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Phase 3b > Infectious diseases > Flashcards

Infectious diseases Flashcards

1
Q

What is the first line antimicrobial treatment for CAP?

A

Co-amoxiclav + clarithromycin

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2
Q

What antibiotic can be given in CAP if penicillin allergic?

A

Cefuroxime + clarithromycin

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3
Q

What is the first line antimicrobial treatment for HAP?

A

Doxycycline

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4
Q

What is the first line antimicrobial treatment for infective exacerbation of COPD?

A

Doxycycline

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5
Q

What is the first line antimicrobial treatment for cellulitis?

A

Flucloxacillin

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6
Q

What does strep bacteria look like under the microscope?

A

Gram positive cocci chains (strep = strip)

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7
Q

What does staph bacteria look like under the microscope?

A

Gram positive cocci clusters

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8
Q

What is the first line antimicrobial treatment for a UTI?

A

Nitrofurantoin

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9
Q

What is the second line antimicrobial treatment for UTI?

A

Trimethoprim

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10
Q

When is trimethoprim CI and why?

A

Pregnancy
Teratogenic as folic acid antagonist

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11
Q

What should you prescribe with trimethoprim?

A

Folic acid

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12
Q

What is the first line treatment for H pylori?

A

PPI
Amoxicillin
Clarithromycin/metronidazole

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13
Q

What can cause C diff?

A

C antibiotics, fluoroquinolones, broad spectrum penicillins

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14
Q

What is the first line antimicrobial treatment for C diff?

A

Vancomycin

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15
Q

What is the first line antimicrobial treatment for candidiasis?

A

Nystatin

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16
Q

What is the first line antimicrobial treatment for meningococcal septicaemia?

A

Cefotaxime (children ceftriaxone)

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17
Q

What antimicrobials can be given for prevention/contacts of meningitis?

A

Clarithromycin or rifampicin

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18
Q

Name 3 community aquired infections

A

Pneumonia, meningitis, skin infections, gastroenteritis, UTI, STI

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19
Q

What is sepsis?

A

A aberrant or dysregulated immune response to an infection resulting in wide spread inflammatory response affecting organs and tissues

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20
Q

Name 3 complications of sepsis

A

AKI, delirium, shock, multi-organ failure, septic shock

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21
Q

When should the sepsis 6 be completed by?

A

Within one hour of diagnosis of sepsis

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22
Q

What is the sepsis 6?

A
  • Senior clinician attendance
  • O2 if required sats < 92%
  • Bloods (lactate, glucose, FBC, U&E, CRP, clotting) + cultures
  • IV Abx (max dose, broad spectrum)
  • IV fluids (up to 20ml/kg in boluses)
  • Monitor -> NEWS2, urine output, lactate (at least hourly)
    BUFALO
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23
Q

What should be considered before prescribing antibiotics?

A

Indication
- Is there an infection?
- Likely pathogen?
- Does it need antimicrobial therapy?
Site of infection
- Does the site affect choice of antimicrobial? ie can it get across BBB or get into prostate? IV/oral?
Patient
- Adverse effects eg risk of C diff, liver/renal function, allergy
- Drug-drug interactions
- Pharmacodynamics with renal/liver impairment

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24
Q

What pathogens can cause CAP?

A

Strep pneumoniae
HiB
Legionella

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25
Q

What pathogens can cause infective exacerbations of COPD?

A

Strep pneumoniae
HiB
Moxarella cararrhalis

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26
Q

What pathogens can cause UTI?

A

E coli

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27
Q

What pathogens can cause cellulitis?

A

Staph aureus
MRSA

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28
Q

What pathogens can cause bacterial meningitis?

A

Strep pneumoniae
GBS
N meningitidis
HiB
Listeria

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29
Q

What is Hepatitis B?

A

Enveloped DNA virus

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30
Q

Name 3 areas in the world where we see higher rates of HBV

A

East Asia
Africa
Amazon basin

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31
Q

Name 3 groups in the UK where there might be higher rates of HBV

A

Migrants from high prevalence countries
Minorities - Roma/Slovaks
IV drug users

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32
Q

What are the 2 routes of transmission of HBV?

A

Vertical - from mother to baby
Horizontal - sexual (much more infective than HIV/HCV), blood transfusions and procedures such as dialysis/operations, needles/sharps, household transmission

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33
Q

What are the 2 antigens of clinical importance in HBV?

A

Surface antigen - HBsAg
Envelope antigen - HBeAg
(Core antigen)

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34
Q

What is the role of the HBsAg antigen (surface antigen) in HBV?

A

Detected in blood during current infection, used for diagnostic confirmation
Genetically produced for vaccine use

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35
Q

What is the role of the HBeAg antigen (envelope antigen) in HBV?

A

Assessment of phase of infection

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36
Q

What 3 antibodies for HBV are of clinical importance?

A

Surface antibody - HBsAb
Envelope antibody - HBeAb
Core antibody - HBcAb

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37
Q

What is the role of the HBsAb antibody (surface) in diagnosing HBV?

A

Indicated immunity to HBV following immunisation or infection

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38
Q

What is the role of the HBeAb antibody (envelope) in diagnosing HBV?

A

Appears in later phase of disease as evidence of immune response

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39
Q

What is the role of the HBcAb antibody (core) in diagnosing HBV?

A

Found in most people exposed to HBV. Doesn’t differentiate between acute, chronic, or past infection.
Not found in people due to immunisation

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40
Q

What other structure other than antibodies and antigens are important in HBV diagnosis?

A

HBV DNA

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41
Q

What is the role of the HBV DNA in diagnosing HBV?

A

Measured and quantified, helps determine grade of replication and activity of the virus

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42
Q

When might you treat acute HBV and why?

A

Fulminant hepatitis
Can cause liver failure (increasing INR) so treated to prevent liver failure and subsequent liver transplant

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43
Q

What is the definition of a chronic HBV infection?

A

Infection persisting beyond 6 months

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44
Q

When is HBV frequently acquired and what affect does this have on the rate of acute infections becoming chronic?

A

At birth/childhood
Birth -> in highly infective mothers 90% risk of becoming chronic
Childhood -> 30-50% risk of becoming chronic
Adulthood -> 5% risk (higher in immunosuppressed)

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45
Q

How can the risk to neonates of becoming infected with chronic HBV be reduced?

A

HBV Ig and immunisation at birth (risk reduced to 7%)

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46
Q

What is the risk of having undiagnosed HBV?

A

Complications - cirrhosis/liver cancer
High risk of liver cancer even without cirrhosis
Oncogenic virus

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47
Q

What is the purpose of HBV treatment?

