Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

YEAR 3 - SEMESTER 1 > CASE 6 - HIV/HEPATITIS > Flashcards

CASE 6 - HIV/HEPATITIS Flashcards

1
Q

Name the 2 types of HIV and the patients they affect

A

HIV-1 worldwide pandemic, ~36 million people

HIV-2 West Africa/Europe, 1-2 million people, generally slower progression than HIV-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Name the family and viral characteristics of HIV

A

FAMILY: retroviridae

CHARACTERISTICS: ssRNA transcribed to double-stranded DNA by reverse transcriptase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Name the antigen that is essential for HIV cell attachment

A

gp120

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the life cycle of HIV

A
  1. HIV gp120 binds to a CD4 receptor on CD4 cell AND a co-receptor
  2. Fusion and release of genetic material
  3. HIV ssRNA transcribed to dsDNA by reverse transcriptase enzyme
  4. Once it becomes dsDNA, it is integrated into the host by integrase
  5. This T cell/CD4 cell basically just becomes a factory for more and more HIV RNA through normal cellular processes
  6. HIV virion assembled and released
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is HIV transmitted?

A
  1. Mucous membranes/blood/tissue (below the skin) being exposed to INFECTED BODILY FLUIDS (e.g. blood, semen, vaginal fluid, breast milk)
  2. Mother to child transmission (particularly during delivery)

Sexual transmission most common

It is NOT transmitted through direct contact (e.g. hugging, kissing, sharing cutlery) or droplets or airborne

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Name 5 factors that increase risk of HIV transmission

A

HIGH VIRAL LOAD in the source (most important)

Concurrent STI (e.g. syphilis) - mucous membranes exposed, easier for HIV to gain access

Bleeding or gential/rectal trauma

Drug use

More sexual partners

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What type of immunity is most important when responding to HIV?

A

Cell-mediated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

HIV subverts the immune system in the following ways:

  1. Infects CD4 cells that control normal immune response
  2. Integrates into host DNA
  3. High rate of mutation (moving target)
  4. Hides in ‘immune-privileged’ tissues
  5. Induces a cytokine environment that the virus uses to its own replication advantage

Explain how each strategy makes it more difficult for the immune system to fight it.

A
  1. Infects CD4 cells that control normal immune response: impairs immune function, facilitates opportunistic infections and the development of malignancies.
  2. Integrates into host DNA: difficult for immune system to recognise it.
  3. High rate of mutation (moving target): when HIV is recognised and wiped out, the other ones that have mutated and present a different antigen will NOT be targeted.
  4. Hides in ‘immune-privileged’ tissues: e.g. brain, bone marrow, reproductive organs where immune cells don’t routinely enter.
  5. Induces a cytokine environment that the virus uses to its own replication advantage: changes the regulation of the immune system by invading CD4 cells, using it to replicate themselves.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

The precipitous, massive, and concealed depletion of CD4 cells causes impaired ability to…

(2 things)

A
  1. Recognise new infections/antigens
  2. Maintain immune memory responses (i.e. old infections that the host once developed immunity against will still infect them)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Looking at a graph of the natural history of HIV, explain what is being shown by the two different lines

(google an image)

A
  1. Depletion of CD4 cells in the first 4 weeks
  2. Acute HIV syndrome as large-scale dissemination of the virus occurs

A small recovery of the CD4 count corresponds with a period of clinical latency (lasts anywhere from a few years to decades) as the viral load drops.

CRITICAL POINT REACHED: CD4 count becomes low enough that the person develops infections and malignancies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

An estimated __ to __% of people remain asymptomatic / unaware that they have contracted HIV

A

An estimated 10 to 60% of people remain asymptomatic / unaware that they have contracted HIV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Are there any specific HIV symptoms?

A

NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is HIV seroconversion illness / acute retroviral syndrome and when does it typically manifest?

A

Seroconversion = body producing antibodies in response to the virus.

