse effects:

__________, ____________ , myalgia, lipodystrophy, hyperglycemia.

A

paraesthesia

rhabdomyolysis

96
Q

HIV PROTEASE INHIBITORS

Specificic adverse effects:

Atazanavir causes ___________________ but has less effects on _________ and __________

A

raised bilirubin levels

lipodystrophy and hyperglycemia.

97
Q

Inhibitors of HIV fusion

Example: __________,_________

A

enfuvirtide, ibalizumab

98
Q

Inhibitors of HIV fusion

Mechanism of action:

Enfuvirtide: binds to ______ to inhibit fusion of HIV with host cells CD4 molecules. It is usually given by ________ injection.

Ibalizumab: binds to _________ and prevent fusion with HIV

A

GP41 ; subcutaneous

CD4 molecules

99
Q

Inhibitors of HIV fusion

Uses: used in treatment of HIV in combination with other ARV drugs when ———————————- or ___________________________

A

resistance becomes a problem or when there is intolerance to other antiretroviral drugs.

100
Q

Inhibitors of HIV fusion

Side effects:

Enfuvirtide:______ symptoms and __________ reactions.

A

flu-like

hypersensitivity

101
Q

HIV Integrase Strand Transfer inhibitors (ISTIs)

Examples:
•
– 1st generation: ralte________ and elvite_____.
•
– 2nd generation: dolute_______ and bicte______

A

gravir; gravir

gravir; gravir

we aRE BaD

102
Q

HIV Integrase Strand Transfer inhibitors (ISTIs) cont’d

Side effects of raltegravir:
– Common: headache, nausea, diarrhoea, weakness,insomnia.

– Rare: _______ ,________,_______ , pyrexia, diaphoresis, rashes, _____ failure, nephrolithiasis, depression, _____ behaviours, anxiety and paranoia.

A

hepatitis, thrombocytopenia, rhabdomyolysis

renal; suicidal

103
Q

HIV Integrase Strand Transfer inhibitors (ISTIs)

Mechanism of action:- they inhibit the __________ enzyme which is responsible for integration of the viral DNA with the infected cell DNA.
Uses: HIV/AIDS infection (with other ARVs)

A

viral integrase

104
Q

Entry Inhibitors or CCR5 antagonists

Examples: mara____, apla______ and vicri______.

A

viroc

viroc

viroc

105
Q

Entry Inhibitors or CCR5 antagonists

Mechanism of action-

maraviroc binds to ______ and blocks its association with the HIV gp _____ thereby preventing _____________

However some HIV can also enter the host cell through _________. Therefore hiv ___________ is essential for efficacy.

A

CCR5 ; 120; entry into the host cell.

CXCR4

tropism test

106
Q

Maturation Inhibitors

Examples: __________ and __________

A

vivecon and bevirimat

107
Q

Maturation Inhibitors

Mechanism of action-

they inhibit the conversion of ________ to _________ leading to formation of (infective or non infective ?) virions with ________

A

viral polyprotein

mature capsid

non infective

defective core.

108
Q

Maturation Inhibitors Examples: vivecon and bevirimat

Uses: HIV/AIDS in combination with other ARV drugs

T/F

A

T

109
Q

Pharmacotherapy of antiretroviral
Principles involved:

– start treatment as soon as __________

– use combination of at least _________ different antiretroviral drugs (______)

– monitoring of _________ and _________

– change treatment regimen if viral plasma concentration persists or increases.

A

HIV is diagnosed

three; HAART

plasma viral load and cd4+ cells count

110
Q

At present, HIV infection has no cure.

T/F

A

T

111
Q

However, the virus can be reduced to an ___________ level in the blood with ___________.

A

undetectable

HAART

112
Q

ART FOR TREATMENT NAÏVE
PATIENTS (2014 GUIDELINES)
1. Tenofovir/emtricitabine + _______/______

  1. Tenofovir + emtricitabine + _______
  2. Tenofovir/emtricitabine + ______/______
  3. Tenofovir/emtricitabine + ________
  4. Tenofovir/emtricitabine +________/cobicistat
  5. Tenofovir/emtricitabine + _______
  6. Abacavir/lamivudine + dolutegravir in (HLA*B-5701 negative)

_____________ could be used to replace emtricitabine in all the regimen.

A

darunavir; ritonavir

efavirenz

atazanavir; ritonavir

raltegravir

Elvitegravir

dolutegravir

Lamivudine

113
Q

Prevention of mother to child transmission of HIV (PMTCT)

Mother to child transmission happens when HIV, the virus that causes AIDS, is passed from a mother to her unborn baby during ________,_______, or ________.

A

pregnancy, labour, childbirth or during breastfeeding

114
Q

Prevention of mother to child transmission of HIV (PMTCT)

The main aim in treating pregnant women with antiretroviral drugs is to ____________ and to ________________.

A

avoid damage to the fetus

prevent mother to child transmission of HIV

115
Q

Scheduled caesarean delivery can not prevent MTCT of HIV.

T/F

A

F

Scheduled caesarean delivery could also prevent MTCT of HIV.

116
Q

PMTCT

Breastfeeding mother

Mother: continue _____ being used from ________________________________ and thereafter.

Infant: ______ started within _____ of birth till ______ after ___________

A

HAART ; before conception throughout pregnancy, breastfeeding

nevirapine; 6-72hrs

one week; stoppage of breastfeeding.

117
Q

PMTCT

Non-breastfeeding mother:

mother: same as above

Infant: ______ started within ______ after birth for _________

A

nevirapine

6-72hrs

6 weeks.

118
Q

HIV post exposure prophylaxis

WHO recommendations are administration of

a)_______/_________+ _______/______for ____ days
OR

(b) ________ /________ + ______/ ————-for _____ days

_________ could replace emtricitabine in either case. And patient should avoid unprotected sex during this period.

A

TENOVOFIR; EMTRICITABINE

LOPINAVIR; RITONAVIR ; 28

TENOFOVIR ; EMTRICITABINE

ATAZANAVIR; RITONAVIR; 28

Lamivudine

TELl R or TEAm R

119
Q

________ ARV has been controversially said to be teratogenic

A

efavirenz

120
Q

No ARV has been clearly stated to be teratogenic

T/F

A

No ARV has been clearly stated to be teratogenic except efavirenz controversially.

121
Q

efavirenz should be avoided in pregnant and child-bearing age women

T/F

A

T

House Pharmacology (50 decks)

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