A

To control viral replication

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48
Q

What is the treatment for HBV?

A

Pegylated interferon alpha (weekly injectable for 48 weeks)
Oral anti-virals (tenofovir or entecavir ODS)

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49
Q

What advice should be given to HBV carriers?

A

Avoid having unprotected sex unless partner has been vaccinated and is immune
Avoid needle sharing
Avoid sharing toothbrushes or razors
Avoid drinking alcohol

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50
Q

What is hepatitis C?

A

BBV
Six genotypes

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51
Q

How is HCV transmitted?

A

Parenteral -> IV drug usage or infection via blood products before identification and testing of virus, needle stick injuries, unclean tattoo needles
Risk of household transmission low
Sexual and vertical transmission uncommon

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52
Q

What are the symptoms of an acute HCV infection?

A

Most asymptomatic
15% malaise, RUQ pain +/- jaundice

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53
Q

What is the rate of spontaneous HCV clearance?

A

15-30%

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54
Q

What is the prognosis of chronic HCV infection?

A

1/3 develop ESLD within 25 years of infection
1/3 ESLD beyond 25 years
1/3 never progress to ESLD

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55
Q

What are the side effects of HCV infection?

A

ESLD, hepatocellular carcinoma
Essential mixed cryoglobulinaemia
Membranoproliferative glomerulonephritis
Porphyria cutanea tarda
Autoimmune thyroid disease in women

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56
Q

How is HCV diagnosed?

A

Hep C antibody test -> if ever been exposed, doesn’t mean actively infection
HCV RNA -> active infection

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57
Q

What clinical assessment occurs for those with HCV?

A

Baseline liver fibrosis scan
If advanced fibrosis/cirrhosis then screening for hepatocellular carcinoma
Screened for other causes of chronic liver disease and counselled regarding alcohol
Hep A and B vaccination if not immune

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58
Q

What screening is there for hepatocellular carcinoma?

A

Alpha feto-protein (AFP)
USS

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59
Q

What is the aim of HCV treatment?

A

Cure

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60
Q

What is the definition of cure in HCV treatment?

A

Undetectable HCV RNA in blood 12 weeks after end of treatment (sustained virological response SVR12)

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61
Q

What does HCV treatment entail?

A

8/12 weeks direct antiviral drugs
95% cure rate

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62
Q

Name 3 places where the incidence of TB is high worldwide

A

SE Asia
Western Pacific
Africa

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63
Q

How is TB spread?

A

Droplet spread

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64
Q

How is TB diagnosed?

A

Sputum ideally (depends on infection site)
Acid fast bacilli special stain -> Ziehl-Neelson stain/Auramine-Phenol
Mycobacterial culture
2-8 weeks to grow
Speciation and genotyping resistance
PCR testing

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65
Q

What are the 4 drugs of treatment for TB and their length of treatment?

A

Rifampicin (6 months)
Isoniazid (6 months)
Pyrazinamide (2 months)
Ethambutol (2 months)

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66
Q

Name the main side effects of rifampicin

A

Red colouring of urine, sweat, tears, soft contact lenses
Hepatitis
GI upset

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67
Q

Name the main side effects of isoniazid

A

Parasthesia
Hepatitis

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68
Q

Name the main side effects of pyrazinamide

A

N&V
Muscle/joint pain
Hepatitis

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69
Q

Name the main side effects of ethambutol

A

Visual changes
Optic neuritis

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70
Q

How is the treatment regimen different for CNS TB?

A

12 months
+ adjunctive steroids

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71
Q

What is multi-drug resistance TB?

A

TB resistance to at least isoniazid and rifampicin due to poor adherence/management of TB

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72
Q

What other infection is highly associated with TB?

A

HIV

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73
Q

What contact screening can be done to help diagnose TB?

A

Mantoux test
Interferon gamma release assay (Quantiferon)

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74
Q

What is the chemoprophylaxis for TB?

A

Isoniazid for 6-9 months

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75
Q

When can you get a false negative from a HIV infection?

A

2-3 weeks post infection

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76
Q

What 2 markers are important for HIV diagnosis and monitoring?

A

CD4 count
Viral load

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77
Q

What does CD4 count tell us in terms of HIV?

A

Determine how immunocompromised patient is

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78
Q

What is a normal CD4 count?

A

450-1600 per microlitre of patient’s blood

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79
Q

What infections are more common in patients with a CD4 count < 200?

A

P jiroveccii pneumonia (PCP)
Toxoplasmosis

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80
Q

What infections are more common in patients with a CD4 count < 50?

A

Mycobacterium avium intracellulare
CMV

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81
Q

What does viral load tell us in terms of HIV?

A

Quantity of virus per ml of patients serum
If uncontrolled viral load > 50,000
If well controlled undetectable

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82
Q

Name 3 HIV CNS associated illnesses

A

Dementia
Toxoplasmosis
CNS lymphoma
Encephalitis -> CMV, herpes

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83
Q

Name 3 HIV skin associated illnesses

A

Molluscom contageousum
Kaposi’s sarcoma
HSV ulcers

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84
Q

Name 3 HIV respiratory associated illnesses

A

Recurrent pneumonia
TB
Pneumocystitis pneumonia
Candidiasis

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85
Q

Name 3 HIV GI associated illnesses

A

Cryptosporidiosis diarrhoea
Candidiasis
Hep A/B/C
Anal cancer

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86
Q

Name 3 other HIV associated illnesses

A

Cervical cancer
Lung cancer
CMV retinitis

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87
Q

What is the treatment for HIV?

A

Highly Active Anti-Retroviral Therapy (HAART)
At least 3 anti-retroviral drugs -> act on the virus in different ways and reduce emergence of resistance

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88
Q

When should you give antibacterial prophylaxis in HIV patients?

A

CD4 < 200

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89
Q

What prophylactic treatment can be given to HIV patients?

A

Co-trimoxazole (against PCP/toxoplasma/bacterial infections, s/e rash/bone marrow suppression)
Nebulised pentamidine (against PCP, administered in negative pressure side room as teratogenic)
Azithromycin (MAI if CD4 < 50)
Valganciclovir (CMV treatment)

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90
Q

What prevention of HIV is there?

A

Pre-exposure prophylaxis (PrEP)
Post exposure prophylaxis (PEP)
Antenatal screening and treatment for mothers with HIV

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91
Q

What types of immunodeficiency are there?

A

Congenital
Acquired
Iatrogenic

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92
Q

What can cause acquired immunodeficiency?

A

Diabetes
Cirrhosis
Renal failure
HIV

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93
Q

What can cause idiopathic immunodeficiency?

