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year 4 CDM 2 > Case 13: TB, Hepatitis > Flashcards

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.
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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
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3
Q

Treatment for latent TB

A

three months of isoniazid and rifampicin or six months of isoniazid only. Rule out active TB

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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.

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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
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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
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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
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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.
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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)
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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
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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.
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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.
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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.
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14
Q

When is NAAT usedin TB diagnosis:

A
  • Diagnosing TB is patients with HIV or <16
  • Risk factors for multidrug resistance
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15
Q

Screening tests for TB

A
  • TST test or IGRA.
  • If any positive or active TB suspected: Chest x-ray, Sputumstain and culture
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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.
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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
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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)
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19
Q

Vitamin D and TB

A

Vitamin D deficiency associated with risk of TB infection + more severe infection

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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
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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

year 4 CDM 2 (39 decks)

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