Infectious diseases Flashcards
Mode of transmission of each hepatitis vaccine
A = Food and drink contaminated with faeces of an infected individual. B = blood transmission. C = blood transmission. D = blood or sexual contact. E = raw/undercooked meat.
Which hepatitis’ are there vaccines for?
A, B (some protection over D)
Non hepatitis virus causes of hepatitis
Autoimmune
Alcohol
EMV and CMV
Short term/acute symptoms of hepatitis
Nausea Right upper quadrant abdo pain Fatigue + malaise Jaundice Myalgia and arthralgia
Which hepatitis virus’ cause acute and which cause chronic hepatitis and what time scale defines which it is?
Acute = All can occur as acute symptoms. Chronic = B, C, D.
Chronic = infection longer than 6 months.
Complications of chronic hepatitis
Cirrhosis
Liver failure
Hepatocellular carcinoma
Investigation for immunity to hepatitis B
HBsAb - Hepatitis B surface antibody (either from vaccine or previous infection). Vaccine injects HBsAg which mounts immune response and produces HBsAb to give immunity (as no HBeAg or HBcAg injected no chance of acquiring chronic viral hepatitis).
Investigation to show current Hep B infection
Abnormal LFTs Positive: HBsAg HBeAg (from replication) Viral load high on PCR HBcAb with esp high IgM
Treatment of acute hepatitis B
Self-limiting so no treatment.
Ways to spread Hep B
Risky sexual behaviours (HBV > HCV for sexual transmission)
Vertical - mother to newborn.
Sharing needles.
Blood transfusions and dialysis.
Treatment for hepatitis B
Nucleoside reverse transcriptase inhibitors.
Tenofovir or Entecavir.
Prevent DNA replication (can still produce cell proteins). Reduces HBeAg. Potentiates seroconversion and limits liver damage.
Ways to spread Hep C
Needle sharing
Needle injuries at work
Tattooing needles
Bloodstained toothbrushes
Symptoms of acute hep C
None, flu-like not worth seeing doctor about.
Extra-hepatic manifestations of hepatitis C
Glomerulonephritis Cryoglobinaemia Autoimmune thyroid disease Porphyria cutanea tarda Lichen planus
Ix for Hep C
Enzyme immunoassay and immnoblot assay for Hep C antibodies.
PCR for HCV RNA.
How many genotypes fo Hep C are there?
6🤙
Chronic liver disease with Hep C
1 in 3 with chronic HCV infection will get end stage liver disease.
Need close follow up for cirrhosis and HCC.
Tumour marker for hepatocellular carcinoma
AFP - alpha fetoprotein.
Treatment for Hep C
Is curative! Novel = Direct acting antiviral drugs. NS3/4A protease inhibitors e.g. Grazoprevir. NS5A inhibitors e.g. Velpatasvir. NS5B inhibitors e.g. Sofosbuvir.
Who are most at risk for chronic Hep B infection
Perinatal or early childhood infected patients.
Investigations for suspected viral hepatitis
LFTs - elevated ALT/AST, alk phos and bilirubin, low albumin. FBC - microcytic anaemia Coagulation - can have high INR/PT Serology Ultrasound of liver AFP for HCC Liver biopsy
Hep B = Serum HbSAg, HbS IgM antibodies
Investigations to show chronic Hep B infection
Positive: HBsAg HBeAb HBcAb esp high IgE Viral load lower on PCR
No HbsAb as they obviously cant clear the virus and HBsAb is the only antibody to resolve virus.
‘Resolved’ Hep B infection pathophysiology and investigations
4% a year resolve. This can occur after a chronic infection of many years or after an acute infection.
The only resolves when complete seroconversion from HBsAg to HBsAb.
Ix: positive for
HBcAb esp high in IgE
HBeAb
HBsAb
Difference between Hep B and Hep C
Hep B is a DNA virus and is harder to treat - never cured only resolved.
Hep C is a RNA virus so able to cure patients.
Investigations for Hep A
IgM antibody for HAV in acute illness and long term high IgG HAV antibodies.
Abnormal LFTs
Elevated serum bilirubin
Management of Hep A
Supportive care - fluids, good nutrition.
Hep A vaccine
IV immunoglobulins
Pathophysiology of Hep D
Can replicate independently once inside cell but require HBV surface antigen for propagation.
Organism for TB
Mycobacterium tuberculosis
Risk factors for TB
HIV Older age (weaker immune system) Vit D deficiency DM Immunosppression e.g chemo/steroids Silicosis and lung fibrosis disease Alcohol and smoking Poverty
S+S of pulmonary TB
Night sweats Haemoptysis Chronic cough Weight loss Fever Malaise, fatigue, anorexia
O/E: Tachypnoea High temp Hypoxia Clubbing Apical lung sounds
Investigations for pulmonary TB
3 x Acid Fast Bacilli of sputum sample.
