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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
Action of oseltamivir
Neuraminidase inhibitor
26
NS3-4A protease
Serine protease | Produces several enzymes and structural proteins for virus
27
NS5B RNA Polymerase
Copies RNA viral genome
28
NS5A
Ex. Ledipasvir | Protein required for HCV replication and assembly
29
Information and target for Simeprevir (OLYSIO) Sofosbuvir Ledipasvir
Hep C Serine Protease Inhibitors Simeprevir - NS3-4A Sofosbuvir - NS5B Ledipasvir - NS5A (domain 1)
30
Function of GP120 and GP41
GP120/41 is a complex on the outside of a virus (continuation of the core of the virus) that attaches on CD4/CCR5/CXCR4
31
Which chemokine receptors are needed for HIV virus to attach
CD4 and CCR5
32
T/F integrate use the LTR in double stranded DNA to insert the HIV copy into the host genome
TRUE
33
Herpes virus: Type Examples
DNA | Chicken pox, herpes, CMV
34
Hepatitis B is what category and what kind of virus
Hepadnavirus | DNA
35
Influenza A,B,C are what kind and type of virus
Orthomyxovirus | RNA
36
RSV is what kind a type of virus
Paramyxovirus | RNA
37
Hep C is what kind and type of virus
Flaviviridae | RNA
38
From outside to in, general structure parts of virus (4)
Envelope Capsid coat/capsomere Enzymes Nucleic acid core
39
How many viruses cause human disease
<50
40
Size of virus
0.02-0.3 um
41
Important receptor for HIV
CD4/CCR5 CXCR4
42
Important receptor for Influenza
Neuraminic acid on glycoproteins
43
Which cells have CD4/CCR5 receptors
Th Lymphocytes Monocytes/macrophages Neurons in CNS
44
What are LTRs and what do they do
Long terminal repeat: sequences at end of genome Used for integration into host Drives transcription of HIV genome in host DNA
45
As HIV replication increases, CD4 cell # _
Decreases
46
6 types of antiretroviral drugs
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
Fusion/adhesion inhibitor of HIV
Enfuvirtide
48
CCR5 antagonist (name)
Maraviroc
49
3 HIV integrase inhibitors
Raltegravir Dolutegravir Elvitegravir
50
Immune reconstitution syndrome
Immune system comes back, attacks other microbes. Inflammation
51
How does reverse transcriptase contribute to HIV mutagenesis
It’s error prone, lacks error correction system. Increases rate of mutation in cDNA
52
How do nucleoside/tide inhibitors of reverse transcriptase work
Resemble nucleosides but lack 3’OH necessary for continued polymerization.
53
Nucleoside/tide inhibitors of RT work on which HIV
Both
54
Lamivudine:
Hep B and HIV treatment | Cytosine Analog, incorporated into cDNA. Causes chain termination.
55
NRTIs: What Effective against:
Nucleoside reverse transcriptase inhibitor | Effective against HIV 1/2 and some HBV
56
Zidovudine:
1st effective anti-HIV drug
57
``` NNRTI: What Works on what: Resistance? Specific example ```
Non-nucleoside reverse transcriptase inhibitor Works on HIV-1 ONLY Rapid resistance when used alone (mutations in RT) Nevirapine
58
What do HIV proteases do? Effects?
Cleave gag-pol polyprotein Produces active enzymes and structural proteins
59
Protease inhibitors are combined with what
Reverse transcriptase inhibitors
60
HIV strains resistant to other protease inhibitors are often responsive to _
Tipranavir
61
Consequences of enabling or disabling oncogene or tumor suppressor gene on growth and death
Inactivating tumor suppressor genes causes cancer Activating oncogenes results in cancer
62
Growth factors that trigger an increase in cyclin D can stimulate _
Cells back into the growth cycle of cancer
63
Necrosis vs apoptosis
A: controlled N: rupture, spilled contents
64
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 _
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
Reason for combination therapy
Drug resistance Resistance is limited by using multiple agents with different mechanisms
66
T/F myelosuppression is a rare side effect of cytotoxic anti-cancer therapeutics
FALSE - common
67
3 main mechanisms of cytotoxic therapies
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
How does DNA damage cause necrosis, apoptosis and inhibition of mitosis
Damage causes rxn involving PARP DNA breaks activate kinase signaling, inducing protein p53
69
What is methotrexate and what does it do?
Resembles folate Inhibits dihydrofolate reductase, ultimately blocking DNA synthesis Also Causes hair loss, NV and loss of appetite
70
5-fluoro uracil is a _ that is ultimately activated to a version attached to deoxyribose forming _, Which inhibits thymidylate synthase which lowers _ and _
Base analog FdUMP TMP and DNA synthesis
71
Mitotic spindle poisons vincristine and paclitaxel: Mechanism Effect
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
What does topoisomerase do
Unwind supercoiling DNA generated by polymerases as they move along DNA
73
How does etoposide cause necrosis, apoptosis and inhibition of mitosis
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
Ways to cause DNA damage in cancer cells (5)
Radiation Covalent modification of DNA by reactive drug DNA strand breaking agent Anthracyclines Topoisomerase inhibition
75
T/F radiation and photodynamic agents induce ROS that damage DNA and produce PARP
TRUE
76
Covalent modifiers of DNA do what
React with DNA producing damage and associated PARP and consequences
77
Anthracyclines do what 3 things
Intercalate between bases of DNA Induce ROS that damage DNA Inhibit topoisomerase
78
5 things that cause GERD
1. Hiatal hernia 2. Abnormalities in LES function 3. Defects in esophageal contractions 4. Defects in emptying stomach 5. Excess production of acid
79
Heartburn, indigestion, GERD and peptic ulcers are all treated by drugs that either _ or _
Reduce intragastric acidity or promote GI mucosal defense
80
Proton pump inhibitors do what
Inhibit hydronium-potassium pump, preventing the production of acid
81
H2 blockers: What Common one
H2 receptors stimulate gastric acid secretion, blockers block that Cimetidine (Tagamet) is common. Less important now
82
What does proglumide do Good side effect
Inhibits GI motility and reduces gastric secretions (gastrin receptor antagonist) Enhances analgesia produced by opioid drugs, prevents and reverses tolerance to them.
83
Anti-nausea and vomiting drugs
Anti-muscarinic
84
4 types of laxatives
Bulk forming Osmotic Stimulant Fecal softeners
85
3 ways anti-diarrheal agents work
Soak up water Anti-secretory Decrease intestinal motility
86
Lower the pH, the less _ will be available, making it tough to remineralize
(PO4)3
87
How does fluoride work
Boosts ability of saliva to return lost minerals to tooth enamel before cavities can develop
88
Tooth with all fluoride instead of hydroxide would have:
Smaller crystals Better H bonding Decreased solubility
89
Healthy gums microbes Unhealthy gums microbes
H: G+, facultative anaerobes U: G-, obligate anaerobes
90
Chlorhexidine is a _
Bisbiguanide
91
Mechanism of chlorhexidine (3 things)
Ruptures bact Cell membrane Binds salivary mucins, reduces pellicle, inhibiting plaque bacteria colonization Binds bacteria
92
Mechanism of triclosan
Inhibits fatty acid synthesis
93
Cetylpyridinium chloride is a _
Quaternary ammonium compound
94
Probiotic organism to prevent caries
Strep salivarius
95
Order of effectiveness of mouthwashes
Chlorhexidine CPC Essential oils
96
How does potassium nitrate desensitize teeth
Depolarizers nerve and prevents it from repolarizing and sending pain signals to brain

Spring 2018 (18 decks)

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