SYMPTOMS TYPICALLY OCCUR WITHIN A MONTH OF INFECTION

It is not always accompanied by a flu-like illness, but this is a possibility.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the symptoms of acute retroviral syndrome / seroconversion illness?

A 
Fever, lethargy, malaise, fatigue
Myalgia, arthralgia
Headache
Lymphadenopathy
Maculopapular rash
Pharyngitis
Anorexia/nausea/vomiting/weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

When primary HIV infection resolves, the body enters a period known as…?

A

Clinical latency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Outline the diagnostic approach to HIV, including:

  1. Screening test
  2. Confirmatory test
  3. Detection of viral RNA
A
  1. Screening test: 4th-generation antibody-antigen test which detects antibodies and HIV antigen (p24 viral core protein) - becomes positive 2-6 weeks after exposure
  2. Confirmatory test: HIV-1/HIV-2 antibody differentiation immunoassay (first-choice confirmatory test). Can detect both HIV-1 and HIV-2 in ∼20 minutes.
  3. Detection of viral RNA: detects HIV RNA in serum or plasma and can quantify the number of copies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

List 3 advantages of the 4th-generation antibody-antigen test

A
  • High specificity and a sensitivity of almost 100%
  • Quicker identification of HIV infection since it looks for the p24 antigen (which appears before antibodies do)
  • Can detect HIV as soon as 1 month after infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which of the following can be detected the soonest?

  • p24 antigen
  • RNA
  • Antibodies
A

RNA

Followed by p24 antigen and then antibodies

(look up image of HIV window period)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is a normal CD4 count?

A

500-2000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Name 2 opportunistic infections or malignancies that occur at each of the following CD4 counts:

CD4 cell count 200-500

CD4 cell count 50-200

CD4 cell count <50

A

CD4 cell count 200-500:
Herpes zoster, pneumococcal pneumonia, oral candidiasis, TB

CD4 cell count 50-200:
non-Hodgkin’s lymphoma, kaposi sarcoma (classical tumour associated w/HIV), primary CNS lymphoma, CNS toxoplasmosis, PJP

CD4 cell count <50: disseminated MAC, CMV retinitis, cryptosporidiosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

The WHO classifies individuals with confirmed HIV infection according to clinical features and diagnostic findings. Give an example of a findings that belongs in each of the following categories

  • Primary HIV infection
  • Clinical stage 1
  • Clinical stage 2
  • Clinical stage 3
  • Clinical stage 4
A
  • Primary HIV infection: acute retroviral syndrome or asymptomatic
  • Clinical stage 1: persistent generalised lymphadenopathy (PGL) or asymptomatic
  • Clinical stage 2: unexplained moderate weight loss (<10%), recurrent bacterial/viral/fungal infections
  • Clinical stage 3: unexplained severe weight loss (>10%), recurrent bacterial/viral/fungal infections, unexplained anaemia, unexplained neutropenia, unexplained persistent fevers, unexplained chronic diarrhoea (>1 month), chronic thrombocytopenia
  • Clinical stage 4: AIDS-defining conditions (e.g. kaposi sarcoma, pneumocystitis pneumonia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

A patient presents with chronic thrombocytopenia, unexplained chronic diarrhoea, and unexplained anaemia. 4th-generation antibody-antigen testing reveals that they are HIV-positive.

What clinical stage of HIV infection is this typical of?

A

Clinical stage 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

A patient presents with kaposi sarcoma. 4th-generation antibody-antigen testing reveals that they are HIV-positive.

What clinical stage of HIV infection is this typical of?

A

Clinical stage 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Name 5 risk factors for HIV

A

MSM (men who have sex with men)

Occupational exposure (e.g. DASA)

IVDU

Coming from a country w/high HIV burden (e.g. south-east asian, africa)

Vertical transmission (mother-to-child)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Why is it not feasible to only test for the p24 antigen?

A

p24 rises rapidly (~2 weeks in), but also falls as the body mounts an immune response.

