17 - TB, HIV, STIs Flashcards

1
Q

What is the pathophysiology of TB infection?

A

- Mycobacterium Tuberculosis

  • Spread by aerosol droplets causing pulmonary infection
  • Pulmonary infection can then spread haematogenously in the body
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2
Q

What is the difference between active and latent TB?

A

Latent: Asymptomatic due to containment of TB in granulmoa. Will have positive skin testing but they are not infectious and no x-ray findings.

Lifetime reactivation of 10-15%

Active: Can be due to primary infection or reactivation. Patient is symptomatic and contagious

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3
Q

What are the different types of active TB?

A

Classified by the site affected e.g:

  • Pulmonary TB
  • Lymph node TB
  • TB meningitis
  • Milliary TB
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4
Q

What are some causes of latent TB reactivation?

A
  • HIV
  • Immunosuppression
  • Increasing age
  • Organ transplant
  • Drug use
  • Malnutrition
  • Immigrating to UK from endemic areas
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5
Q

Latent TB is asymptomatic so how is it diagnosed?

A

Screening with:

  • CXR
  • Interferon gamma testing (quantiFERON or T-spot)
  • Tuberculin skin testing (Mantoux)
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6
Q

How do the following tests for TB work:

  • Tuberculin Skin Testing
  • QuantiFERON
  • T-spot test
A

NO TEST CAN DISTINGUISH BETWEEN ACTIVE AND LATENT!

Mantoux: Intradermal injection of PPD tuberculin, size of skin induration determines positivity. If positive cannot distinguish between latent, active or BCG

QuantiFERON: Blood test where T-cells are mixed with TB antigen to see how much interferon gamma they release. Pre-exposed T-cells release more. Negative in BCG. Cannot tell difference between active and latent

T-Spot Test: Same as above but instead of whole blood, isolate lymphocytes. Good if patient has low amount of lymphocytes

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7
Q

What is the cause of a false negative QuantiFERON test?

A

Immunosuppression as not enough T cells to release interferon gamma!

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8
Q

What people are offered screening for latent TB?

A

Asymptomatic patients with high risk for TB:

  • Immigrants from high prevalence countries
  • Close contacts e.g family
  • Healthcare workers
  • HIV positive
  • Starting immunosuppressive therapy
  • Prisons and homeless
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9
Q

How is latent TB treated?

A

Balance between risk of developing active disease and side effects of treatment (hepatotoxicity)

If >35 high risk of hepatotoxicity so only treat if risk factors of reactivation e.g HIV, immunosuppressants

If risk of hepatotoxicy use 3 months of isoniazid (with pyroxidine) + rifampicin

OR 6 months of just isoniazid (with pyroxidine)

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10
Q

What are some of the signs and symptoms of active TB?

A

Symptoms:

  • Non-resolving cough
  • Low grade fever
  • Night sweats
  • Weight loss
  • Haemoptysis
  • Pleurisy

Signs:

  • Clubbing
  • Cachexia
  • Lymphadenopathy
  • Hepatosplenomegaly
  • Erythema nodosum
  • May be pericardial rub
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11
Q

What general investigations should you do if you suspect pulmonary TB?

A

Imaging: CXR, CT, MRI

Samples: 3 early morning sputum smear , sputum cultures as gold standard, NAAT

Biopsy: lymph nodes

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12
Q

What could you find on imaging of acitve TB?

A

CXR: mediastinal lymphadenopathy, cavitating pneumonia, pleural effusion

CT: lymphadenopathy

MRI: leptomeningeal enhancement in TB meningitis

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13
Q

How long do sputum cultures, sputum smears and NAAT tests for TB take?

A

Sputum Culture: takes 6 weeks so start ATT before samples back, GOLD STANDARD

Sputum Smear: 3 early morning sputum samples for AFB. If positive then isolate. Takes 1-2 days

NAAT: PCR takes 8 hours due to DNA/RNA amplification. Can also detect drug sensitivities

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14
Q

What would you see histologically on a biopsy of a TB infected lymph node?

A

Granulomas with caseating central necrosis

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15
Q

Once the results are back for the sputum smear for TB, in a suspected case of TB, what is the management?

A

Smear positive: indicates high bacterial load so high infectivity so needs ATT immediately

Smear negative: Bronchoscopy +/- EBUS (biopsy of pulmonary lymph nodes). Once these samples are taken and sent for AFB test then start ATT

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16
Q

What investigations should you do if you suspect extra-pulmonary TB?

