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Spring 2018 > Pharm Final > Flashcards

Pharm Final Flashcards

1
Q

Time dependent drug

A

Concentrations in blood must be maintained for a period to inhibit cell growth

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2
Q

Ideal antibacterial

A 
Stable
Soluble
Diffusible
Slow excretion
Large therapeutic index
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3
Q

Drug that is both static and cidal

A

Vancomycin

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4
Q

Empiric therapy

A

Give antibiotics based on best guess

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5
Q

Example of synergism in the notes

A

Beta-lactam + aminoglycoside
-cell wall inh. -protein synth. Inh

AG’s can get into the cell wall because of the beta-lactams

Only synergistic for G+ (cell wall)

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6
Q

Fungal cell walls contain chitin and _

A

B-Glucans

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7
Q

Mycobacteria cell walls are made of what

A 
Phospholipids
Mycolic acids
Arabinogalactan
Murein
Cytoplasmic membrane
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8
Q

_ is the leading killer of people HIV infected

A

Tuberculosis

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9
Q 
Roles of:
antigen presenting cells
Helper T cells
Cellular and humoral immunity
Interferon

In rxn to infection

A

APC- take up and digest/present antigens

HTC: makes interleukin 2, makes interferon

Cell immunity: killer cells kill infected cells

Humoral: T helper contacts B cell holding antigen, B cell makes antibodies

Interferon: activates killer cells, induces resistance of other host cells to virus

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10
Q

How can antibodies affect a virus

A

Bind and neutralize virus

Recognize complex so it can be phagocytosed and destroyed

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11
Q

Passive vs. active immunization

Characteristics of both types of immunization

A

Active: antigen induces cell and humoral immunity, takes weeks

Passive: give antiviral immunoglobulin

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12
Q

How is interferon produced?

What is its role in suppressing viruses?

A

Interferon producing cells express receptors that recognize viral DNA/RNA and make interferon.

It circulates and activates interferon receptors on other cells, inducing expression of genes that promote resistance to viruses. Also activate NK cells

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13
Q

Considerations regarding spectrum activity of antiviral agents

A

Work on one genome type (usually) and sometimes on one type of virus in class.

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14
Q

Base-analog concepts (p31)

A

Resemble bases

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15
Q

Details about acyclovir:

  • Selective metabolic activation in _
  • Competitive inhibition
  • Incorporation into DNA
  • Viral polymerase cannot _

Spectrum:

A

Virus infected cells

Add another base causing termination

HSV1>2>VZV

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16
Q

Acyclovir (Zovirax, Sitavig):

Mechanism of action, virus family affected, uses

A

S

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17
Q

Ganciclovir (cytovene)

Mechanism of action, virus family affected, use

A

M: phosphorylated, inhibits dGTP on polymerase, inhibits elongation after incorporation into DNA

CMV

Prophylaxis and treatment of CMV

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18
Q

Lamivudine

Mechanism of action, virus family affected, use

A

M: competes with dCTP to inhibit reverse transcriptases

hep B and HIV

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19
Q

Docosanol (abreva)

Mechanism of action, virus family affected, use

A

Inhibits attachment of enveloped viruses to cells

HSV1/2, HH6, CMV
Influenza, RSV

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20
Q

Importance of thymidine Kinase and UL97 kinase

A

TK phosphorylates acyclovir to human Kinase

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21
Q

Do host enzymes affect metabolic activation for base analogs?

A

It looks like viral enzymes do (thymidine kinase)

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22
Q

What is the role of M2 protein and action of amantadine in influenza

A

M2: allows genome release within cells

A: prevents uncoating of inf. A virus after entry into host cell and release by blocking M2

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23
Q

Importance of neuraminic (Sialic) acid

A

Cleavage of neuraminic acid disrupts binding of viral hemagglutinin to cell

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24
Q

Importance of neuraminidase

A

Hydrolyzes terminal neuraminic acids from proteins and other host cells.

Ultimately allowing viral release

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25
Q

Action of oseltamivir

A

Neuraminidase inhibitor

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26
Q

NS3-4A protease

A

Serine protease

Produces several enzymes and structural proteins for virus

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27
Q

NS5B RNA Polymerase

A

Copies RNA viral genome

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28
Q

NS5A

A

Ex. Ledipasvir

Protein required for HCV replication and assembly

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29
Q

Information and target for
Simeprevir (OLYSIO)
Sofosbuvir
Ledipasvir

A

Hep C Serine Protease Inhibitors

Simeprevir - NS3-4A
Sofosbuvir - NS5B
Ledipasvir - NS5A (domain 1)

