Case 13: TB, Hepatitis Flashcards
1
Q
TB: CXR
A
- Primary: hilarlymphadenopathy effusion, pulmonary infiltrates, calcification.
- Reactivation: upper lobe cavitary lesion with mediastinal adenopathy
- thick walled cavities/ cavitating consolidation
- nodular tree in bud pattern
- Necrotic adenopathy
- Disseminatedmiliary tuberculosisgives an appearance ofmillet seedsuniformly distributed across the lung fields.
2
Q
Summary of TB investigations
A
- FBC, U+Es, LFTs, bone profile, CRP/ESR
- Blood borne virus screen - Hep B/C/HIV
- Sputum x 3 for AFB smear/TB culture and routine M, C and S
- -CXR
3
Q
Treatment for latent TB
A
three months of isoniazid and rifampicin or six months of isoniazid only. Rule out active TB
4
Q
Monitoring TB
A
Gain in weight, improving cough and sputum, sputum smear and culture ‘conversion’ (i.e. sputum becomes smear then culture negative). Patients often get paradoxically worse for 2-6 weeks before clinically improving. Radiological improvement lags behind clinical improvement.
5
Q
Treatment for active TB
A
- Intensive phase:two months of isoniazid + rifampin + pyrazinamide + ethambutol.
- Continuation phase (if fully better and sensitive after two months):four months of isoniazid + rifampin.
- Without sensitisation you may continue a third drug if cant resample
- If TB and CNS involvement treat for 12 months
6
Q
General principles for treating TB
A
- Testing for other infectious diseases (e.g.,HIV,hepatitis Bandhepatitis C)
- Testing contacts for tuberculosis (contact tracing)
- Notifying UK Health Security Agency(UKHSA) of suspected cases
- Isolating patients with active tuberculosisto prevent spread (usually for at least 2 weeks of treatment)
- Aspecialist MDTguides management and follow-up
7
Q
Monitoring treatment for TB
A
- Sputum samples (microscopy and culture) should be obtained for acid-fast bacilli smear and culture at monthly intervals until two consecutive cultures are negative.
- If treatment failure (positive cultures after four months of therapy) or relapse: drug susceptibility testing should be done
8
Q
Side effects of TB drugs
A
- Hepatotoxicity is an important adverse effect of isoniazid, rifampin, and pyrazinamide.
- Pyridoxine (vitamin B6) is given with isoniazid to prevent peripheral neuropathy.
- Rifampicincan causered/orange secretions, such as urine and tears. It is apotent inducerof thecytochrome P450 enzymesand reduces the effects of drugs metabolised by this system, i.e.COCP.
- Pyrazinamide can causehyperuricaemia(high uric acid levels), resulting ingout and kidney stones.
- Ethambutol can causecolour blindness and reduced visual acuity.
9
Q
How to manage Rifampicin drug interactions
A
- Oestrogens (use alternative contraception)
- steroids (double normal dose)
- phenytoin (increase dose)
- sulfonylureas (consider alternatives if diabetic control deteriorates)
- anticoagulants e.g. warfarin and DOACs (increase INR monitoring)
10
Q
Multidrug resistance TB
A
- TB resistant to at least both isoniazid and rifampin.
- A longer, individualised regimen vs a shortened, standardised regimen: 9 to 18 months.
- Management of drug-resistant TB requires expert consultation.
- Levofloxacin (or moxifloxacin) + bedaquiline + linezolid is a commonly used regimen
11
Q
Extensively drug resistant TB
A
- Resistant to at least isoniazid, rifampin, fluoroquinolones as well as either aminoglycoside (amikacin, kanamycin) or capreomycin or both.
- Treatment consists of an intensive and continuation phase for prolonged duration.
- The regimen consists of at least five drugs: susceptible first-line drugs if any, a fluoroquinolone, bedaquiline, linezolid, and additional oral agents (clofazimine, cycloserine, or terizidone).
- A different regimen for treatment of XDR-TB is 26-week regimen including bedaquiline, pretomanid, and linezolid.
12
Q
Complications of TB
A
- Pulmonary: Haemoptysis, Pneumothorax, Bronchiectasis, Pulmonary destruction, Fistula, Tracheobronchial stenosis, Malignancy, Chronic pulmonary aspergillosis.
- Tuberculous effusions and empyema.
- Miliary TB: massive spread with multiple organ involvement.
- Septic shock.
13
Q
Screening for latent TB infection is done for:
A
- Individuals with recent exposure (contacts).
- Health care workers.
- Homeless shelters and prisons.
- Individuals with increased risk of reactivation: HIV.
- If patient is starting immunosuppressants.
- Travellers from high-incidence countries.
14
Q
When is NAAT usedin TB diagnosis:
A
- Diagnosing TB is patients with HIV or <16
- Risk factors for multidrug resistance
15
Q
Screening tests for TB
A
- TST test or IGRA.
- If any positive or active TB suspected: Chest x-ray, Sputumstain and culture
16
Q
TB- prevention
A
- Isolate patient (short-term, until two weeks after initiating treatment), treat the contacts.