A

NAAT: any sterile body fluid so lumbar puncture or pericardiocentesis if suspect meningeal/pericardial TB

AFB: take biopsies of lymph nodes, pleura, colon and send for AFB staining, histological exam and culture

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17
Q

Why is there a paradoxical reaction at the start of Anti-TB therapy?

A

As bacteria die there is an increase in inflammation causing worsening symptoms

If TB is in sites where additional swelling cannot be tolerated e.g meningeal, pericardial, then give steroids at the start of ATT

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18
Q

How does a patient with CNS TB/TB meningitis present and what should you do to diagnose this?

A

Presentation: INSIDIOUS ONSET, personality change, headache, meningitic, comotose over several weeks

Diagnosis:

- Lumbar puncture: high protein, low glucose, lymphocytosis

- MRI: leptomeningeal enhancement

  • Everyone with milliary TB needs LP to exclude TB meningitis
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19
Q

Why is it important to know if a patient has TB meningitis before starting ATT?

A

Need to give steroids when starting treatment as paradoxical reaction can be fatal!

Also need 12 months of treatment not 6

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20
Q

How might pericardial TB present and what is the importance of this?

A
  • Often pericardial effusion so pericardial rub and Kussmaul’s sign
  • Can get pericarditis

- Need to give steroids at start of ATT as paradoxical reaction can lead to tamponade

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21
Q

How do you know a patient has milliary/disseminated TB and how do you treat it?

A
  • CXR/CT shows foci of granulomas throughout the lung, heart, joints etc

- Need to have neuroimaging and LP to exclude CNS involvement

- Do not withold treatment whilst awaiting biopsies, start ATT as soon as you know no CNS involvement

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22
Q

What are some symptoms of the following extrapulmonary TB:

  • Spinal
  • Skin
  • Genitourinary
  • GI
A

Spinal: local pain and bony tenderness

Skin: lupus vulgaris, apple jelly nodules

Genitourinary: dysuria, frequency, haematuria, infertility, genital ulceration

GI: colicky abdominal pain and vomiting

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23
Q

How is active TB treated?

A

Treat all TB the same apart from CNS, Pericardial, MDR

2 months quadruple therapy:

  • Rifampicin
  • Isoniazid (+Pyroxidine)
  • Pyrazinamide
  • Ethambutol

4 more months: (10 more months if CNS)

  • Rifamipicin
  • Isoniazid (+Pyroxidine)
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24
Q

When should you suspect MDR TB and what should you do wit this?

A
  • Previous incomplete TB treament
  • Birth or resident in country with MDR TB
  • Need to do NAAT if high risk of resistance to check for resistance
  • Need good infection control in negative pressure room and masks/PPE
  • Specialist advice treatment with at least 6 agents using
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25
Q

How does the treatment regime change for pericardial TB, CNS TB and MDR TB?

A

Pericardial: need steroids at start of treatment

CNS: need steroids at start of treatment and 12 months instead of 6

MDR: Use second line drugs and at least 6

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26
Q

What are the side effects of each of the ATT drugs?

A

Rifampicin: hepatitis + , urine/tears turn orange

Isoniazid: peripheral neuropathy, colour blind, hepatitis ++

Pyrazinamide: hepatitis +++

Ethambutol: optic neuropathy/reduced visual acuity

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27
Q

What monitoring needs to be done before and during ATT to combat the side effects?

A

Before: baseline LFTs and visual acuity

During: LFTs (if they derange can stop and gradually reintroduce or use liver-friendly regime but this takes 24 months), monthly visual acuity

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28
Q

What are the infection control measures on the ward with a new TB case?

A

- Nurse in negative pressure side room until 2 weeks of treatment, need to wear mask when leaving room

  • If ward has immunocompromised patients (e.g HIV), need to be in side room for whole stay on ward
  • Smear positive patients can go home but need to quarantine until 2 weeks of treatment

- Only need to wear FFP3 mask/aprons if MDR TB or aerosol generating procedures

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29
Q

What infection control measures with a new TB take place off the ward?

A
  • Inform public health
  • Contact tracing to CXR or Quantiferon close contacts
  • Refer to TB nurses
30
Q

What should all patients admitted to an IDU be offered?

A

Blood bourne infection screen

  • HIV
  • Syphillis
  • Hepatitis B/C
31
Q

When should patients be offered bacterial STI screening on IDU?

A
  • Any patient requesting testing
  • Any patient identified to be high risk of STI due to history
  • All patients already known to have a STI (Including blood-bourne infections)
32
Q

How should you take a sexual history?

