Session 6- Blood Borne Viruses- HIV and Hepatitis Flashcards

1
Q

HIV life cycle

A

1- free virus
2- binding and fusion- binds to CD4 receptor
3-virus penetrates cell
4-reverse transcription RNA TO DNA
5- integration- viral DNA is combined with the cells own DNA by the integrase enzyme
6- transcription- when infected cell divides viral DNA is read and long chain proteins are made
7- assembly viral protein chains come together
8- budding- immature virus pushes out of cell membrane with it

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2
Q

transmission

A

: Contact of infected bodily fluids with mucosal tissue /
blood / broken skin – sexual contact, blood transfusion, contaminated needles,
vertical transmission to fetus during delivery. Some medical procedures carry a risk
of transmission

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3
Q

what happens when CD4 cell count drops

A

Once CD4 cell count drops below 350 cells/µl you begin to get more symptoms – a cold you can’t shake, athlete’s foot

Once less than 200 cells/µl – you begin to see severe infections,
AIDS defining symptoms and cancers linked with HIV/AIDS.

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4
Q

diagnostic tools for HIV

A
– a) serology – detects
both antigens (viral proteins) and antibodies to HIV in the blood,

b) PCR – detects the
viral nucleic acid

c) rapid testing

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5
Q

treatment of HIV

A

Every patient is treated as soon as possible with ARVs (anti-retroviral drugs)
regardless of CD4

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6
Q

how do antiretroviral drugs work

A

Anti-retroviral drugs work by targeting the binding (CCR5 – entry inhibitor), the
enzymes responsible for incorporation of viral DNA into host DNA (Integrase
inhibitor), for breaking down the large proteins into smaller units (protease inhibitor)
during the maturation phase of the viral life cycle and reverse transcriptase (Nonnucleoside reverse transcriptase inhibitor (NNRTI ) – non-competitive inhibitor or
Nucleoside reverse transcriptase inhibitor (NRTI) - competitive substrate inhibitor)

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7
Q

strategies to reduce prevalence of HIV

A
  • Increase condom usage
  • ARV treatment as prevention
  • Wide-spread testing/screening
  • Prevention of mother-to-child transmission
  • Post-exposure prophylaxis (PEP)
  • Pre-exposure prophylaxis (PrEP)
  • Male circumcision
  • Combine the above
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8
Q

what viruses cause collateral liver damage

A

EBV- Epstein Barr Virus
CMV- cytomegalovirus
VZV- Varicella Zoster

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9
Q

icteric sclera

A

white of eye turns yellow

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10
Q

what kind of hepatitis does viral hepatitis cause

A

intrahepatic

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11
Q

what does raised bilirubin indiacte

A

either the pre-hepatic, intrahepatic or extrahepatic

processing of this product.

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12
Q

what does raised ALT AST indicate

A
If ALT (Alanine transaminase) or AST
(Aspartate aminotransferase) are elevated it tells us there is hepatocyte damage and the problem is
intrahepatic.
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13
Q

ALT

AST

A

alanine transaminase

aspartate aminotrasnferase

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14
Q

raised ALP indicates…

A
If ALP (Alkaline phosphatase) is elevated
there is a problem in the biliary tract- extra hepatic
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15
Q

transmission if Hep B

A

Transmission is predominantly vertical (75% of cases globally) but also through
sexual contact, intravenous drug use, close household contacts (low risk) where
there is significant blood exposure and health care workers via needle stick injuries.

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16
Q

symptoms of hep b

A

jaundice, fatigue, abdominal pain,

anorexia/nausea/vomiting and arthralgia (joint pain)

17
Q

HEP B serology

A

in a blood test you can detect HBsAg & HBsAb, HBeAg

& HBeAb, HBcAb (IgM followed by IgG (HBcAg is undetectable in blood))

18
Q

C diff

A

Clostridioides difficile [klos–TRID–e–OY-dees dif–uh–SEEL]

a gram-positive, anaerobic, spore-forming bacillus that is responsible for the development of antibiotic-associated diarrhoea and colitis (bowel inflammation).