- Reportable condition to the local health authorities. (notifiable disease)
- Close contacts: Screened for active TB symptoms, CXR and interferon gamma release assay ≥6 weeks after exposure.
17
Q
BCG vaccine
A
- BCG vaccination: children in high-risk region, health-care workers, and other individuals based on exposure status
- Should not be administered to individuals with decreased immunity.
- Take Mantoux test before and only give if negative. Live vaccine
18
Q
Who do you offer DOT to
A
- do not adhere to treatment (or have not in the past)
- have been treated previously for TB
- have a history of homelessness, drug or alcohol misuse
- are currently in prison, or have been in the past 5years
- have a major psychiatric, memory or cognitive disorder
- are in denial of the TB diagnosis
- have multidrug‑resistant TB
- are too ill to administer the treatment themselves
- DOT: directly observed therapy. Can have VOT (video observed therapy)
19
Q
Vitamin D and TB
A
Vitamin D deficiency associated with risk of TB infection + more severe infection
20
Q
Drug induced Liver injury (DILI)
A
- Can be caused by all TB medication but most likely Pyrazinamide
- Causes acute hepatitis, cholestasis or granulomatous hepatitis
- Often asymptomatic – or abdo pain, jaundice, fatigue, N+V, itching
- If ALT > 3 x baseline (with symptoms), or > 5 x baseline (without symptoms), or if bilirubin rises – STOP all treatment unless really bad TB in which case continue 2 non-hepatotoxic drugs
- Reintroduce the anti-TB drugs to full dose over 10 days
21
Q
Pericardial TB
A
- causes pericardial effusion which an compromise cardiac function causing heart failure
- Investigations: urgent CT scan of thorax/abdomen, urgent echocardiogram, pro-BNP level, diuretics and pericardiocentesis +/- drain with samples sent for cytology and routine culture/AFB smear/TB culture and PCR.
- Treatment: standard TB treatment, High dose steroids (60 mg prednisolone, weaned to 30 mg over 2-3 weeks, weaned off by 2 months
22
Q
Viral gastroenteritis
A
- Acute inflammation of the lining of the stomach and small intestine
- Most common organism is Norovirus in adults and Rotavirus in children
- Clinical diagnosiswhich presents with a self-limiting episode of diarrhoea, nausea and vomiting lasting <14 days
- Other less common causes: Adenovirus (children), Sapovirus (adults)
23
Q
Rotavirus
A
- Almost every child is infected by 5th birthday. Infection causes long lasting immunity
- Faeco-oral transmission
- UK: oral rotavirus vaccine
24
Q
Norovirus
A
- Faeco-oral
- No long lasting immunity
- Spreads in hospitals, residential homes or schools
25
Q
Viral gastroenteritis: clinical features
A
- Acute diarrhoea: 3 or more stools per day less than <14 days. Watery non-bloody
- Vomiting
- Mild fever
- Abdominal pain
26
Q
Clinical signs of significant dehydration
A
- Dry mucous membranes
- Tachycardia
- Hypotension
- A thin, thready pulse
- Reduced urine output
27
Q
Viral gastroenteritis investigations
A
If dehydrated: FBC,U&E before commencing IV fluids
28
Q
When would you need a stool sample in viral gastroenteritis
A
- Diarrhoea which is persistent, lasting >14 days
- Blood or pus in the stool
- High suspicion of non-viral gastroenteritis
- Recent history of hospitalisation and antibiotic therapy
- Recent foreign travel history
29
Q
When would urgent fluid resuscitation be needed in viral gastroenteritis
A
- Systolic blood pressure <100
- Heart rate >90
- Cool peripheries
- Respiratory rate >20
- NEWS score >5
30
Q
When would a patient be admitted to hospital for viral gastroenteritis
A
- If they are unable to to maintain oral intake due to vomiting
- Some elderly individuals >60 years old, who are more at risk of severe dehydration
- Abdominal tenderness
- Diarrhoea lasting 10 days or more
31
Q
Conservative management for viral gastroenteritis
A
- Symptomatic support and fluid/electrolyte replacement
- Oral rehydration salts if high risk of poor outcomes
- Hygiene: don’t share towels or flannels, wash soiled clothes separately
- If working in hospitals, schools or care homes don’t return to work until 48hrs after diarrhoea and vomiting have stopped
32
Q
Complications of viral gastroenteritis
A
- Dehydration and electrolyte disturbance: renal injury, persistent acidosis and circulatory failure. Can cause sodium abnormalities and Hypokalaemia
- AKI
- Lactose intolerance: can last several weeks or be permanent
33
Q
Causes of acute hepatitis
A
- Most common: Hep A, E, B
- Relatively common: Hep C, EBV, CMV
- If immunosuppressed: VZV, HSV, adenovirus
- Drugs (especially paracetamol)
- Others: autoimmune, pregnancy, toxins, ischaemia, malignancy, Wilson disease
- Acute hepatitis: liver inflammation lasting less than 6 months
34
Q
Complications of acute hepatitis
A
- ALF: severe ALF with encephalopathy and impaired synthetic function in a patient without cirrhosis or pre-existing liver disease
- progression to chronic hepatitis which may lead to cirrhosis and HCC
35
Q
Other less common causes of viral hepatitis
A
- Hepatitis C: normally asymptomatic. Majority progress to chronic. Presents similar to Hep A/B/E
- EBV: infective mononucleosis (fever, sore throat, lymphadenopathy, fatigue). Mild hepatitis don’t tend to get jaundice. Increased risk of immunosuppressed
- CMV: like EBV with mild hepatitis. Important if immunosuppressed.