This means you have to get tested very early on in the disease, which is difficult because there may be no symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

MPPD sexual history osce stuff

A

.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Is it likely for HIV to be contracted after one sexual encounter?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

For which patient groups is HIV pre-exposure prophylaxis (PrEP) recommended?

A

Men who have sex with men

Transgender and gender-diverse people

People who inject drugs

Heterosexual men and women with a HIV-positive partner

(there are guidelines for each group based on high vs. medium risk factors. look @ ETG)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is involved in PEP?

A

Take with 72 hours of exposure

28-day course of a 2-drug or 3-drug regimen

Come back for checkups after 1 month, 3 months, and 6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the indications for HIV post-exposure prophylaxis? (PEP)

3 scenarios

A
  • Injury with HIV-contaminated needles or instruments
  • Contamination of open wounds or mucous membranes with HIV-infected fluids
  • Unprotected sexual activity with a known or potentially HIV-infected person
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

When should HIV post-exposure prophylaxis (PEP) be initiated?

How long is it taken for?

A

As soon as ideally possible (ideally within 2 hours of exposure)

GUIDELINES:

  • Within 72 hours of high-risk exposure
  • Taken for 28 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

State the route of transmission for Hepatitis A, Hepatitis B, and Hepatitis C

A

Hepatitis A: Faecal-oral, person-person (e.g. contaminated food or water, household contacts, MSM)

Hepatitis B: Parenteral (e.g. blood, genital secretions), sexual, perinatal

Hepatitis C: Parenteral (intranasal cocaine use is a RF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

State the likelihood of progression to chronic liver disease for Hepatitis A, Hepatitis B, and Hepatitis C

A

Hepatitis A: Never

Hepatitis B: ~10%

Hepatitis C: ~80%

When it comes to viral hepatitis

When it come to viral hepatitis, vowels (A and E) cause only AcutE hepatitis while Consonants (B, C, and D) may have Chronic sequelae as well.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

TRUE OR FALSE? Humans are the only reservoir for Hepatitis A

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

State the following information for HEPATITIS A:

  • Incubation period (& average)
  • Vaccine available?
  • Prevention
  • Site of replication
  • Symptoms
A
  • Incubation period (& average): 2-6 weeks, with an average of 28 days
  • Vaccine available? YES
  • Prevention: Vaccine, clean drinking water
  • Site of replication: GIT
  • Symptoms: fever, jaundice, vomiting, diarrhoea. Usually prodromal symptoms of fever + malaise, THEN jaundice.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Who is more likely to have symptoms of hepatitis A?

A

Adults

Symptoms are rare in children <5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Can you transmit Hep A infection before you are symptomatic?

What is the infectiousness period?

A

YES - can be shed in stool 2-3 weeks before symptoms

Infectious 2-3 weeks prior to symptom onset and 1 week after.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

TRUE OR FALSE? After contracting Hep A, you develop robust immunity.

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Which finding on a LFT would indicate Hep A?

A

Very high ALT (in the thousands)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

ALT > AST indicates…

A

VIRAL HEPATITIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

AST > ALT indicates…

A

ALCOHOLIC LIVER DISEASE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Which diagnostic tests are used for HAV in the following situations:

  • Testing for recent or current infection
  • Testing for past infection
A
  • Testing for recent or current infection: IgM antibody

- Testing for past infection/immunity: IgG antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

State the following information for HEPATITIS B:

  • Incubation period
  • Vaccine available?
  • Prevention
  • Site of replication
  • Symptoms
A
  • Incubation period: 1-6 months
  • Vaccine available? YES
  • Prevention: immunisation, avoiding risky behaviour (e.g. IVDU, sharing sharps, unprotected sex), screening in vulnerable populations
  • Site of replication: liver
  • Symptoms: many times it can be asymptomatic. Risk is that it’s a silent killer –> then present with advanced liver disease.

WHEN SYMPTOMATIC: fever, rash, arthralgia, myalgia, fatigue, nausea, anorexia, jaundice, RUQ pain

Very treatable disease, but you need to detect it (tricky part)

44
Q

Can hepatitis B cause hepatocellular carcinoma (HCC)?