19
Q

microbiology of c diff

A

C. difficile is an anaerobic bacteria. The presence of oxygen is inhibitory to its growth.
Their sensitivity to oxygen limits the conditions under which it can colonise the
human body or cause disease.
C. difficile is a minor component of the bowel microflora. Colonisation of the large
bowel is present in up to 5% of the population.

20
Q

why do patients develop c diff

A

When the balance of gut microorganisms is disrupted, C. difficile starts to dominate
and colonize the large intestine.

after use of antibiotics

21
Q

toxins of C diff

A

C. difficile produces two important types of toxins, A and B.
Toxin A is an enterotoxin that causes excessive fluid secretion, but also stimulates an
inflammatory response and has some effect on damaging cell structure.

Toxin B is a cytotoxin and damages protein synthesis and the cell structure.

22
Q

risk factors associated with Clostroidioes Difficille

A

Antibiotic exposure, older age and hospitalisation Severe illnesses, immune suppression, and gastric acid suppression

23
Q

when to suspect C diff

A

diarrhoea
who has received antibiotics within the previous 3 months, has been recently
hospitalized, and/or has an occurrence of diarrhoea within 48 hours or more after
hospitalization.

24
Q

diagnoses of CDI

A

Tests aim to identify the C. difficile bacteria and the presence of toxin.
Stool assays for C difficile include the following:
 Enzyme immunoassay (EIA): for glutamate dehydrogenase produced by C.
difficile.
 Real-time polymerase chain reaction (PCR) assay for toxin gene
 EIA for detecting toxins A and B

25
Q

treatment of CDI

A

 Mild, antibiotic-associated diarrhoea : Cessation of antibiotic(s) may be the only treatment necessary
 Mild to moderate diarrhoea or colitis: Metronidazole (oral or intravenous) or
vancomycin (oral) for 10 days
 Severe or complicated disease: Vancomycin is considered to produce faster
symptom resolution and fewer treatment failures than metronidazole;

26
Q

preventative measure against spread of c diff

A

 Isolate patients with C. difficile immediately, even if you only suspect CDI
 Wear disposable gloves and gowns when treating patients with C. difficile,
even during a short visit.
 Perform hand hygiene after removing gloves. Alcohol does NOT kill C.
difficile spores. The use of soap and water is more effective than alcoholbased hand rubs.

27
Q

metronidazole

A

oldest antibiotic used to treat CDI.
It is a broad-spectrum antibiotic used to treat anaerobic infections. Metronidazole
kills the vegetative forms of the Clostridioides bacteria but not the spores.

28
Q

vancomycin

A

Vancomycin has excellent activity against C difficile. This agent kills the organism by
inhibiting cell wall synthesis.
Oral vancomycin does not get absorbed and acts directly at the site of infection.
Vancomycin does not cross in the bowel from blood so is only effective when given
enterally. Therefore, IV vancomycin is not used here as it does not act directly on the
site of infection.

29
Q

fidaoxmicin

A

The drug is only available in an oral formulation and systemic absorption
is minimal. Fidaxomicin has bactericidal activity against C. difficile, but reduced
activity against several enteric commensal bacterial species, particularly those
thought to confer colonization resistance against C. difficile

30
Q

MRSA

A

methicillin-resistant Staphylococcus aureus

s a type of Staphylococcus aureus that is resistant to most beta-lactam
antibiotics, antistaphylococcal penicillins (e.g., methicillin, oxacillin), and
cephalosporins

31
Q

how is MRSA spread

A

h skin-to-skin contact with someone who
has an MRSA infection or has the bacteria living on their skin.
The bacteria can also spread through contact with towels, sheets, clothes, dressings
or other objects that have been used by a person infected or colonised with MRSA.
MRSA can survive for long periods on objects or surfaces, such as door handles, sinks,
floors and cleaning equipment.

32
Q

treatment of MRSA

A

doxicyclin

oral trimoxycol

33
Q

transmission of norovirus

A

s mainly faecal-oral and also thought to be respiratory. Can be spread
following ingestion of contaminated food, direct person-to-person contact or
through contact with contaminated surfaces.