36
Q
Testing for acute hepatitis
A
- LFT, INR and albumin
- Hepatitis A IgM, hepatitis B surface antigen, Hepatitis C Ab, Hepatitis E IgM
- Consider testing for EBV and CMV
37
Q
Chronic hepatitis
A
- Inflammation of the liver >6 months
- Causes: viral infection, alcohol, NASH, autoimmune disorders, cholestatic disorders, Metabolic disease
- Main viral causes: HBV, HCV, HDV, HEV (if immunocompromised)
- Causes immune mediated fibrosis of the liver → Cirrhosis and chronic liver failure → HCC
38
Q
Hepatitis A
A
- self limiting infection which spreads through the faecal oral route
- only causes acute hepatitis and not chronic
- Risk factors: travel, MSM, IV drug use, no vaccine
39
Q
Hepatitis A stages
A
- Incubation: 28 days
- Prodromal symptoms (3-10 days): flu-like illness, gastrointestinal symptoms (such as appetite loss, RUQ pain, nausea, vomiting and diarrhoea) and low-grade fevers up to 39C.
- Icteric phase (established illness): lasts 1-3 weeks but up to 12. Symptoms appear after 10 days
- Convalescent stage: recovery after acute illness (up to 6 months). Features of weakness, malaise.
- Full clinical recover: usually symptoms improve 1-3 weeks can last 12
40
Q
Clinical features of Hepatitis A
A
- Symptoms includejaundice, pale stools and dark urine, pruritis (40% of those with jaundice), fatigue, anorexia, vomiting.
- There may beHepatomegaly, Splenomegaly and hepatic tenderness on examination.
- Asymptomatic <6
41
Q
Hepatitis A: acute liver failure
A
- Complication
- Increased risk with age/pre-existing liver disease
- Encephalopathy is usually proceeded by impairement of liver function (jaundice and INR >1.5)
42
Q
Hepatitis A: investigations
A
- First line: PCR for hepatitis A RNA
- Blood tests: hep A serology of serum sample (IgM or IgG)
- LFT’s: raised ALT/AST (in the 1000’s), raised bilirubin and ALP
43
Q
Hepatitis A: IgM and IgG
A
- Positive HAV-IgM and positive HAV-IgG suggests acute hepatitis A infection. Can confirm with PCR
- Negative HAV-IgM and positive HAV-IgG suggests past hepatitis A infection or vaccination.
44
Q
Hepatitis A: Management
A
- Notify public health England and contact tracing: infectious during incubation period and 1 week after jaundice onset (should be in side room with own toilet)
- Rest and hydration
- Anti-emetics: Metoclopramide or cyclizine unless impaired liver function
- Avoid food preparation, work or school, and sexual contact for 7 days after symptom onset
- Follow patients up every 1-2 weeks until amino-transferase is normal
45
Q
How long is Hep A infectious for
A
during incubation and 1 week after onset of jaundice
46
Q
Hep A prevention
A
- improved sanitation and hygiene
- education: transmission, drink bottled water
- hep A vaccine for high risk groups
- Can give contacts hepatitis A vaccine and HNIG (Human Normal Immunoglobulin) to prevent infection
47
Q
Who gets the Hepatitis A vaccine
A
- Travellers to endemic areas
- Men whom have sex with men
- IVDU
- Chronic liver disease
- Haemophilia
- Occupational risk e.g. lab workers, sewage workers
- Following exposure to infected individual
- Given >2 weeks before required and booster after 6-12 months
- An inactive vaccine- 2 are given
48
Q
Hepatitis E
A
- RNA hepevirus
- spread by the faecal-oral route
- incubation period: 3-8 weeks (40 days)
- common in Central and South-East Asia, North and West Africa, and in Mexico
- causes a similar disease to hepatitis A, but carries a significant mortality (about 20%) duringpregnancy
- does not cause chronic disease or an increased risk of hepatocellular cancer
- Sporadic and Classical subtypes
49
Q
Hepatitis E subtypes: Classical (genotype 1/2)
A
- more common in resource limited countries
- Like hep A
- spread by faeco-oral route: due to travel in endemic areas
- Higher mortality.
- At risk groups: travellers, young adults 15-40, pregnant women (severe infection)
- Asymptomatic in children
50
Q
Hep E subtype: sporadic (genotype 3/4)
A
- More common in recourse rich countries i.e. the UK
- At risk groups: age, male, no increased mortality in pregnancy