A

Radiotherapy
Cytotoxic chemotherapy
Immunosuppressive medication
Splenectomy

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94
Q

What is a haematopoietic stem cell transplant?

A

Stem cells from patient (autologus) or donor (allogenic)
Condition regimen to eradicate cancer/bone marrow stem cells
Stem cells infused into patient
Supportive medication given as stem cells graft
Monitor late effects

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95
Q

What is neutropenia?

A

Low neutrophil count

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96
Q

Who is at higher risk of neutropenia?

A

Chemotherapy patients who received it in the last 6 weeks
Received in high dose chemotherapy/bone marrow transplant in last year
Haematological condition causing numeric or functional (not working properly) neutropenia

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97
Q

Where are the common infections in neutropenic patients?

A

IV lines
Oral cavity
Sinuses
Lungs
Skin
Perineal region
Urinary tract

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98
Q

What is neutropenic sepsis?

A

Life-threatening complication of chemotherapy and haematopoietic stem cell transplant
Can have minimal signs of infection and may not have pyrexia

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99
Q

What should you do with a suspected neutropenic sepsis patient?

A

Cultures from IV lines, sputum/bronchoalveolar lavage, urine ect
Empirical Abx treatment started promptly

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100
Q

What symptoms might neutropenic patients have when septic?

A

Pallor
Mottled skin
Tachycardia
Altered mental state
Anxiety
Increased resp rate

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101
Q

What treatment for neutropenic sepsis can be given to autograft/non-transplant patients?

A

Piperacillin/taxobactam + gentamicin
Mild penicillin allergy -> ceftazidime + gentamicin
Severe penicillin allergy -> teicoplanin + PO ciprofloxacin

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102
Q

What treatment for neutropenic sepsis can be given to allograft patients?

A

Meropenem + teicoplanin
Mild penicillin allergy -> meropenem + teicoplanin
Severe penicillin allergy -> discuss with micro

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103
Q

Why are solid organ transplant recipients immunosuppressed?

A

Require continuous immunosuppressant medication to prevent rejection

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104
Q

What infections can be present in patients within the first month of their solid organ transplant?

A

Nonsocomial: wound infection, pneumonia, IV line infection
Reactivation of previous infection: TB, strongyloidiasis

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105
Q

What infections can be present in patients within the first 1-6 months of their solid organ transplant?

A

Viral: CMV, EBV, HBV
Opportunistic: PCP, legionella, aspergillosis, listeria

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106
Q

What infections can be present in patients after 6 months of their solid organ transplant?

A

Progressive viral: CMV, HBV
Opportunistic: PCP, cryptococcus, listeria, nocardia
Community acquired: S pneumoniae, influenze

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107
Q

What biologic drugs are most at risk of causing reactivation of TB or HBV?

A

Anti-TNF

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108
Q

What vaccinations should be given to patients to patients with asplenia?

A

Pneumococcal
Meningococcal ACWY
MenB
Annual flu

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109
Q

Name 3 groups of patients in whom live vaccines are CI

A

Primary immunodeficiency
HIV
Immunosuppressive therapy

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110
Q

What can be given to immunosuppressed patients who have been exposed to measles/chickenpox as post-exposure prophylaxis?

A

Measles -> IVIg
Chickenpox -> IVIg/acyclovir

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111
Q

What are sewage workers more at risk of?

A

Gastroenteritis
Hepatitis
Leptospirosis (rats)

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112
Q

What are farm workers more at risk of?

A

Orf
Coxsackie
Coxiella

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113
Q

What are aberttoir workers more at risk of?

A

Anthrax

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114
Q

What are the military more at risk of?

A

Anthrax

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115
Q

What are sex workers more at risk of?

A

STDs
Syphilis
HBV
HIV

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116
Q

What are health workers more at risk of?

A

HBV
LRTI

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117
Q

What are canoeist more at risk of?

A

Leptospirosis
Gastroenteritis

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118
Q

What are cavers more at risk of?

A

Histoplasmosis

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119
Q

What are trekkers more at risk of?

A

Lyme disease
Tick-borne diseases

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120
Q

What are fresh water swimmers more at risk of?

A

Schistosomiasis
Crytosporidia

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121
Q

What can parrots put you more at risk of?

A

Chlamydia psittacci

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122
Q

What can terrapins put you more at risk of?

A

Salmonellae

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123
Q

What can rodents put you more at risk of?

A

Rat bite fever

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124
Q

What can cats put you more at risk of?

A

Toxoplasmosis
Toxocara

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125
Q

What can dogs put you more at risk of?

A

Campylobacter
Capnocytophaga

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126
Q

What can tropical fish put you more at risk of?

A

Mycobacterium marinum

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127
Q

What can IV drug usage put you more at risk of?

A

HBV
HCV
HIV
Soft tissue infection
Endocarditis

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128
Q

What can a Hx of head injury put you more at risk of?

A

Meningitis
Sinusitis

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129
Q

What can alcoholism put you more at risk of?

A

TB
Pneumonia
HIV

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130
Q

What is an antibiotic?

A

Molecule that works by binding a target site on a bacteria
Points of a biochemical reaction crucial to survival of bacterium
Crucial binding site varies with antibiotic class

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131
Q

What classes of antibiotics interrupt cell wall synthesis?

A

Beta lactams
Vancomycin
Teicoplanin

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132
Q

Name the 4 types of beta-lactams

A

Penicillins
Cephalosporins
Carbapenems
Monobactams

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133
Q

Name 3 penicillins

A

Penicillin V
Flucloxacillin
Amoxicillin/ampicillin
Piperacillin

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134
Q

Name 3 cephalosporins

A

Cefalexin
Cefuroxime
Ceftriaxone
Ceftazidime

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135
Q

Name a carbapenem

A

Meropenem
Ertapenem
Imipenem

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136
Q

Name a monobactam

A

Aztreonam

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137
Q

How do beta-lactam antibiotics work?

A

Targets peptidoglycan in cell wall
Larger in gram positive bacteria so tends to be more effective in treating gram positive infections
Bind covalently and irreversibly to the penicillin binding proteins
Leads to hypo-osmotic or iso-osmotic environment
Only active against rapidly multiplying organisms
Poorly penetrate mammalian cells so ineffective in treatment of intracellular pathogens

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138
Q

What is targeted in nucleic acid synthesis?

A

DNA gyrase
RNA polymerase

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139
Q

Name the antibiotic class that targets DNA gyrade

A

Quinolones

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140
Q

Name a quinolone antibiotic

A

Ciprofloxacin
Levofloxacin
Moxifloxacin

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141
Q

Name an antibiotic that targets RNA polymerase

A

Rifampicin

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142
Q

Name another antibiotic that targets nucleic acid synthesis

A

Metronidazole

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143
Q

What can be targeted in protein synthesis?