A

YES - it is an oncogenic virus

45
Q

In which age group is the risk of HBV-related chronic liver disease highest?

A

Younger populations

The younger you are when you get Hep B, the more likely it is to become chronic HBV infection (–> chronic liver disease –> cirrhosis –> HCC or liver failure)

46
Q

HBV isolated core antigens (HBcAg) are not routinely checked in clinical practice.

When would you test for HBV core antigens?

A

When there will be immunosuppression (e.g. chemotherapy, organ transplantation)

Because there’s a chance that it will become reactivated - the cccDNA remains in the liver, but does not circulate in blood

47
Q

Which of the HBV markers (HBsAg, HBcAg, HBeAg, HBV DNA, Anti-HBS) would be positive and negative in the following situations:

  • HBV infection
  • HBV resolved infection
  • Immunity
A
  • HBV infection: HBsAg positive (HBV SURFACE ANTIGEN IS IMPORTANT IN ACTIVE INFECTION), Anti-HBcAg positive (IgM in acute, IgG in chronic), HBV DNA positive, Anti-HBS positive (Surface antibody).
  • HBV resolved infection: Anti-HBS and Anti-HBc IgG, HBsAg and HBV DNA negative
  • Immunity: everything negative except for Anti-HBS

look there was a good table in the lecture

https://www.youtube.com/watch?v=eocRM7MhF68 (good osmosis vid)

48
Q

Which factors assist Hep B in persisting as a chronic infection? (Name 3)

A
  • Integrates into host DNA
  • High mutation rate
  • Antiviral therapy doesn’t target cccDNA
49
Q

How does Hep B cause liver disease?

A

The virus itself is not hepatotoxic. Liver damage comes from the immune response.

  1. Foreign virus
  2. Immune activation
  3. Inflammation and necrosis of liver due to immune reaction
  4. Inflammation and necrosis –> liver disease
50
Q

Which types of hepatitis are transmitted via the faecal-oral route?

A

Vowels (A and E) are bowels (transmitted fecal-orally) and usually only cause AcutE hepatitis

51
Q

Give 3 examples of parenteral transmission

A

Contact w/infected blood:

  • Shared needles
  • Occupational exposure (e.g. needlestick injury)
  • Blood transfusion
  • Organ transplant
  • Tattoos, piercings
52
Q

Risk factors for progressive fibrosis in Hep B include:

  1. Host factors
  2. Viral factors
  3. Environmental factors

Name 2 risk factors that belong in each category

A
  1. Host factors: older, male, immunocompromised
  2. Viral factors: having genotype C, high HBV DNA
  3. Environmental factors: concurrent infections (HCV, HIV), alcohol, smoking, diabetes, obesity
53
Q

What are the 4 possible outcomes of acute infection with HBV?

(good flow chart in Robbins)

A
  1. Subclinical disease
  2. Acute hepatitis
  3. Chronic hepatitis
  4. Carrier
54
Q

Is current HBV anti-viral therapy curative?

A

NO - doesn’t target cccDNA

Helps control the disease and hopefully:

  • Prevent progression to HCC
  • Prevent vertical transmission
55
Q

HBV SUMMARY

A

There are acute and chronic infections

Risk of liver disease, cirrhosis, and liver cancer

Antiviral therapy does not eradicate cccDNA

56
Q

State the following information for HEPATITIS C:

  • Incubation period
  • Vaccine available?
  • Prevention
  • Site of replication
  • Symptoms
A
  • Incubation period: 2 weeks - 6 months
  • Vaccine available? NO
  • Prevention: in Australia, highly prevalent amongst IVDU. Prevention = needle exchange programs, TREATMENT AS PREVENTION (esp in vulnerable populations, e.g. homeless). Safe sex.
  • Site of replication: liver
  • Symptoms: mostly asymptomatic (80%).