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30
Q

Function of GP120 and GP41

A

GP120/41 is a complex on the outside of a virus (continuation of the core of the virus) that attaches on CD4/CCR5/CXCR4

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31
Q

Which chemokine receptors are needed for HIV virus to attach

A

CD4 and CCR5

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32
Q

T/F integrate use the LTR in double stranded DNA to insert the HIV copy into the host genome

A

TRUE

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33
Q

Herpes virus:
Type
Examples

A

DNA

Chicken pox, herpes, CMV

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34
Q

Hepatitis B is what category and what kind of virus

A

Hepadnavirus

DNA

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35
Q

Influenza A,B,C are what kind and type of virus

A

Orthomyxovirus

RNA

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36
Q

RSV is what kind a type of virus

A

Paramyxovirus

RNA

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37
Q

Hep C is what kind and type of virus

A

Flaviviridae

RNA

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38
Q

From outside to in, general structure parts of virus (4)

A

Envelope
Capsid coat/capsomere
Enzymes
Nucleic acid core

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39
Q

How many viruses cause human disease

A

<50

40
Q

Size of virus

A

0.02-0.3 um

41
Q

Important receptor for HIV

A

CD4/CCR5 CXCR4

42
Q

Important receptor for Influenza

A

Neuraminic acid on glycoproteins

43
Q

Which cells have CD4/CCR5 receptors

A

Th Lymphocytes
Monocytes/macrophages
Neurons in CNS

44
Q

What are LTRs and what do they do

A

Long terminal repeat: sequences at end of genome

Used for integration into host
Drives transcription of HIV genome in host DNA

45
Q

As HIV replication increases, CD4 cell # _

A

Decreases

46
Q

6 types of antiretroviral drugs

A
  1. Nucleoside/tide Reverse Transcriptase Inhibitors
  2. Non-nucleoside Reverse Transcriptase Inhibitors
  3. Protease Inhibitors
  4. Fusion/Adherence Inhibitors
  5. CCR5 Antagonist
  6. Integrase Inhibitors
47
Q

Fusion/adhesion inhibitor of HIV

A

Enfuvirtide

48
Q

CCR5 antagonist (name)

A

Maraviroc

49
Q

3 HIV integrase inhibitors

A

Raltegravir
Dolutegravir
Elvitegravir

50
Q

Immune reconstitution syndrome

A

Immune system comes back, attacks other microbes. Inflammation

51
Q

How does reverse transcriptase contribute to HIV mutagenesis

A

It’s error prone, lacks error correction system. Increases rate of mutation in cDNA

52
Q

How do nucleoside/tide inhibitors of reverse transcriptase work

A

Resemble nucleosides but lack 3’OH necessary for continued polymerization.

53
Q

Nucleoside/tide inhibitors of RT work on which HIV

A

Both

54
Q

Lamivudine:

A

Hep B and HIV treatment

Cytosine Analog, incorporated into cDNA. Causes chain termination.

55
Q

NRTIs:
What
Effective against:

A

Nucleoside reverse transcriptase inhibitor

Effective against HIV 1/2 and some HBV

56
Q

Zidovudine:

A

1st effective anti-HIV drug

57
Q 
NNRTI:
What
Works on what:
Resistance?
Specific example
A

Non-nucleoside reverse transcriptase inhibitor

Works on HIV-1 ONLY

Rapid resistance when used alone (mutations in RT)

Nevirapine

58
Q

What do HIV proteases do?

Effects?

A

Cleave gag-pol polyprotein

Produces active enzymes and structural proteins

59
Q

Protease inhibitors are combined with what

A

Reverse transcriptase inhibitors

60
Q

HIV strains resistant to other protease inhibitors are often responsive to _

A

Tipranavir

61
Q

Consequences of enabling or disabling oncogene or tumor suppressor gene on growth and death

A

Inactivating tumor suppressor genes causes cancer

Activating oncogenes results in cancer

62
Q

Growth factors that trigger an increase in cyclin D can stimulate _

A

Cells back into the growth cycle of cancer

63
Q

Necrosis vs apoptosis

A

A: controlled
N: rupture, spilled contents

64
Q

Cancer results from _

Growth factor tyrosine kinase signaling can stimulate _ via _

Growth factor signaling can also repress _ and promote _

Anti-cancer drugs may inhibit _ and/or cause _

A

Imbalance b/t cell growth and death

Mitosis via cyclin D

Apoptosis and promote cell survival

Mitosis and cause necrosis or apoptosis to reduce a cancer

65
Q

Reason for combination therapy

A

Drug resistance

Resistance is limited by using multiple agents with different mechanisms

66
Q

T/F myelosuppression is a rare side effect of cytotoxic anti-cancer therapeutics

A

FALSE - common

67
Q

3 main mechanisms of cytotoxic therapies

A
  1. Inhibition of nucleotide or DNA synthesis
  2. Block critical proteins needed for cell growth and survival
    - Microtubule and topoisomerase
  3. Cause DNA damage
68
Q

How does DNA damage cause necrosis, apoptosis and inhibition of mitosis

A

Damage causes rxn involving PARP

DNA breaks activate kinase signaling, inducing protein p53

69
Q

What is methotrexate and what does it do?