A

50s subunit
30s subunit

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144
Q

Name the antibiotic class + 3 other antibiotics that target the 50s subunit

A

Macrolides
Clindamycin
Linezolid
Chloramphenicol
Streptogramins

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145
Q

Name a macrolide

A

Erythromycin
Clarithromycin
Azithromycin

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146
Q

Name the 2 antibiotic classes that target the 30s subunit and an example for each

A

Tetracyclines -> doxycycline
Aminoglycosides -> gentamicin

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147
Q

Name an antibiotic that targets folate synthesis

A

Sulphonamides -> sulphamethoxazole
Trimethoprim
Co-trimoxazole

148
Q

What are the direct consequences of bacterial infections?

A

Destroy phagocytes or cells in which bacteria replicate

149
Q

What are the indirect consequences of bacterial infections?

A

Inflammation - eg necrotic cells
Immune-pathology - eg antibody
Diarrhoea

150
Q

What are the toxin effects of bacterial infections?

A

Exotoxin - protein production
Endotoxin - gram negative

151
Q

What is bactericidal role of antibiotics?

A

Kills the bacteria > 99.9% in 18-24 hours
Antibiotics that inhibit cell wall synthesis
Useful if poor penetration, difficult to treat infections, or need to eradicate infections quickly eg meningitis

152
Q

What is bacteriostatic role of antibiotics?

A

Prevent growth of bacteria
Kill > 90% in 18-24 hours
Defined as ratio of minimum bacterial concentration to minimum inhibitor concentration of > 4
Antibiotics that inhibit protein synthesis, DNA replication, or metabolism
Reduces toxin production and endotoxin surge less likely

153
Q

What is the minimum inhibitory concentration?

A

Amount of Abx required to clear the infection (determined by turbidity in lab)
Required at the side of infection
Lowest MIC doesn’t mean best antibiotic

154
Q

What is also important along with MIC?

A

Time dependent killing
Concentration dependent killing

155
Q

What is time dependent killing?

A

Time that serum concentrations remain above the MIC during the dosing interval
t>MIC
- Beta-lactams
- Clindamycin
- Macrolides
- Oxazolidinones

156
Q

What is concentration dependent killing?

A

How high the concentration is above MIC
Peak concentration/MIC ratio
- Aminoglycosides
- Quinolones

157
Q

What happens to cause antibiotic resistance?

A

Change antibiotic target -> changes molecular configuration of binding site/masks it
Destroy antibiotic
Prevent antibiotic access
Remove antibiotic from bacteria

158
Q

What is intrinsic resistance?

A

All subpopulations of species equally resistant
eg aerobic bacteria unable to reduce metronidazole to active form

159
Q

What is required resistance and how can this occur?

A

Previously susceptible bacterium obtains ability to resist activity of particular antibiotic
Spontaneous
Horizontal gene transfer

160
Q

What happens in spontaneous resistance?

A

New nucleotide base pair change in amino acid sequence change to enzyme or cell structure reduced affinity or activity of antibiotic

161
Q

What happens in horizontal gene transfer?

A

Transduction -> from bacteriophages, transfer DNA
Transformation -> take up free DNA from environment and incorporate into chromosomes
Conjugation -> plasmid transferred from one bacteria to another

162
Q

What other signs may you get in encephalitis?

A

Confusion
Reduced GCS

163
Q

Why would you give steroids in meningitis? When might you stop them?

A

Improves disability outcomes in pneumococcal meningitis
Stop when proved not pneumococcal meningitis

164
Q

If a patient has a penicillin allergy what would you give for meningococcal septicaemia?

A

Depends on type of allergy
Rash/diarrhoea -> likely to be okay with 3rd gen cephalosporins
More severe -> chloramphenicol, meropenem

165
Q

What is the s/e of chloramphenicol?

A

Aplastic anaemia

166
Q

When would you not do an LP?

A

Rash -> bleeding risk as DIC, diagnosis often known if rash
Raised ICP
Shock
Coagulation abnormalities

167
Q

What are the signs of raised ICP?

A

Papilloedema
Reduced GCS and deteriorating
Seizures
Relative bradycardia and hypertension
Focal neurological signs
Abnormal posture/posturing

168
Q

What would the CSF look like for a viral cause of meningitis?

A

Clear, normal opening pressure
High WCC -> lymphocytes
Normal protein and glucose

169
Q

What would the CSF look like for a bacterial cause of meningitis?

A

Turbid, elevated opening pressure
High WCC -> neutrophils
High protein, low glucose

170
Q

Name 2 viruses that can cause meningitis

A

HSV
VSV

171
Q

What is the treatment for viral meningits/encephalitis?

A

Acyclovir for HSV and VSV

172
Q

Which of viral meningitis and viral encephalitis is often not treated?

A

Viral meningitis
Often resolves on its own but patient often feels unwell for months after resolved

173
Q

What is the prophylaxis for close contacts of meningitis cases? Which is better in pregnancy?

A

Ciprofloxacin or rifampicin
Rifampicin in pregnancy

174
Q

What does the CURB65 score stand for?

A

Confusion
Urea > 7mmol/L
RR > 30
BP systolic < 90 or diastolic < 60
Age > 65

175
Q

What extra pulmonary signs can legionella cause?

A

SiADH -> so low Na
Abnormal LFTs, RUQ pain
Diarrhoeal prodrome

176
Q

How can legionella be diagnosed?

A

Urinary legionella antigen test
Sputum culture/PCR

177
Q

What is the preferred treatment for legionella?

A

Ciprofloxacin

178
Q

What are the 4 bacteria that can cause bloody diarrhoea?

A

CESS
Campylobacter
E coli
Salmonella
Shigella

179
Q

What other causes of infective gastroenteritis would you consider if someone had been abroad?

A

Amoeba + parasites (3 stool samples required)

180
Q

Which bacteria can cause haemolytic uraemic syndrome?

A

E coli 0157H1

181
Q

What is haemolytic uraemic syndrome?

A

HUS
Triad of haemolytic anaemia, thrombocytopenia, and AKI

182
Q

When would you not give antibiotics in infective gastroenteritis?

A

HUS -> makes this worse
< 2 weeks diarrhoea and getting worse

183
Q

When would you have a lower threshold for treating infective gastroenteritis?

A

Immunocompromised
Old/frail
Shigella

184
Q

What is the antibiotic choice for infective gastroenteritis?

A

Ciprofloxacin
Campylobacter -> azithromycin/erythromycin

185
Q

What type of bacteria does ciprofloxacin cover?

A

Gram negative

186
Q

Should you give loperamide in suspected infective gastroenteritis cases?

A

No
Can make worse
Need at least 3 negative stool samples before prescribed

187
Q

What clinical features may someone with infective endocarditis have?

A

Anaemia -> of chronic disease if had for a while, or blood haemolysed around infection
Fever, night sweats, malaise, SOB
New/changed murmur
Thrills
Janeway lesions, splinter haemorrhages (hands)
Roth spots (eyes)
Creps -> HF
Septic emboli

188
Q

What is important when performing blood culture in suspected IE?

A

At least 3 from 3 different sites at least 30 mins apart
Bugs that can cause it can also be contaminants

189
Q

Why should you do a urine dip in a suspected IE case?

A

Haematuria
Very sensitive for IE

190
Q

What is the criteria used to support IE diagnosis?

A

Modified Duke’s

191
Q

Name 3 organisms that can cause IE

A

Staph epidermis
Strep viridans
Enterococci
GBS
Staph aureus (IVDU)
Fungal (immunocompromised)

192
Q

What is most likely to be the cause of IE in a patient who has recently been catheterised?

A

Enterococci
Often found in urine and may have been disturbed

193
Q

What type of bacteria is enterococci?

A

Gram negative

194
Q

What S&S might you get in an IVDU with IE?

A

R sided valves involved
Septic pulmonary emboli
No Hx of heart conditions
Needle tract marks
Staph aureus often causative

195
Q

What is the treatment for IE?

A

Ceftriaxone

196
Q

What is the treatment for IE in an IVDU?

A

Staph aureus -> flucloxacillin + gentamicin

197
Q

What if the treatment for IE in prosthetic valves?

A

Vancomycin + gentamicin +?rifampicin

198
Q

What length of treatment should someone with IE get?

A

4-6 weeks

199
Q

When should you get a surgical review in IE?

A

Prosthetic valves
HF develops
Uncontrolled
>1cm vegetations
New emboli whilst on treatment

200
Q

Name 3 complications of IE

A

HF
Stroke from emboli
Pericarditis
Aortic root abscess

201
Q

What are the S&S of aortic root emboli?

A

Fever
New or changing murmur
Valvular dehiscence
Weight loss
Poor appetite
Systemic embolisation
CHF features

202
Q

What is important to rule out in patients who have travelled abroad to tropical areas?

A

Malaria
Typhoid

203
Q

What is the significance of P falciparum?

A

Most severe malarial illness
Can deteriorate very quickly

204
Q

What does the parasitaemia % suggest?

A

Level of parasite in blood
Anything above 2 is worrying, more likely to develop complex malaria

205
Q

How is malaria treated orally?

A

Artemether with lumefantrine

206
Q

How is malaria treated IV?

A

Artesunate

207
Q

When should you treat malaria with IV drugs?

A

If cannot tolerate eg can’t eat/drink, vomiting
More severe complications eg cerebral malaria/haemolysis

208
Q

How does P falciparum cause severe malaria?

A

‘Sticky’ parasite
Causes clogging up of small blood vessels

209
Q

Name some cerebral complications of malaria

A

Coma/seizures
Cerebral oedema
Reduced GCS

210
Q

Name some pulmonary complications of malaria

A

ARDS
Oedema

211
Q

Name some haemolytic complications of malaria

A

Anaemia
Excreted through kidneys and causes blockages therefore AKI
DIC

212
Q

Name some other complications of malaria

A

Sepsis
Spontaneous bleeding/coagulopathy
Hypoglycaemia
Metabolic acidosis
Nephrotic syndrome
Jaundice
Splenic rupture

213
Q

Name 2 antimalarial drugs used for prophylaxis

A

Chloroquine
Proguanil
Atovaquone
Doxycycline

214
Q

Why is mefloquine no longer used as antimalarial prophylaxis/treatment?

A

Neuropsychiatric side effects

215
Q

Why are patients with diabetes more at risk of cellulitis?

A

Poor diabetic control compromises the immune system
Foot disease increases risk of infection

216
Q

What are the most common pathogens causing cellulitis?

A

Staph aureus
Strep pyogenes

217
Q

How can you tell the difference between a staph and strep infection?

A

Pustules/folliculitis -> staph
Spreading diffused inflammation -> strep

218
Q

How might you tell if a patient has an anaerobic infection?

A

Foul smelling discharge

219
Q

What types bugs are diabetics more at risk of?

A

Gram negative

220
Q

Why do you keep a patients leg elevated with cellulitis?

A

Helps reduce oedema/pain

221
Q

How might septic arthritis present?

A

Active and passive movement of joint reduced
Pain and swelling around joint

222
Q

How might necrotising faciitis present?

A

Creptius when touch the tissue
Rapid onset
Very unwell
Pain out of proportion to normal cellulitis/what can be seen

223
Q

What is a normal CD4 count?

A

> 500

224
Q

What CD4 count characterises AIDS?

A

< 200

225
Q

What infections are patients with HIV more at risk of with a CD4 count > 500?

A

Post-primary TB

226
Q

What infections/neoplasms are patients with HIV more at risk of with a CD4 count 200-500?

A

Bacterial
Primary TB
B-cell
Non-Hodgkin’s lymphoma
Primary CNS lymphoma
Kaposi’s carcoma
Hodgkin’s

227
Q

What infections are patients with HIV more at risk of with a CD4 count < 200?

A

Cryptococcus/other fungal
C,V
Pneumocystis Carinii

228
Q

What infections are patients with HIV more at risk of with a CD4 count < 50-100?

A

Mycobacterium avium-intracellulare complex

229
Q

What investigations can be done for PCP?

A

Sputum culture -> sputum induction then broncheoalveolar lavage if needed
Cultures
Beta-D glucan -> marker in blood for diagnosis and monitoring

230
Q

What is the treatment for PCP?

A

Co-trimoxazole + prednisolone for 5 days

231
Q

What prophylaxis is used to prevent infection in HIV patients?

A

Depends on CD4 count
When count < 200 PCP + toxoplasma -> co-trimoxazole PO
When count < 50 cover for mycobacterium

232
Q

What is the main type of infective cause of jaundice?

A

Hepatitis C
Also CMV, EBV, any infection causing haemolysis

233
Q

What is the typical history of a hep B infection?

A

Immune tolerance -> immune clearance (immunity)
If no immune clearance = chronic
Chronic = immune control -> causes sx when immune escape

234
Q

How do you tell if a hep B infection has become chronic?

A

After diagnosis of acute infection, check core antigen/surface antigen to determine whether still infected

235
Q

What public health things need to happen when someone is diagnosed with hep B?

A

Contact tracing
Vaccination of close contacts -> immune/current infection check before vaccination
Monitor for vertical transmission in chronic to children if female

236
Q

What does a gram film differentiate between?

A

Gram +ve and gram -ve bacteria

237
Q

What colour are gram +ve bacteria on gram film?

A

Purple

238
Q

What colour are gram -ve bacteria on gram film?

A

PiNk

239
Q

What are the 2 types of gram +ve cocci?

A

Streptococci and staphylococci

240
Q

How can you tell the difference between strep and staph?

A

Strep = chains (strip)
Staph = clusters

241
Q

How can different types of strep be differentiated?

A

Blood agar for haemolysis

242
Q

What are the 3 different types of haemolysis?

A

Beta
Alpha
Gamma

243
Q

What strep are beta haemolytic?

A

Beta haemolytic strep
Antigenic group -> A, B, C, G

244
Q

What strep are alpha haemolytic?

A

Viridans strep
S pneumoniae

245
Q

How can you differentiate between alpha haemolytic streps?

A

Optochin test
- Viridans strep = resistant
- S pneumoniae = sensitive

246
Q

What strep is gamma haemolytic?

A

Enterococci

247
Q

How can you tell the different between different types of staph?

A

Coagulase/DNAse test

248
Q

What type of staph is +ve on the coagulase/DNAse test?

A

S aureus

249
Q

What type of staphs are -ve on the coagulase/DNAse test?

A

Coagulase -ve staph

250
Q

How can you tell the difference between Group A strep and Group B strep?

A

Bactracin test
Group A strep = bactracin sensitive
GBS = bactracin resistant

251
Q

Name a group A strep

A

S pyogenes

252
Q

Name a GBS

A

S agalaticae

253
Q

What are the 2 different types of gram +ve bacilli?

A

Aerobic (non-spore forming)
Anaerobic (spore forming)

254
Q

Name an aerobic gram +ve bacilli

A

Listeria
Corneybacterium

255
Q

Name an anaerobic gram -ve bacilli

A

Clostridium

256
Q

What are the 4 different shapes of gram -ve bacteria?

A

Diplococci
Comma-shaped
Bacilli
Coccobacilli

257
Q

Are gram -ve diplococci aerobic/anaerobic?

A

Aerobic

258
Q

How do you tell the difference between gram -ve diplococci?

A

Maltose utilisation
No -> N gonorrhoea, Moxarella
Yes -> N meningitidis

259
Q

How can you tell the difference between the 2 different bacilli (comma-shaped and bacilli) apart from shape?

A

Comma-shaped -> all are oxidase +ve

260
Q

How can you tell the difference between comma-shaped gram -ve bacteria?

A

Type of media it grows in/product/temperature it grows in
Grows in 42 -> C jejuni
Grows in alkaline media -> V cholerae
Urease producing -> H pylori

261
Q

Name 2 coccobacilli

A

H influenzae
B pertussis
Pasteurella
Brucella
F tularensis

262
Q

How can you differentiate between different types of gram -ve bacilli?

A

Lactose fermentation

263
Q

How do you tell the difference between different types of lactose fermenting gram -ve bacilli?

A

Speed at which lactose is fermented
Slow vs fast

264
Q

Name a slow lactose fermenting gram -ve bacillus

A

Citrobacter
Serratia

265
Q

Name a fast lactose fermenting gram -vs bacillus

A

E coli
Klebsiella
Enterobacter

266
Q

How can you tell the difference between non-lactose fermenting bacilli?

A

Oxidase test

267
Q

Name an oxidase +ve gram -ve bacilli

A

Pseudomonas

268
Q

How do you tell the difference between oxidase -ve gram -ve bacilli?

A

H2S production

269
Q

Name a non-H2S producing oxidase -ve gram -ve bacilli

A

Shigella
Yersinia

270
Q

Name a H2S producing oxidase -ve gram -ve bacilli

A

Salmonella
Proteus

271
Q

What valves are most commonly involved in IE?

A

Left side - mitral/aortic

272
Q

What valves are most commonly affected in IE in IVDU?

A

Right side - tricuspid/pulmonary

273
Q

How common is prosthetic valve endocarditis?

A

20% cases

274
Q

What is the difference between early/late prosthetic valve endocarditis?

A

Early -> occurs with 12/12 of surgery, contamination intraoperatively (S aureus)
Late -> more than 12 months post-op, CAI

275
Q

What 3 key factors are involved in IE?

A
  1. Transient bacteraemia
  2. Damage to valvular tissue
  3. Vegetations
276
Q

What are the vegetations in IE made of?

A

Platelet-fibrin matrix

277
Q

Why is IE difficult to treat?

A

Poor vasculature in endocardium so difficult for Abx to penetrate

278
Q

What complications can vegetations lead to?

A

Septic emboli
L sided -> strokes/cerebral abscesses
R sided -> mycotic aneurysms, PE, pulmonary abscesses

279
Q

What is the most common causative organism in IE?

A

S aureus

280
Q

What gram +ve bacteria can cause IE?

A

S aureus
Strep viridans -> dental work
Enterococci

281
Q

What gram -ve bacteria can cause IE?

A

HACEK organisms
- Haemophilus spp
- Aggregatibacter actinomycetemcomitans
- Cardiobacterium spp
- Eikenella corrodens
- Kingella kingae
Pseudomonas
N elongata

282
Q

What fungi can cause IE?

A

Candida
Aspergeillus

283
Q

What causes culture -ve endocarditis?

A

31% all cases
1. Abx started before blood cultures
2. Fastidious organisms eg HACEK

284
Q

What are the RF for IE?

A

Intrinsic
- Valve problems
- Hypertrophic cardiomyopathy
- Structural heart disease with turbulent flow VSD/PDA
- Prosthetic heart valves
- Previous infection including rheumatic fever
Extrinsic
- IVDU
- Invasive vascular procedure
- Poor dental hygiene/dental infections

285
Q

What are the S&S of IE?

A

Fever, rigors, malaise, night sweats, weight loss
Anaemia - fatigue, SOB
Tachycardia
New/changing heart murmur
Splinter haemorrhages, Osler nodes, Janeway lesions (hands)
Roth spots (eyes)
Clubbing (late sign)
Mild splenomegaly
Bi-basal lung creps (HF)
Clinical features of emboli eg Sx of stroke

286
Q

Name 4 DDx of IE

A

Autoimmune
- SLE -> non-infective endocarditis
- Antiphospholipid syndrome -> thromboemboli, cardiac valve disease
- Vasculitis
- PMR -> myalgia, raised CRP
- Reactive arthritis
Infection
- Lyme disease
- Meningitis
- TB
Neoplastic
- Atrial myxoma -> fever, new murmur

287
Q

What investigations should you do in IE?

A

Vital signs, ECG, urine dip
Blood cultures -> 3 sets, at least 30 mins apart from 3 different sites
FBC, CRP, U&E
TTE (+ TTO, CXR, CT chest)

288
Q

What is the diagnostic criteria for IE?

A

Duke’s criteria

289
Q

What is the management of IE?

A

IV abx 2/52 then oral
Treatment for at least 6/52 in prosthetic valve
Treatment for at least 2-6/52 in native valve

290
Q

What are the indications for surgery in IE?

A

If prosthetic valve involved -> urgent surgical review
1. HF (severe valve disease, pulmonary oedema, cardiogenic shock)
2. Uncontrolled infection
3. Prevention of embolism (large vegetations)

291
Q

Name 3 local complications of IE

A

Valve destruction
HF (secondary to regurg)
Arrhythmias and conduction disorder
MI
Pericarditis
Aortic root abscess

292
Q

Name 2 systemic complications of IE

A

Emboli
Immune complex deposition eg glomerulonephritis
Septicaemia
Death (mortality 30-40%)

293
Q

What are pacemakers made of?

A

Generator -> sub-dermal in sub-clavian area (generally L side)
Leads -> cephalic/subclavian vein

294
Q

What is a demand pacemaker?

A

Paces on demand, paces/inhibits, inhibits if beat noticed

295
Q

How many leads can a pacemaker have?

A

1/2/3

296
Q

Where does the lead go in a single lead pacemaker?

A

R ventricle

297
Q

Where do the leads go in a dual lead pacemaker?

A

R atrial/ventricular
Paces both

298
Q

When might you use a single lead pacemaker?

A

Permanent AF

299
Q

When might a single lead pacemaker have the lead in the RA rather than the RV?

A

SAN disease in young people eg sick sinus syndrome with good AV node

300
Q

When might you use a dual lead pacemaker?

A

All other scenarios

301
Q

What is it called when you have a 3 lead pacemaker?

A

Cardiac resynchronisation therapy

302
Q

What is cardiac resynchronisation therapy used in and how does it work?

A

HF
Often not synchronised contraction of ventricles in HF which can worsen cardiac function
3rd lead -> coronary sinus to pace L ventricle
RV and LV pump at same time which also improved CO

303
Q

What is the definition of pacemaker dependent?

A

Absence of intrinsic rhythm 30 beats/min during back-up pacing after switching off pacemaker

304
Q

What are the 2 types of BBB?

A

Left and right BBB

305
Q

What does R BBB look like on an ECG?

A

QRS > 120ms
RSR’ pattern in V1-V3
Wide, slurred S wave in lateral leads - I, aVL, V5-6
MaRRoW M = V1, W = V6

306
Q

What is R BBB and what can cause it?

A

No depolarisation through R bundle of His
Physiological/pathological

307
Q

What does L BBB look like on ECG?

A

QRS > 120ms
Dominant S wave V1
Broad, monophasic R wave lateral leads - I, aVL, V5-6
Absent Q wave in lateral leads
R wave > 60ms V5-6
WiLLiaM W = V1, M = V6

308
Q

What is L BBB and what causes it?

A

No depolarisation through L bundle of His, always pathological

309
Q

What is Wolff-Parkinson White syndrome?

A

Accessory pathway causing ventricular stimulation -> bypasses AVN
Most cases sporadic
Associated with congenital heart disease eg Ebstein’s anomaly + autosomal dominant PRKAG2 mutation

310
Q

Who does WPW syndrome often affect?

A

Males 30-40

311
Q

What does WPW look like on ECG?

A

Tachyarrhythmia -> short PR < 120ms
Delta wave -> slurred upstroke QRS
Widened QRS > 110ms

312
Q

How can you tell the difference between type A and type B WPW?

A

Type A = L sided -> delta wave I, II, III, aVL, aVR, aVF, R>S in V1
Type B = R sided, -ve delta wave I, II

313
Q

What is sick sinus syndrome?

A

Tachy-brady syndrome
Sinus bradycardia + arrest
+ SAN exit block
+ AF with slow ventricular response
Often need ambulatory monitoring as intermittent
Match up periods of symptoms with ECG

314
Q

What are the RF for sick sinus syndrome?

A

Advancing age
Cardiac disease
Electrolyte derangement
Thyroid disease
Medication

315
Q

What is 1st degree heart block?

A

Consistent prolonged PR > 0.02s
Every P wave followed by QRS
Regular rhythm, QRS normal
Often asymptomatic

316
Q

What is 2nd degree heart block, Mobitz T1?

A

Wenckebach phenomenon
Irregular rhythm,
P waves present, not all followed by QRS
PR progressively lengthens then QRS dropped
QRS otherwise normal

317
Q

What is 2nd degree heart block, Mobitz T2?

A

Rhythm irregular
More P waves than QRS
PR interval normal with occasional dropped QRS
QRS normal/broad

318
Q

What is 3rd degree heart block?

A

Complete
Variable rhythm
P wave not associated with QRS
PR interval absent
QRS narrow/broad

319
Q

What is the first line treatment for treating animal bites and why?

A

Co-amoxiclav
Gram +ve and gram -ve cover
2nd line/pen allergic - doxycycline

320
Q

What are the 5 antibiotics that can cause C diff infections?

A

5 C’s
1. Clindamycin
2. Clarithromycin
3. Cephalosporins
4. Co-amoxiclav
5. Ciprofloxacin

321
Q

How can you remember which antibiotics are bacteriocidal?

A

BANG Q R.I.P
- Beta-lactams
- Aminoglycosides
- Nitromidazoles (metro)
- Glycopeptides (vanc)
- Quinolones
- Rifampicin
- Polymyxins

322
Q

How can you remember which antibiotics are bacteriostatic?

A

MS COLT
- Macrolides (erythromycin)
- Sulfonamides
- Chloramphenicol
- Oxazolidinones
- Lincosamides (clindamycin)
- Tetracyclines

323
Q

What is the difference between bacteriocidal and bacteriostatic antibiotics?

A

Bacteriocidal - irreversible, inhibits, cell wall formation, MBC = conc required to kill 99.9% of bacterial population
Bacteriostatic - reversible, inhibits DNA replication + protein synthesis, works with the immune system, MIC

324
Q

What is the innate immune response?

A

First line
Macrophages ,phagocytosis, neutrophils, dendritic cells, natural killer cells, complement and natural antibodies
Hours

325
Q

What is the adaptive immune response?

A

T lymphocytes - helper and cytotoxic
B lymphocytes + antibodies
Cytokines
Days

326
Q

How might a primary immunodeficiency condition present?

A

Infection
Autoimmune disorders
Auto-inflammatory disorders
Malignancy

327
Q

Name an infection that can cause secondary immunodeficiency

A

Viral (HIV, herpes groups)
Bacterial, mycobacterial
Parasitic

328
Q

Name 3 causes of secondary immunodeficiency

A

Infections
Malignancy
DM, CKD, liver cirrhosis, malnutrition
Autoimmune diseases
Relative - pregnancy, stress, ageing
Splenectomy
Immunosuppressive therapy

329
Q

What are the main barriers to disease-free survival after a solid organ transplant?

A

Infection
Malignancy

330
Q

What infections might people with solid organ transplants get?

A

Nosocominal infections
Reactivation of infections
Donor-derived infections
Community aquired infections
Type of infection depends on time since transplant

331
Q

What infections may be present in SOT recipients < 4 weeks post-transplant and why?

A

Effects of immunosuppressive not evident yet
Surgical complications -> SSI, ischaemic graft, haematomas, urinomas, pleural effusions, bile leak
Line related infection
Hospital acquired pathogens
Organisms -> bacteria (intra-abdominal, pulmonary), candida (liver, intestinal transplant), HSV reactivation
Donor derived
Prophylaxis - broad spectrum IV antibiotics, fluconazole, acyclovir

332
Q

What infections may be present in SOT recipients1-6 months post-transplant and why?

A

Period of maximal immunosuppression to avoid rejection therefore greatest risk of development of infection
CMV (most common concern)
HSV, HHV-6
HBV, HVC if untreated
BK virus in kidney transplant
Respiratory viruses - adenovirus, RSV, metapneumovirus, influenza, parainfluenza
GI - norovirus, CMV, cryptosporidium, microsporidium
Strongyloides
TB
Cryptococcus

333
Q

What prophylaxis can be given to patients with1-6 months post SOT?

A

Septrin
Valganciclovir
Aspergillus specific

334
Q

What infections may be present in SOT recipients >6-12 months post-transplant and why?

A

Stable so reducing immunosuppression unless rejection
Late CMV (after stopping prophylaxis)
Community acquired infection
PTLD
JC virus, PML
Listeria, nocardia (not if on septrin)

335
Q

What are the 3 sources of stem cells for transplants?

A

Autologous - patients own cells
Syngeneic - identical twin
Allogenic - sibling, a related, or unrelated donor

336
Q

What are the 3 steps of stem cell transplants?

A

Induction chemotherapy - for acute leukaemia
Condition chemotherapy - high dose chemo +/- TBI
Transplant - administration of stem cells

337
Q

What is the the risk of infection in stem cell transplants?

A

Prolonged and severe neutropenia
Immunosuppressive regimen, T cell depletion
Severe acute and extensive chronic graft vs host disease and its therapy

338
Q

What is pre-engraftment?

A

From treatment to neutrophil recovery
Approx day 20 - 30

339
Q

What are the main infection risks during the pre-engraftment period?

A

HSV
Respiratory viruses
Gram +ve and -ve organisms
Candida

340
Q

When is early post-engraftment?

A

From engraftment to day 100

341
Q

What are the main infection risks during the post-engraftment period?

A

Respiratory viruses
CMV
VZV
Gram +ve and -ve organisms
Pneumocystis jirovecci

342
Q

When is last post-engraftment?

A

From day 100

343
Q

What is neutropenic fever?

A

Dose-dependent effect of cytotoxic chemotherapy or immunosuppressive agents

344
Q

What is the definition of neutropaenia?

A

ANC < 1

345
Q

How does the risk of neutropaenic sepsis change?

A

Rises as neutrophil count falls
Higher in those with prolonged duration of neutropenia > 7 days, liver or kidney failure

346
Q

What are the most common infectious causes of neutropaenic fever?

A

Bacteria

347
Q

What are the common sites of infection in neutropaemic fever?

A

IV lines
Oral cavity
Sinuses
Lungs
Skin
Perineal region
Urinary tract

348
Q

What is the treatment for neutropaenic sepsis?

A

Tazocin + gent
If penicillin allergy teic + PO cipro

349
Q

What are the two biologics?

A

Monoclonal antibodies
Small molecule targeted therapies

350
Q

What is the role of biologics?

A

Selectively targets cells and pathways, carry a theoretical advantage over traditional methods of immunosuppression
Indications for biologic therapy broadened
Infections increasingly recognised as a complication

351
Q

How can you identify monoclonal antibodies?

A

Mabs

352
Q

What do monoclonal antibodies target?

A

Cytokines - IL and TNF alpha
Lymphocytes - T, B cells, or both

353
Q

What are TNF alpha monoclonal antibodies used for?

A

Inflammatory arthritis
IBD

354
Q

Name a TNF alpha monoclonal antibody

A

Infliximab
Adalimumab
Etanercept
Golimumab
Certolizumab

355
Q

What infectious are TNF alpha monoclonal antibodies associated with?

A

TB ++++
Common bacterial infections
Invasive fungal infection
Reactivation of HBV
HSV

356
Q

How can you prevent infection with biologic treatment?

A

Interferon gamma release assay + CXR
BBV screen
VZV serology
Vaccines -> flu, pneumococcal, HBV, VZV, HPV

357
Q

Name an IL-1 monoclonal antibody

A

Anakinra

358
Q

Name an IL-2 monoclonal antibody

A

Basiliximab

359
Q

Name an IL-5 monoclonal antibody

A

Mepolizumab
Reslizumab

360
Q

Name an IgE monoclonal antibody

A

Omalizumab

361
Q

Name a CD20 monoclonal antibody

A

Rituximab
Ocrelizumab
Omalizymab

362
Q

What are small molecule targeted therapies?

A

Chemically synthesised
Smaller and simpler models
Good oral availability
Short half-lives

363
Q

Name a small molecule targeted therapy

A

Ibrutinib
Acalaburtinib

364
Q

How can you recognise small molecule targeted therapies?

A

‘Ib’

365
Q

What is worse - steroids or biologics - in terms of infection risk?

A

Steroids
Steroid + biologic = highest risk

366
Q

What are the highest infections risks with rituximab treatment?

A

HBV reactivation
Moderate risk of serious bacterial infections

367
Q

What precautions are recommended for patients having rituximab treatment?

A

Screening for HBsAg and anti-HBc antibody
Pneumococcal + VZV vaccines
Tenofovir or entecavir treatment for HBV or monitoring

Phase 3b (6 decks)

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