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B9W4 > PBL 1 > Flashcards

PBL 1 Flashcards

1
Q

Outline the HIV replication cycle

A

HIV uses gp120 to bind to CD4 receptor and a co-receptor
HIV and CD4 membranes fuse and the capsid is released inside
HIV releases and uses reverse transcriptase to convert RNA to DNA
integrate allows insertion of viral DNA to the cells DNA to form proviral DNA
It uses the machinery of the cell to make HIV proteins which move to the surface of the cell and assembles into immature HIV
Immature HIV pushes itself out of the cell with protease to form mature HIV

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2
Q

What are some common co-receptors on the CD4 T cells?

A

CCR5

CXCR4

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3
Q

Describe what happens in the acute infection stage of HIV?

A

HIV enters the body and takes over macrophages/dendritic cells/T cells
There’s a large spike in HIV replication. And viral load and a drop in CD4 T cells

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4
Q

What symptoms do we see in the acute HIV infection? Why?

A

1-2 weeks of flu like symptoms due to seroconversion as the body first produces antibodies

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5
Q

When is the risk of passing on HIV the highest?

A

During the acute infection

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6
Q

How long does the clinical latency last?

A

2-10 years

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7
Q

What happens during the clinically latent phase of HIV?

A

The virus steadily affects more cells so viral load slowly increases and T cell number slowly decreases

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8
Q

What is the the normal T cell count?

A

500-1200 cells per cubic mm

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9
Q

What is the T cell lymphocyte count during AIDS?

A

Less than 200 cells per cubic meter

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10
Q

What symptoms are experienced during AIDS?

A

Persistent fever
Fatigue
Weight loss
Diarrhoea

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11
Q

What are some common AIDS-defining conditions?

A

Pneumocystis jiroveci pneumonia
HIV related encephalopathy
Invasive cervical cancer
Fungal infections

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12
Q

What are ELISA tests?

A

Enzyme linked immunoassay

Detects antibodies in the blood

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13
Q

What is a NAT test? When can it test for HIV?

A

Nucleic acid test
blood tests used to detect the genetic material of viruses and bacteria in your blood
10-33 days after exposure

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14
Q

When can antibody tests detect HIV?

A

23-90 days after exposure

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15
Q

What is the recommended test for detecting HIV?

A

Antibody/antigen test

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16
Q

When does an antibody/antigen test work?

A

18-45 days after exposure

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17
Q

Where did HIV come from?

A

Simian immunodeficiency virus in chimpanzees from central Africa

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18
Q

How can you vertically transmit HIV?

A

Across the placenta during pregnancy
During childbirth due to cervical secretions and blood
During breastfeeding

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19
Q

What should you do to prevent vertical transmission of HIV?

A

Start taking antiretroviral medication by week 24 of pregnancy
Have a c section if the viral load is over 1000
The baby will need to take anti HIV drugs for a period of time after birth
HIV tests done on the baby at birth 6 weeks, 12 weeks and 18 months
Breast feeding is not advised

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20
Q

why is it important to take antiretroviral therapy?

A

to help people live longer, happier lives and reduce the risk of transmission to others

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21
Q

how long does it take on antiretrovirals to reach an undetectable viral load?

A

6 months

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22
Q

what are the 7 classes of antiretroviral therapies?

A
  • nucleoside reverse transcriptase inhibitors
  • non-nucleoside reverse transcriptase inhibitors
  • integrase inhibitors
  • protease inhibitors
  • entry inhibitors
  • attachment inhibitors
  • post-attachment inhibitors
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23
Q

how do nucleoside reverse transcriptase inhibitors work?

A

they compete for reverse transcriptase’s binding site so that RNA cannot be converted to DNA

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24
Q

how do non-nucleoside reverse transcriptase inhibitors work?

A

they bind directly to an allosteric site on reverse transcriptase, inhibiting its action

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25
Q

how do integrase inhibitors work?

A

stop integrase from working, which stops HIV DNA from entering CD4 cell’s DNA

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26
Q

how do protease inhibitors work?

A

they block the activity of portease so that the resulting virions released by the cells are immature and cannot infect new cells

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27
Q

what are 2 types of entry inhibitors?

A

CCR5 inhibitors and fusion inhibitors

28
Q

how do attachment inhibitors work?

A

they bind to gp120 on HIV envelopes, preventing the virus from attaching to the CD4+ receptor on immune cells

29
Q

how do post-attachment inhibitors work?

A

they bind to CD4+ receptors on T cells, preventing the HIV gp120 protein from changing its shape to engage with co-receptors

30
Q

what is PEP?

A

post-exposure prophylaxis
HIV treatment every day for 1 month for those following high risk exposure to stop the virus from replicating and reducing HIV spread

31
Q

when should you start PEP?

A

within 72 hours of coming into contact with the virus

32
Q

what is PrEP?

A

pre-exposure prophylacis
HIV medicine for people at risk of getting HIV
taken every day

33
Q

when on PrEP, how long does it take to reach maximum protection from HIV?