A

Resembles folate

Inhibits dihydrofolate reductase, ultimately blocking DNA synthesis

Also

Causes hair loss, NV and loss of appetite

70
Q

5-fluoro uracil is a _
that is ultimately activated to a version attached to deoxyribose forming _,
Which inhibits thymidylate synthase which lowers _ and _

A

Base analog
FdUMP
TMP and DNA synthesis

71
Q

Mitotic spindle poisons vincristine and paclitaxel:
Mechanism
Effect

A

V: bind to tubulin dimers, added to end of new tubule and stops polymerization. Chromosome can’t segregate in M-phase

P: bind tubulin, inhibit disassembly of tubulin in microtubules. Microtubules can’t function, can’t segregate

72
Q

What does topoisomerase do

A

Unwind supercoiling DNA generated by polymerases as they move along DNA

73
Q

How does etoposide cause necrosis, apoptosis and inhibition of mitosis

A

Etoposide inhibits topoisomerase II by making it so DNA can’t separate from enzyme after it breaks the strand. This causes a double strand break.

74
Q

Ways to cause DNA damage in cancer cells (5)

A

Radiation

Covalent modification of DNA by reactive drug

DNA strand breaking agent

Anthracyclines

Topoisomerase inhibition

75
Q

T/F radiation and photodynamic agents induce ROS that damage DNA and produce PARP

A

TRUE

76
Q

Covalent modifiers of DNA do what

A

React with DNA producing damage and associated PARP and consequences

77
Q

Anthracyclines do what 3 things

A

Intercalate between bases of DNA
Induce ROS that damage DNA
Inhibit topoisomerase

78
Q

5 things that cause GERD

A
  1. Hiatal hernia
  2. Abnormalities in LES function
  3. Defects in esophageal contractions
  4. Defects in emptying stomach
  5. Excess production of acid
79
Q

Heartburn, indigestion, GERD and peptic ulcers are all treated by drugs that either _ or _

A

Reduce intragastric acidity or promote GI mucosal defense

80
Q

Proton pump inhibitors do what

A

Inhibit hydronium-potassium pump, preventing the production of acid

81
Q

H2 blockers:
What
Common one

A

H2 receptors stimulate gastric acid secretion, blockers block that

Cimetidine (Tagamet) is common. Less important now

82
Q

What does proglumide do

Good side effect

A

Inhibits GI motility and reduces gastric secretions (gastrin receptor antagonist)

Enhances analgesia produced by opioid drugs, prevents and reverses tolerance to them.

83
Q

Anti-nausea and vomiting drugs

A

Anti-muscarinic

84
Q

4 types of laxatives

A

Bulk forming
Osmotic
Stimulant
Fecal softeners

85
Q

3 ways anti-diarrheal agents work

A

Soak up water
Anti-secretory
Decrease intestinal motility

86
Q

Lower the pH, the less _ will be available, making it tough to remineralize

A

(PO4)3

87
Q

How does fluoride work

A

Boosts ability of saliva to return lost minerals to tooth enamel before cavities can develop

88
Q

Tooth with all fluoride instead of hydroxide would have:

A

Smaller crystals
Better H bonding
Decreased solubility

89
Q

Healthy gums microbes

Unhealthy gums microbes

A

H: G+, facultative anaerobes

U: G-, obligate anaerobes

90
Q

Chlorhexidine is a _

A

Bisbiguanide

91
Q

Mechanism of chlorhexidine (3 things)

A

Ruptures bact Cell membrane
Binds salivary mucins, reduces pellicle, inhibiting plaque bacteria colonization
Binds bacteria

92
Q

Mechanism of triclosan

A

Inhibits fatty acid synthesis

93
Q

Cetylpyridinium chloride is a _

A

Quaternary ammonium compound

94
Q

Probiotic organism to prevent caries

A

Strep salivarius

95
Q

Order of effectiveness of mouthwashes

A

Chlorhexidine
CPC
Essential oils

96
Q

How does potassium nitrate desensitize teeth

A

Depolarizers nerve and prevents it from repolarizing and sending pain signals to brain

Spring 2018 (18 decks)

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