A

Symptoms: discharge, genital skin problems, pain, dysparaunia, unusual PV bleeding, anal symptoms

Exposure: sexual contacts in past 3 months including what sex is the partner and what type of sex (oral, anal, vaginal), contraceptive method, type and duration of relationship, ask men if ever had sex with man, STI history

Other: LMP, last smear, HPV vaccine history, consensual sex

33
Q

How do you perform a genital examination on a patient if you suspect them to have an STI?

A

Have a chaperone for all

Check oral and anal area for all!

Men:

  • Retract foreskin
  • Inspect urethral meatus for discharge
  • Look at skin
  • Check scrotum

Women:

  • Vulval exam
  • Speculum
  • Bimanual examination
34
Q

What tests are done on an STI screening for asympomaic patients?

A

All are testing for GC/CT!!

- Pregnancy test

- First pass urine (men only)

- Vulvovaginal swab (insert as far as possible and sweep) and put into NAAT medium

- Pharyngeal swab and put into NAAT

- Rectal swab (2cmin and rotate) and put into NAAT medium

35
Q

What additional tests are done on a STI screen for symptomatic patients?

A

- Urethral discharge charcoal swab for GC culture

- Vaginal discharge charcoal swab for GC, Trichomoniasis and Candida culture from posterior fornix

- If ulceration viral swab for HSV1/HSV2 PCR

- Anal discharge: charcoal swab for GC culture, viral swab for HSV

- Conjunctivitis: GC/CT NAAT

36
Q

How does syphillis present?

A

Treponema Pallidum

Primary: macule then papule then painless ulcer

Secondary: maculopapular rash, mucous patches, lymphadenopathy, hepatitis, headache, fatigue

Tertiary: neurosyphillis, cardiovascular, gumma

37
Q

How is syphillis diagnosed and treated?

A

Dx: PCR and Serology

Mx: IM benzylpenicillin

38
Q

What are the following for Chlamydia Trachomatis:

  • Presentation
  • Diagnosis
  • Treament
  • Complications
A

- Presentation: often asymptomatic, urethral discharge, dysuria, intermenstrual bleeding, dysparaunia

- Diagnosis: NAAT on first pass urine or vulvovaginal swabs

- Treament: Azithromycin or Doxycycline, Partner tracing, avoid sexual contact until treatment complete

- Complications: Reactive arthritis, epididymo-orchitis, PID, ectopic prefnancy, infertility

39
Q

What are the following for Neisseria Gonorrhoeae:

  • Presentation
  • Diagnosis
  • Treament
  • Complications
A

Presentation: urethral/vaginal discharge, dysuria, asymptomatic

Diagnosis: NAAT on first void urine or vaginal swab, can also culture

Treatment: IM Ceftriaxone, contact tracing, avoid sex during treatment

Complications: prostatitis, epididymitis, reactive arthritis, PID

40
Q

What are the following for non-gonococcal urethritis:

  • Presentation
  • Diagnosis
  • Treament
  • Complications
A

Caused by C.Trachomatis, Mycoplasma Genitalium, Trichomonas Vaginalis

41
Q

What are the following for Trichomonas Vaginalis:

  • Presentation
  • Diagnosis
  • Treament
  • Complications
A

- Presentation: yellow vaginal discharge, itch, asymptomatic in men

- Diagnosis: NAAT, culture, microscopy

- Treament: Metronidazole, contact tracing, avoid sexual intercourse

- Complications: risk of preterm delivery and low birth weight

42
Q

What are the following in bacterial vaginosis:

  • Presentation
  • Diagnosis
  • Treament
  • Complications
A

Caused by Gardnerella Vaginalis

- Presentation: thin grey fishy discharge, asymptomatic

- Diagnosis: gram stain, check vaginal pH >4.5

- Treatment: oral or PV metronidazole

- Complications: PID

43
Q

What are the following in genital candidiasis:

  • Presentation
  • Diagnosis
  • Treament
A

- Presentation: itch, dysparaunia, cottage cheese discharge

- Diagnosis: microscopy and culture

- Treament: clotrimazole cream, oral fluconazole, no need to treat partner

Those who are pregnanct, diabetic, immunosuppressed or on antibiotics are at great risk of candida

44
Q

How does HIV get into the body to cause infection?

A

Sexual transmission, sharing needles, blood tranfusions, vertical transmission etc

HIV binds to CD4 receptors on helper T cells to get in

45
Q

How is the transmission of HIV prevented?

A

- Wear condoms

- Post exposure prophylaxis: given up to 72h after for 28 days. Test for HIV 8-12 weeks after exposure

- PrEP

- Avoid breast feeding and have C-section

46
Q

How does early HIV present?

