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Disease and Defense > Test 2 (week 2) > Flashcards

Test 2 (week 2) Flashcards

1
Q

What is the best known pathogenic yeast?

A

Candida albicans. Candida is in the gastrointestinal and vaginal microbiomes (normal flors)

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2
Q

causes lung infections that often spread to the skin and central nervous system.

A

Cryptococcus neoformans

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3
Q

eukaryotic single-cell organisms (protozoa) or complex multi-cellular organosms (Helminths)

A

parasites

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4
Q

either single cell organisms (typically yeast) or complex multi-cellular forms (mold)

A

fungi

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5
Q

typically form thread-like hyphae and usually form conidia (spores)

A

molds

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6
Q

tapeworms made up of an attachment end (scolex) with many, many segments (proglottids)

A

cestodes

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7
Q

roundworms

A

nematodes

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8
Q

leaf-shaped flukes that infect the gastrointestinal tract.

A

trematodes

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9
Q

How are filoviruses transferred?

A

Filoviruses are transmitted through direct contact with blood or bodily fluids (saliva, sweat, feces, urine, vomit, breast milk, and semen).

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10
Q

Filoviruses initially infect _____.

A

macrophages and dendritic cells

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11
Q

How do filoviruses typically enter human populations?

A

Filoviruses typically enter human populations by handling bushmeat (wild animals hunted for food) and contact with infected bats

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12
Q

where do you typically see yellow fever today?

A

Today, yellow fever is found primarily in subtropical areas of Africa and South America

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13
Q

What carries yellow fever to humans?

A

mosquitos

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14
Q

How does the Hantavirus get to humans?

A

Hantaviruses cause persistent infections of rodents and may cause disease in humans following transmission through aerosolized excreta

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15
Q

What are the two most common species of plasmodium that infect humans?

A

P. falciparum

P. vivax

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16
Q

describe the Exoerythrocytic stage (1st stage) in plasmodium life cycle

A

** no symptoms of disease are seen in this stage**
Sporozoites introduced at bite site in mosquito saliva–>
Infects hepatocytes and undergoes asexual replication
(Product of replication are merozoites)

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17
Q

Describe the erythrocytic stage (second stage) in plasmodium life cycle.

A

Merozoites infect red blood cells (RBCs).
Asexual replication occurs in RBCs.
-Ring-stage (Early Trophozoites)

-Late Trophozoites
-Schizonts
Some merozoites develop into male and female gametocytes within RBCs

this stage is where you see clinical manifestations

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18
Q

What causes the cyclic fever spikes in plasmodium infections?

A

spikes occur when RBCs are lysed by parasites

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19
Q

The quartan fever cycle is characteristic of ____.

A

malaria

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20
Q

The tertian fever cycle is characteristic of _____.

A

P. falciparum

P. vivax

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21
Q

how are plasmodium parasites transmitted to humans?

A

Transmitted through the bite of a female Anopheles mosquito

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22
Q

What is the treatment plan for plasmodium vivax?

A

P. vivax – give chloroquine and then primaquine

23
Q

What is the treatment plan for plasmodium falciparum (poses greatest risk of mortality)?

A

pretty much anything but chloroquine

24
Q

describe positive polarity RNA viruses.

A
  • viral RNA genome directly serves as mRNA

- synthesizes viral encoded transcriptase

25
Q

Describe negative polarity RNA viruses.

A
  • Viral RNA genome CANNOT serve as mRNA
  • Viral RNA transcriptase must be included within virion
  • The transcriptase copies genomic RNA into complementary positive-sense mRNA that is used to synthesize viral proteins
26
Q

Where does viral RNA replication occur?

A

cytoplasm

27
Q

Where does viral DNA replication occur?

A

nuclues

28
Q

Which RNA virus is not replicated in the cytoplasm?

A

influenza–> happens in nucleus

29
Q

Which DNA virus is not replicated in the nucleus?

A

poxvirus–> happens in cytoplasm

30
Q

What is the MOA of Acyclovir (and other herpes drugs for that matter)?

A

are analogs of nucleosides that prevent DNA chain elongation

31
Q

What are the prototype herpes drugs?

A

Acyclovir

32
Q

Which is metabolized in the liver: NRTIs or NNRTIs?

A

NNRTIs; because of this, you can see drug interactions

33
Q

What are the different classes of drugs used to treat HIV?

A

NRTIs, NNRTIs, protease inhibitors, and entry inhibitors

34
Q

What is the mechanism of action of NRTIs?

A

NRTIs are analogs of nucleosides but lack a 3’ hydroxyl group
–>Attachment of the next nucleotide is impossible

35
Q

What is the mechanism of action of NNRTIs?

A

bind to site on viral transcriptase and prevent further RNA to DNA synthesis

36
Q

What is the mechanism of action of protease inhibitors?

A

inhibit the HIV proteases needed to assemble the coat structures correctly

37
Q

What is the mechanism of action of entry inhibitors?

A

Attachment of many HIV strains requires two receptors on human cells
Drugs bind to this receptor or the proteins that can block attachment and entry of HIV into the cell

38
Q

What are the prototype NRTIs?

A

Abacavir, Didanosine, Lamivudine

39
Q

What are the prototype NNRTIs?

A

Efavirenz, Nevarapine

40
Q

What are the prototype protease inhibitors?

A

Retonavir, Atazanavir

41
Q

What are the prototype entry inhibitors?

A

Miravoc, Enfuvirtide

42
Q

What is the prototype CMV drug?

A

Ganciclovir

43
Q

What are the general adverse effects of NRTIs?

A

Lactic acidosis producing:

Hepatomegaly, steatosis (higher fat storage in cells)

44
Q

What are the general adverse effects of NNRITs?

A

multiple drug interactions since it is degraded in the liver

45
Q

What are the general adverse effects of Protease inhibitors?

A

-Use in HAART has led to carbohydrate and lipid metabolism disorders
-Cross-inhibits endogenous lipid-regulating proteins
-Leads to altered body fat disposition
“buffalo hump” and gynecomastia
-Hyperglycemia and insulin resistance

46
Q

What is the MOA of Amantadine and Rimantadine?

A

Block the M2 proton ion channel of the virus
-Inhibits uncoating of the virus in cells
Thus preventing replication

47
Q

What are the adverse effects of Amantadine and Rimantadine?

A

GI, dizziness, slurred speech

48
Q

What are the primary influenza drugs?

A

Oseltamivir, Zanamivir

49
Q

What are the primary Hepatitis drugs?

A

Interferon-alpha, Ribavirin

50
Q

What is the MOA for Oseltamivir and Zanamivir

A
  • Inhibit neuraminidase A and B

- Reduce viral spreading

51
Q

What is the MOA for interferon-alpha?

A
  • Host cytokine that exerts complex antiviral, immunomodulatory and antiproliferative actions
  • Enhances phagocytic activity of macrophages
  • Augmentation of the proliferation and survival of cytotoxic T cells.
52
Q

What are the adverse effects of interferon-alpha?

A 
GI irritation
flu-like syndrome 
fatigue 
severe depression 
alopecia 
thyroid dysfunction
mental confusion
53
Q

What is the MOA for Ribavirin?

A

Prodrug – when active, represents RNA nucleotide; Inhibits GTP formation, mRNA capping, and block RNA-dependent polymerases
IT MUST BE USED WITH ANOTHER ANTIVIRAL DRUG, DOES NOT LIKE BEING ALONE

54
Q

What are the adverse effects of ribavirin?

A

hemolytic anemia

Disease and Defense (3 decks)

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