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Med School > IIIR3b > Flashcards

IIIR3b Flashcards

1
Q

Where do NK cells come from?

A

bone marrow from a common NK and T cell progenitor

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2
Q

What interferons activate NK cells?

A

interferon alpha/beta: augments cytolytic activity

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3
Q

What interleukins activate NK cells?

A
  1. IL-15: needed for development and is constantly needed, increases cytotoxicity
  2. IL-12/18: augments INF-gamma production
  3. IL-2: induces proliferation, increases cytotoxicity
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4
Q

What are NK cells especially good at?

A

fighting viruses

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5
Q

What will make an NK cell kill another cell?

A
  1. The absence of an MHCI receptor, and

2. An activating reaction from the other cell

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6
Q

What are Id2, MCM4 and TF Nfil3 (E4B4) for?

A

They are all important in T cell development.

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7
Q

How do NK cells indirectly participate in fighting viral infections?

A

IFN-alpha/gamma activates them, as do cytokines released from infected cells.

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8
Q

How do NK cells directly participate in fighting viral infections?

A

KIR (Ly49 in mice) helps the NK cell recognize infected cells. If MHCI is absent, KIR helps NK to bind and kill. If MHCI is present, KIR inhibits the attack.

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9
Q

What is an NKG2D ligand?

A

It is a “kill me” signal put up by infected cells. NK cells have NKG2D receptors.

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10
Q

What must NKG2D pair up with in order to work?

A

DAP10.

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11
Q

What type of cell does HIV target?

A

CD4+ T lymphocytes

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12
Q

What are the 3 steps of entry for HIV?

A
  1. bind to CD4
  2. bind co-reeptor, either CCR5 or CXCR4
  3. fuze membrane
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13
Q

Where does HIV turn RNA into DNA?

A

cytoplasm

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14
Q

What is the role of integrase?

A

It brings the viral DNA into the nucleus to be inserted into the host DNA

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15
Q

How many HIV clades are there?

A

A-O. B is common in US, C is common in Africa.

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16
Q

What is normal CD4 levels? When does a person have AIDS?

A 
normal = 450-500 CD4 cells per microliter
AIDS = <200 CD4 cells per microliter
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17
Q

What HLA type do elite controllers have?

A

HLAB57

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18
Q

Whys is HIV so hard to fight?

A

B cells can make Abs, and CTL cells will attack, but CD4+ cells are the ones that regulate the B cell and CTL cells. Also, rapid mutation rates.

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19
Q

How does Lamivudine work?

A

It is a reverse transcriptase inhibitor. It lacks an -OH on the 3’ carbon of the nucleoSide. If it is incorporated, the chain has to stop.

20
Q

How does Ritonavir work?

A

Protease inhibitor. It mimics the transition state of the protease.

21
Q

How does Ritonavir help potentiate other drugs?

A

it is a P450 inhibitor (cyp 3A4 to be exat), so other drugs (Saquinavir) is not metabolized as fast. Greatly increases the area under the curve.

22
Q

How does resistance develope?

A

One point mutation, either 184V or L90M.

23
Q

What is Amantadine?

A

An anti-influenza drug that works by blocking the M2 proton pump to the endosome which the virus needs to uncoat itself.

24
Q

What is neuraminidase? Name a neuraminidase inhibitor?

A

It is what helps the new viral bud to cut off its oligosaccharide and be free. Neuraminidase inhibitors, like Oseltamivir, is given as a prodrug.

25
Q

What are three fungi that live commensaly with humans?

A
  1. Candida
  2. Malassezia
  3. Pneumocystis jiroveci
26
Q

Ringworm

A

species of microsporun, trichophyton and epidermophyton floccosum

27
Q

pityriasis veriscolor

A

infects oily areas of skin and can change pigment of host

28
Q

dermatophytes

A

athlete’s foot, fungi that infects keratinous tissue, 3 main groups: microsporum, trichophyton, epidermophyton

29
Q

Sporotrichosis

A

Rose handler’s disease, happens traumatically and then spreads along lymphatics, Dx’ed with culture

30
Q

What are the 5 major fungi that cause infection?

A
  1. aspergillosis
  2. candidiasis
  3. cryptococcosis
  4. mucormycosis
  5. pneumocystosis
31
Q

When dimorphic fungi become morpho-type locked, what happens to them?

A

They become avirulent.

32
Q

What are 3 types of candidiasis?

A
  1. oropharyngeal
  2. esophageal
  3. vulvovaginits
    * all three have white patches that are painful
33
Q

What are some opportunistic fungal pathogens?

A

aspergillus, non-aspergillus (mucorales, fusarium, scedosporium), candida, pneumocystis, cryptococcus*

34
Q

What are some primary pathogenic fungi?

A

histopasma, coccidioides, blastomyces, sporothrix, paracoccidioides, cryptococcus*

35
Q

What is a dimorph?

A

Mold outside, and yeast inside.

36
Q

What are the four steps after you cut yourself?

A
  1. vasoconstriction
  2. primary hemostasis (platelet adhesion/aggregation)
  3. clot formation
  4. resolution
37
Q

How do vWF and collagen help platelets? What does GPIb do?

A

Platelets see them in the subendothelium and that helps them bind. GPIb also helps platelets bind, and it undergoes conformational change and becomes GPIIb and IIIa after the platelet joins.

38
Q

What does ADP do?

A

It is a platelet agonist which activates and recruits more platelets.

39
Q

How does the Fibrin know where to go?

A

the platelet plug begins to show negatively charged phosphlipids, this pulls them to the site.

40
Q

What change do RBCs undergo?

A

They go from erythrocyte to polyhedrocyte.

41
Q

How does the clotting stop?

A

endothelial cells secrete negative regulators such as prostacyclin, ADPase and nitric oxide.

42
Q

How is fibrin made?

A

thrombin acts on fibrinogen.

43
Q

What is the most important factor for making thrombin?

A

Tissue factor.

44
Q

Prothrombin time and Partial Thromboplastin Time do what?

A

They are measures of clotting abilities. They measure slightly different mechanisms, so the results can help to identify which co-factor might not be working.

45
Q

What are 4 ways to regulate coagulation?

A
  1. Tissue Factor Pathway Inhibition
  2. Antithrombin III
  3. Protein C Pathway
  4. Blood Flow

Med School (24 decks)

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