A

Usually 2-4 weeks after infection:

  • Flu like symptoms
  • Rash
  • Myalgia
  • Persistent generalised lymphadenopathy
47
Q

What are some tests you can do for HIV?

A

ELISA blood test: Used to test blood at 4 weeks after exposure and takes a few days. Looks for p24 antigen and HIV antibodies. If positive need serological confirmatory test.

Rapid point of care testing: Uses finger prick or mouth swab and rapid results. Need confirmatory test. Can only use 3/12 post exposure

48
Q

Once someone has had a positive test for HIV, what are some oher baseline investigations that should be done?

(NB - read image)

A
  • Confirmatory HIV test
  • CD4 count
  • HIV viral load
  • HIV resistance profile
  • HLAB*5701 (for abacavir sensitivity)
  • Serology for Hep A/B/C and Syphillis
  • Toxoplasm IgG, Measles IgG, Varicella IgG, Rubelle IgG
  • FBC, U+Es, LFTs, bone profile lipid profile
  • Annual cervical cytology
49
Q

What are some investigations done on newly diagnosed HIV patients to check fro co-infections?

A
  • TB culture
  • Fungal culture and stain
  • Cryptococcal antigen
  • Toxoplasma PCR
  • Viral PCR (EBV, CMV, HSV, VZV)
50
Q

What is the risk of HIV transmission from a needle-stick injury from a person not on ART and what measures should take place after this injury?

A

1 in 300!

  • Bleed wound and put under running water
  • Seek advice from occupational health
51
Q

Apart from baseline investigations when a patient is newly diagnosed with HIV, what else needs to be carried out?

A

Contact tracing!!!!

52
Q

What are the complications of HIV?

A
  • Complications of immune dysfunction (opportunistic infections and malignancy)
  • Complicating comorbidity
  • Complications of treatment e.g side effects of drugs
53
Q

How do the following opportunistic infections in HIV present and how are they treated:

  • Pneumocystis Jirovecii
  • Candidiasis
  • Cryptococcus Neoformans
  • Toxoplasma Gondii
A

Opportunistic infections that occur when CD4<200

54
Q

How do the following opportunistic infections in HIV present and how are they treated:

  • CMV
  • Cryptosporidum
  • Kaposi’s Sarcoma
  • Lymphoma
A
55
Q

How does HIV infection complicate co-moribidity?

A

- Increased risk of CVD: ART causes dyslipidaemia and HIV is pro-atherosclerotic

- Increased risk of osteoporosis: side effect of ART

- HIV can have co-infection with HepB/C and TB

56
Q

What are some infection/malignancies HIV patients are more suspectible to?

A
  • Latent infections: CMV, EBV, HSV, Varicella Zoster
  • Candida
  • Pneumocystis Jirovecci
  • Lymphoma
  • Kaposi’s sarcoma
  • TB
57
Q

What are the aims of ART?

A

Reduce viral load in order to:

  • Allow immunological recovery
  • Prevent progression
  • Reduce mortality
  • Littlest side effects
58
Q

What are the 5 different drug classes involved in ART and what is their mechanism of action?

A

- CCR5 antagonsits: inhibt entry of HIV into cell by blocking CCR5 coreceptor

- NRTI/NNRTI: inhibit reverse transcriptase so viral RNA cannot be converted into DNA so cannot be integrated into nucleus

- ISTI: inhibit integrase so stops HIV DNA integrating into nucleus

- Protease inhibitors: stops protease and maturation of virus particles

- Pharmacokinetic enhancers: increase effectiveness of ARV drugs allowing lower doses to be used

59
Q

What are some examples of the 5 different drug classes used in ART?

A

- CCR5 Inhibitors: Maraviroc

- NRTI: Tenofovir/Emtricitabine (Truvada) or Abacavir/Lamivudine (Kivexa)

- NNRTI: Rilpivirine

- PI: Atazanavir, Darunavir

- Integrase Inhibitors: Dolutegravir, Elvitegravir

- Boosters: cobicistat, ritonavir

60
Q

What is the ART regime?

A

Two NRTI’s plus one of:

  • Ritonavir boosted protease inhibitor
  • NNRTI
  • Integrase inhibitor

Give multiple drugs to prevent resistance

61
Q

What needs to be done before starting ART?

A

- Counselling: explain benefits of ART (not cure), explain lifelong, resistance, side effects, necessary monitoring, partner testing

- Screen for infections and malignancy: e.g TB, HepB/C

- Baseline tests: CD4, viral load, FBC, LFTs, electrolytes, creatinine, pregnancy test, viral genotype for drug resistance

- Review usual medications for drug interactions

62
Q

What monitoring is done during ART?