When symptomatic: acute viral hepatitis (fever, malaise, arthralgia, myalgia, RUG pain, hepatomegaly, jaundice, pruritus, nausea, vomiting, diarrhoea.

57
Q

Is Hepatitis C curable?

A

YES

Newer tablets also act against all different strains of Hep C

58
Q

How is hepatitis C diagnosed?

A
  1. HCV antibody (IF POSITIVE: do more testing)
  2. HCV RNA (maker of active infection)

If HCV RNA is detected –> treatment

59
Q

What are the possible outcomes of acute hepatitis C infection?

A
  1. Resolution ~15%

2. CHRONIC hepatitis (more common in adults, unlike in hepatitis B) ~85%

60
Q

What are the possible outcomes of HBC-related chronic hepatitis?

A

Cirrhosis –> HCC

Cirrhosis –> Stable cirrhosis

Lymphotropism –> lymphoma

61
Q

What is the first-line Hep C treatment regime in Australia?

A

Direct-acting antiviral drugs for hepatitis C are highly effective and well tolerated.

Sofosbuvir + Velpatasvir (1 oral combined tablet), 12 weeks. Epculsa.

Glecaprevir + Pibrentasvir (3 tablets once daily), 8 or 12 weeks (depending if there’s cirrhosis). Maviret.

62
Q

What factors affect the type of antiviral treatment for HCV?

A
  • Cirrhosis
  • HCV genotype and subtype (less relevant now)
  • Prior treatment Hx
  • Comorbidities
  • Other medications (possible interactions)
63
Q

What is the target population for HCV treatment?

A

Intravenous drug users

64
Q

When is someone defined as cured of HCV?

A

Negative HCV RNA 12 weeks AFTER treatment ends

65
Q

What is the most common cause of hepatitis?

A

Viruses

66
Q

What is the first-line treatment for HIV?

A

Antiviral therapy:

2x nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs)

1x Integrase strand transfer inhibitor (INSTI).

e.g. dolutegravir+abacavir+lamivudine (Triumeq)

67
Q

What should be monitored in patients undergoing anti-retroviral therapy for HIV? (many things)

A
  1. Treatment adherence
  2. HIV viral load
  3. CD4 count
  4. Toxicity of antiretroviral therapy (CBC, EUC, LFTs, biochem)
  5. RFs for CVD
  6. RFs for osteoporosis
  7. Screen for cancers
  8. Mental health
  9. Respiratory infections
68
Q

What should be checked before taking PrEP?

A
  • Baseline testing (HIV, HBV, HCV, pregnancy, STIs, kidney function)
  • Advice on reducing risk of STIs and HIV
  • Ensure the patient can attend regular follow-up
69
Q

What should patients be counselled on prior to HIV testing?

A
  • If they do test positive, they will need to notify previous sexual partners (this can also be done via an anonymous text)
  • Agrees to be tested on the basis of understanding the HIV testing procedures, the reasons for testing and is able to assess the personal implications.

(look at the document steph sent)

70
Q

What is the ‘window period’? for HIV?

A

Period after which it is certain that the person being tested for an infection will not seroconvert following exposure to that infection

Officially quoted as 3 months, but most people seroconvert within 6 weeks

71
Q

List 3 side effects of anti-retroviral therapy

A
  • Headache
  • Diarrhoea
  • Lipodystrophy

(note: most adverse effects are common and short-lived)

72
Q

Outline the management of suspected or confirmed exposure to HIV

(according to eTG)

A
  1. If the source is HIV antibody/antigen negative and unlikely to be in the window period, no further follow-up testing of the source or exposed person is required
  2. HIV antibody/antigen test at baseline, then at 4-6 weeks
  3. If PEP is prescribed, re-test at 3 months
73
Q

What criteria must be met before someone is defined as having AIDS?

A

EITHER:

Acquiring an AIDS-defining illness (e.g. kaposi sarcoma, pneumocystitis pneumonia, cerebral toxoplasmosis, primary lymphoma of the brain)

OR

CD4 Cell count of <200 per microlitre of blood

74
Q

What is the goal of anti-retroviral therapy?