If +ve = infective, if -ve doesn’t rule out TB, just less infective/bacteria present.
Blood PCR
CXR - fibronodular opacities in upper lobes with or without cavitation, Gonn focus from calcification and fibrosis around granuloma.
FBC - anaemia, raised WCC
Treatment for pulmonary TB
NOTIFY PHE!!!!!!!! Contact tracing.
Drugs: Isoniazid (H) Rifampicin (R) Ethambutol (E) Pyrazinamide (Z)
Isoniazid + Rifampicin for 6 months daily.
Ethambutol + Pyrazinamide for first 2 months daily only.
Test of cure CXR.
How to treat a TB patient who you are worried wont comply?
Directly Observed Therapy - higher drug doses are given 3 times a week. The patient is observed taking them.
Multi-drug resistant TB
Resistance to at least Isoniazid and Rifampicin.
Patients treated with range of 5-8 drugs for up to 2 years.
Side effects of HREZ drugs
Isoniazid - peripheral neuropathy, agranulocytosis.
Rifampicin - thrombocytopenia, orange urine, many drug interactions including warfarin, oral contraceptives, methadone!
Ethambutol - ocular toxicity.
Pyrazinamide - hepatotoxic, arthralgia, gout/hyperuricaemia.
Latent TB test
Tuberculin skin test / Mantoux test:
- Doesn’t discriminate against those who are vaccinated and those who have previous infection.
- Can get false negative if patient is immunocompromised.
ALTERNATIVE
Interferon Gamma Release Assay (IGRA):
- 2 types = QUANTIferon and T-Spot.
- Distinguishes between vaccinated and latent TB but will also be +ve with active/acute infection.
- Therefore need thorough clinical assessment and CXR.
Locations for extra-pulmonary TB
CNS - TB meningitis TB osteomyelitis TB lymphadenitis Abdominal TB Pericardial TB
Pott’s disease
TB osteomyelitis in the vertebrae.
Pathophyisology of HIV
RNA virus
Enters cells which express CD4 receptor. Mostly T-lymphocytes, macrophages and dendritic cells.
Inside the host’s cell the virus replicates using viral enzymes reverse transciptase and protease) and harnessing host’s proteins to form new viral particles.
Host’s immune system tries to destroy these viral infected cells leading to reduction in CD4 cell count.
Can have host’s immune system control the viral infected cells creating asymptomatic phase (+10yrs) where viral load stays at set point and steady gradual decrease in CD4.
When CD4 T-lymphocyte count is so low that the host is predisposed to opportunistic infections = acquired immunodeficiency syndrome (AIDS).
Risk factors for HIV infection
IVDU needle sharing Unprotected sexual intercourse Vertical transmission to baby Occupational needle stick injury Blood product transfusion e.g haemophiliacs before screening was introduced.
Differential diagnosis for acute primary HIV illness
infectious monoculeosis
S+S in acute, primary HIV illness
Fever Night sweats Myalgia + arthralgia Anorexia Nausea and diarrhoea Lymphadenopathy Maculo-papular rash on trunk and torso Weight loss
Things in a history to suspect HIV
Recurrent UTI Recurrent oral candidias Severe bacteria infections for unexplained reasons e.g. pneumonias. Herpes zoster history Persistent lymphadenopathy Social risk factors
Investigations for HIV/newly diagnosed HIV patient
HIV status via ELISA (p24 antigen), PCR HIV viral load CD4+ count - usually <450cells/mL Offer full STI screen Viral hepatitis antibodies/Blood born virus screen FBC - low Hb U+E LFT and synthetic liver function test esp before starting drugs. Bone profile Tuberculin skin test Urinanalysis
Window period for HIV status testing after exposure
4 weeks. Can get false negative if test immediately after exposure. Give post exposure prophylaxis.
Framework for HIV Management
HAART.
Drug classes used:
Nucleoside reverse transcriptase inhibitors.
Non-nucleoside reverse transcriptase inhibitors, Protease inhibitors.
Entry inhibitors
Fusion inhibitors
Most combinations use 2NRTI and 1PI or NNRTI.
99% reduction in viraemia in 8 weeks.
Can interrupt treatment and can manipulate Rx.
Monitor response with CD4+ count.
Non drug parts = annual flu vaccine, counselling and psych support, annual cervical screening for females, safe sex advice.
Pharmacology, side effects and examples of NRTI
Prevent DNA replication from virus’ RNA.
SE = hypersensitivity (fever/rash)
Examples = Abacavir, Zidovudine
Pharmacology, side effects and examples of NNRT
Prevent DNA synthesis but not as a analogue to nucleotide.
SE = nightmares, hepatotoxic.
Examples = Etravirine, Efavirenz.
Pharmacology, side effects and examples of protease inhibitors
Prevent production of functional proteins from polyprotein.
SE = hyperlipidaemia, diarrhoea, peripheral neuropathy.
Examples = Atazanavir, Darunavir