A

- Viral Load

- CD4 counts: see if need prophylaxis for opportunistic infections

- Check adherance

- Chest for adverse effects: LFTs and Glucose

63
Q

What are the side effects of each class of drug in ART?

A

- NRTI: GI disturbance, anorexia, pancreatitis, hepatic dysfunction, decreased bone mineral density, avoid abacavir in CVD, avoid tenofovir if eGFR<30

- PI: hyperglycaemia, insulin resistance, dyslipidaemia, jaundice, hepatitis

- NNRTI: CNS toxicity, suicidal thoughts, rash, GI disturbance

- Integrase Inhibitor: rash, GI disturbance, insomnia

64
Q

Why is adherance important in ART and how can it be improved?

A

To prevent resistance and disease progression

  • Explore reasons for non-adherance
  • Simplify dosage regime with dossette box
  • Link taking medication to regular daily activity
  • Explain risks of not adhering
65
Q

What support are patients with newly diagnosed HIV given?

A
  • Given HIV nurse for advice, education and social support for patient and their family
  • Community support groups
  • Psychologist referral
66
Q

What prophylaxis is offered to patients with a low CD4 count and why?

A

CD4<200: Offer daily co-trimoxazole to prevent P.Jirovecii Pneuomonia

CD4<50:

Offer Azithromycin weekly to protect against MAI(aka MAC).

Also refer to opthamology for dilated fundoscopy to check for CMV retinitis

67
Q

When is the diagnosis of AIDS given?

A

CD4<200

68
Q

What vaccinations should be given to all HIV patients?

A
  • Hep B
  • Pneumococcus
  • Annual influenzae
69
Q

What drug is given for PEP?

A

Truvada (tenofovir/emtricitabine) for 28 days then do a test 8-12 weeks after exposure

Can be given up to 72h after exposure e.g needlestick, unprotected sex

70
Q

What are the principles of contact tracing in TB?

A
  • Only contact trace close contacts (household members, partners, frequent visitors to house)
  • If symptomatic look for active TB
  • If asymptomatic do Mantoux for latent TB and offer BCG
71
Q

How is latent TB diagnosed?

A

Do mantoux test and if positive rule out active TB by doing CXR and sputum cultures

72
Q

What is the pathophysiology of TB?

A

Primary Ghon’s focus

Transmission:
TB is primarily transmitted through the air when an infected person with active TB disease coughs, sneezes, or talks, releasing respiratory droplets containing the bacteria. Individuals who inhale these droplets may become infected.

Infection and Primary TB:
Once inhaled, the bacteria reach the alveoli (air sacs) of the lungs and are engulfed by macrophages, a type of immune cell. The bacteria can resist destruction within the macrophages.
The infection can lead to primary TB, characterized by the formation of small, localized lesions called granulomas. These granulomas contain immune cells, including macrophages and T lymphocytes, which attempt to contain the infection.

Latent TB Infection (LTBI):
In many cases, the immune response is effective in controlling the infection, leading to a state known as latent TB infection. In LTBI, the bacteria are still present but are held in check by the immune system, and the individual does not exhibit symptoms.
A collection of these granulomas are known as a ghons focus

Reactivation or Progression to Active TB:
In some individuals, especially those with weakened immune systems, the bacteria can escape control and multiply, leading to reactivation of TB. This can occur years after the initial infection.
Factors contributing to reactivation include immunosuppression (HIV infection, certain medications), malnutrition, diabetes, and aging.

Spread of Active TB:
Active TB disease occurs when the bacteria overcome the immune system’s defenses, leading to the destruction of lung tissue and the formation of larger cavities. The bacteria can then spread through the bloodstream to other organs, causing extrapulmonary TB.
If the granulomas spread to the lymph nodes, its then a primary complex

Clinical Manifestations:
Active TB is characterized by symptoms such as persistent cough, chest pain, hemoptysis (coughing up blood), fatigue, weight loss, and night sweats. Extrapulmonary TB can affect various organs, such as the kidneys, bones, and central nervous system.
Immune Response:
The immune response involves both innate and adaptive immunity. Macrophages play a central role in recognizing and attempting to destroy the bacteria. T lymphocytes also contribute to the immune response by releasing cytokines and activating other immune cells.

Granuloma Formation:
Granulomas are a hallmark of TB infection. They are organized structures formed by immune cells attempting to contain the bacteria. While granulomas can prevent the spread of the bacteria, they may also serve as a reservoir for latent infection.