A
  • Slow HIV replication

- Help the immune system recover and fight other infections

75
Q

List 3 things that can raise Alk Phos (ALP)

A
  1. Pregnancy
  2. Cholestasis
  3. Bone growth (e.g. paget’s disease, blastic cancers - prostate, breast)
76
Q

List 2 things that can raise GGT.

GGT can be used in conjunction with ALP to distinguish between…?

A
  1. Cholestasis
  2. Alcohol

Bone growth does NOT cause GGT elevation, so it is a helpful distinguishing feature.

High ALP + Low GGT = not liver-related

77
Q

When do AST and ALT levels rise?

Which one has low specificity for the liver?

Are they indicators of acute or chronic injury?

A

Liver damage

They are markers of hepatic inflammation

AST (also found in bones) has low specificity for the liver. ALT has HIGH specificity for the liver). Both are only good indicators of recent injury.

78
Q

Why is albumin a useful marker of chronic hepatocellulr injury?

A

Has a 20-day half-life

79
Q

GGT levels are found to be raised. How can it be distinguished from alcohol-related pathology vs. cholestasis?

A

In cholestasis, bilirubin and ALP will also be raised

80
Q

INR is both an acute AND chronic marker of liver disease. Raised INR indicates…?

A

Longer clotting time

High INR = Takes longer to clot

81
Q

Why is INR so sensitive to the liver?

A

Depends on many proteins that are synthesised by the liver

82
Q

Why is chlamydia routinely tested for?

A

It is very COMMON and ASYMPTOMATIC

1 in 20 young people have chlamydia and ~75% don’t know they have it

83
Q

Which groups are at risk of contracting gonorrhoea?

A
  • MSM
  • Young Aboriginal and Torres Strait Islander persons
  • Returned travellers
84
Q

Why is it important to do an MC&S for gonorrhoea?

A

Resistance is emerging: need to check sensitivity via MC&S

85
Q

What percentage of women vs. men are asymptomatic when it comes to gonorrhoea?

A

~80% of women are asymptomatic

~10% of men are asymptomatic (typically will have discharge)

86
Q

How is PID diagnosed? Why?

A

Clinically; the cause is POLYMICROBIAL. In 70% of causes, no causative agent is identified.

Hence, waiting for swabs will not affect management

87
Q

Who is at risk of syphilis infection?

A
  • MSM
  • Gender diverse
  • Aboriginal and Torrens Strait Islander persons
  • IVDU
  • Multiple sexual partners
  • Sex overseas
  • Pregnant persons

Anyone with a partner who fits the above criteria

88
Q

Why is syphilis known as the ‘great mimicker’?

A

Signs & symptoms are similar to so many other infectious diseases

Buzz words: palmoplantar rash, maculopapular rash, patchy alopecia, snail trail ulcers in mouth, warty growths

89
Q

Epidemiology for female and male HIV patients in Australia vs. worldwide

A

Australia: 90% men, 10% women

Worldwide: ~56% women

90
Q

When would the Hepatitis B surface antigen (HBsAg) be raised?

What is the corresponding antibody, and when would this be detectable?

A

Acute & chronic infection

Corresponding antibody: Anti-HBS. Present 1-3 months after infection or vaccination. Presence indicates immunity

91
Q

When would the Hepatitis B CORE antigen (HBcAg) be raised?

A

Trick question: HBcAg is not routinely measured in clinical practice because HBcAg forms the nucleocapsid of the virus particle, which lies beneath the viral surface. So HBcAg circulates as a part of the virus but is covered by the HBsAg. It does not circulate as a free protein in significant quantity in the blood.

92
Q

What are the corresponding HBcAg (Hep B core antigen) antibodies? When do they appear?

A

Anti-HBc IgM: indicates recent infection (<6 months)

Anti-HBc IgG: chronic or resolved infection

93
Q

When would the Hepatitis B envelope antigen (HBeAg) be raised?