A

7 days of use

34
Q

what are the 2 types of PrEP?

A

truvada - for all people at risk

descovy - for people at risk except for those assigned female gender at birth

35
Q

what type of anti-retroviral is truvada?

A

a NRTI

36
Q

what type of anti-retroviral is descovy?

A

NRTI

37
Q

what is the common active ingredient in truvada and descovy?

A

emtricitabine

38
Q

what are some prevention methods for HIV?

A 
barrier methods of protection
PrEP
PEP
getting tested
choosing less risky sexual behaviours
limiting the number of sexual partners
never sharing needles/drug equipment
39
Q

what are some ways of transmitting HIV?

A 
vaginal or anal sex
sharing injection equipment 
vertical transmission
blood transfusions
needle stick injuries
40
Q

who are some ‘at risk’ groups for HIV?

A

those with current or past HIV partners or a partner who is from an area with high HIV rates
those living in an area with highest HIV rates
men who have unprotected sex with men
those who inject drugs and share equipment
those who share sex toys
those who have a history of sexually transmitted diseses
those with multiple sexual partners
those who have been raped
those who have had blood products in a country where HIV is not properly screened
babies with untreated HIV mothers

41
Q

how does HIV transmission vary between anal sex and vaginal intercourse?

A

18 times higher with anal sex

42
Q

what causes thrush?

A

overgrowth of the candida species - more common in weaker immune systems/taking medication

43
Q

what is pseudomembranous candidiasis?

A

oral thrush - destruction of epithelium pf skin or mucous membranes causing accumulations of cells. keratin and protein = white lesions

44
Q

what is erythematous candidiasis?

A

red, painful lesions caused by increased blood flow to affected tissues

45
Q

where do you normally find candida?

A

mouth, throat, gut, vagina etc

46
Q

what is invasive candidemia?

A

when the candida infection spreads from your bloodstream to other parts of your body such as your eyes, kidney, liver, and brain

47
Q

what is candidemia?

A

the presence of candida species in the blood

48
Q

what is the first line treatment for thrush?

A

fluconazole or oral nystatin suspension

49
Q

what is the moa of fluconazole?

A

binds to lanosterol 14 alpha demethylase inhibiting the conversion production of ergosterol and the de-methylation of lanosterol. ergosterol is vital for cell membrane integrity so we get disruption of fungal cell (increased permeability as cellular constituents move out) membrane and we get an increase in methol sterols

50
Q

what is the moa of nystatin?

A

It binds to ergosterol, a major component of the fungal cell membrane. When present in sufficient concentrations, it forms pores in the membrane that lead to K+ leakage, acidification, and death of the fungus.

51
Q

what type of antifungal is fluconazole?

A

an azole

52
Q

what type of antifungal is nystatin?

A

polyenes

53
Q

how do polyenes work?

A

It binds to ergosterol, a major component of the fungal cell membrane. When present in sufficient concentrations, it forms pores in the membrane that lead to K+ leakage, acidification, and death of the fungus.

54
Q

what are some examples of polyenes?

A

nystatin and amphotericin B

55
Q

how do azoles work?

A

inhibition of 14α-lanosterol demethylase, a key enzyme in ergosterol biosynthesis, resulting in depletion of ergosterol and accumulation of toxic 14α-methylated sterols in membranes of susceptible yeast species

56
Q

what are some examples of azoles?

A

ketaconazole
clotrimazole
econazole

57
Q

how do allylamines work?

A

inhibiting squalene epoxidase which converts squalene to ergosterol. This leads to squalene accumulation intracellularly which is toxic and so causes rapid cell death

58
Q

what are some examples of allylamines?

A

butenafine
naftifine
terbinafine

59
Q

how do echinocandins work?

A

Inhibit beta-D-glucan synthase which prevents cell wall integrity

60
Q

what are some examples of echinocandins?

A

micafungin, caspofungin, anidulafungin

61
Q

when on treatment for thrush, how long should it take for thrush to clear up?

A

7-14 days

62
Q

how long should you take treatment for thrush if it re-occurs 4 times in a year?

A

up to 6 months- GPs judgement

63
Q

when are you more susceptible to thrush?

A 
skin irritation or damage e.g. sex
taking antibiotics
have poorly controlled diabetes
are immunosupressed
are on HRT
if you are pregnant
64
Q

what can being on antibiotics make you more susceptible to thrush?

A

because they kill off some of the beneficial bacteria that prevent the overgrowth of yeast

65
Q

what are thrush symptoms in women?

A

white vaginal discharge like cottage cheese that doesnt smell
itching and irritation around the vagina
soreness and stinging during sex or when peeing

66
Q

what are thrush symptoms in men?

A

irritation, burning and redness around the head of the penis and under the foreskin
a white discharge like cottage cheese
an unpleasant smell
difficulty pulling back the foreskin

67
Q

what does thrush look like in other areas of the body e.g. armpits or between fingers?

A

red, itchy and painful rash that scales over with a white or yellow discharge

B9W4 (7 decks)

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