What is the corresponding antibody? What do these things indicate?

A

HBeAg indicates active viral replication and HIGH TRANSMISSIBILITY (can be found in acute and chronic infection)

Corresponding antibody: Anti-HBe. Indicates long-term clearance and therefore low transmissibility.

HBEAg indicates highly Enfectious.

https://www.youtube.com/watch?v=h_9EBVPADNE

94
Q

Outline the testing algorithm for HBV

A
  1. Screening: HBsAg + Anti-HBc IgM

2. If HBsAg is positive, measure HBeAg and HBV DNA to determine transmissibility

95
Q

This is a characteristic sign of HIV seroconversion illness that can be found in the mouth.

A

Painful mucocutaneous ulceration

96
Q

Who is more likely to experience symptoms of EBV; adults or children?

A

Adults

97
Q

How do EBV symptoms differ from HIV?

A

EBV: cervical lymphadenopathy. HIV: generalised contender lymphadenopathy.

EBV: maculopapular rash that occurs after treatment with aminopenicillins. HIV: generalised rash.

EBV: possible abdo pain, jaundice & hepatosplenomegaly. HIV: none of the above (but can have other GIT symptoms such as nausea and vomiting)

EBV: tonsilitis and/or pharyngitis. HIV: painful mucocutaneous ulcerations.

HIV: myalgia, arthralgia, headache.

98
Q

Why does viral hepatitis cause jaundice?

A

Liver damage causes the following to occur:

  1. Hepatocytes lose the ability to conjugate bilirubin; UCB leaks into the blood.
  2. Hepatocytes line the bile duct, so when they die, it also allows bile to leak into the blood (containing conjugated bilirubin).

The presence of conjugated and UCB leads to jaundice.

99
Q

What is Hoagland’s sign? Which condition can it be found in?

A

Bilateral upper-eyelid oedema.

An early and transient sign of EBV infection/infectious mononucleosis/glandular fever.

100
Q

What is HAART?

A

Highly-active antiretroviral therapy

A combination of 3 or more antiretroviral drugs used to treat HIV.

101
Q

What is HIV wasting syndrome?

A

Unwanted weight loss of more than 10 percent of a person’s body weight, with either diarrhea or weakness and fever that have lasted at least 30 days.

102
Q

What is the treatment regime for chronic hepatitis B?

A
  1. Pegylated interferon
    Good: No resistance, finite duration of therapy
    Bad: Less well tolerated due to side-effect profile, only moderate antiviral activity
  2. Nucleoside (Lamivudine, Entecavir) and Nucleotide (Tenofovir) analogues
    Good: Potent antiviral effects, few side-effects
    Bad: Risk of resistance with some drugs
103
Q

TRUE OR FALSE? Clinically-significant infection with MAC is uncommon except among people with T-cell immunodeficiency due to AIDS, and immunosuppression resulting from treatment for transplant rejection or autoimmune diseases.

A

TRUE

MAC/Mycobacterium Avium Complex is caused by two types of bacteria: Mycobacterium avium and Mycobacterium intracellulare. It gains entry via respiratory or GIT epithelium.

104
Q

Which drug classes are used for first-line HIV antiretroviral therapy?

A

Two nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs)
+
An integrase strand transfer inhibitor (INSTI)

105
Q

How do we test for Hepatitis B?

Screening & follow-up if positive

A

SCREENING:

  • HBsAg (for active infection)
  • HBcAg (for previous infection)

IF POSITIVE:

  • HBeAg (E antigen found in actively replication cells - gives an indication of HOW INFECTIVE they are)
  • HBV DNA (viral load)
106
Q

Which aspect of the hepatitis B virus is used in the vaccine?

A

Hepatitis B surface antigen (HBsAg)

107
Q

Why might someone who has just received a HBV vaccine test positive in a screening test?

A

Hepatitis B surface antigen (HBsAg) is used in the vaccine

YEAR 3 - SEMESTER 1 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions