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Infection and immunity Flashcards

1
Q

What is an Abscess?

A
  1. A collection of pus that has built up within the tissue of the body
  2. Can develop anywhere in the body
    Most commonly in the skin or inside the body, in an organ or in the spaces between organs
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2
Q

What is the aetiology of Abscesses?

A
  1. Caused by bacterial infection, parasites, or foreign substances, e.g. aspiration pneumonia
  2. Bacterial infection is the most common cause, most common causative pathogen is methicillin-resistant Staphylococcus aureus (MRSA)
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3
Q

What are the presenting symptoms of an Abscess?

A
  1. Skin abscess:
    a. Swollen, pus-filled lump under the surface of the skin
    b. Symptoms of an infection, such as fever and chills
  2. Internal abscess:
    a. Pain in the affected area
    b. Fever
    c. Malaise
    d. Loss of appetite and weight loss
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4
Q

What are the signs of an Abscess on physical examination?

A
  1. Skin abscess:
    a. Smooth swelling under skin
    b. Pain and tenderness
    c. Warmth and erythema
    d. White or yellow pus under the skin
  2. Internal abscess:
    a. Fever
    b. Pain or swelling in the affected area
    c. Dependent on the affected area e.g. lung: cough, dyspnoea, liver: jaundice
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5
Q

What are the appropriate investigations for Abscess?

A
  1. Bloods:
    a. FBC: leukocytosis
    b. CRP/ESR: inflammatory markers
  2. Blood culture: positive for organism
  3. CT/Ultrasound: visualisation of abscess
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6
Q

What is the management for an Abscess?

A

a. If severe intravenous antibiotics
b. Usually consider percutaneous incision and drainage
c. In very rare cases surgical resection/ debridement

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7
Q

What is Behçet’s disease?

A

A complex multisystem disorder associated with presumed autoimmune-mediated inflammation of the arteries and veins

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8
Q

What is the triad seen in Behçet’s disease?

A
  1. Oral ulcers
  2. Genital ulcers
  3. Anterior uveitis
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9
Q

What is the epidemiology of Behçet’s disease?

A
  1. More common in the eastern Mediterranean (e.g. Turkey)
  2. More common in men
  3. Tends to affect young adults (e.g. 20 - 40 years old)
  4. Associated with HLA B51
  5. Around 30% of patients have a positive family history
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10
Q

What are the features of Behçet’s disease?

A
  1. Classically: a) oral ulcers b) genital ulcers c) anterior uveitis
  2. Thrombophlebitis and deep vein thrombosis
  3. Arthritis
  4. Neurological involvement (e.g. aseptic meningitis)
  5. GI: abdo pain, diarrhoea, colitis
  6. Erythema nodosum
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11
Q

What are the investigations for Behçet’s disease?

A
  1. No definitive test
  2. Diagnosis based on clinical findings
  3. Positive pathergy test is suggestive (puncture site following needle prick becomes inflamed with small pustule forming)
  4. Routine bloods, raised inflammatory markers
  5. Imaging to determine organ involvement e.g. angiography
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12
Q

What is the management of Behçet’s disease?

A

Immunosuppression: corticosteroids

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13
Q

What is bursitis?

A

When the fluid-filled sacs (bursa) that cushion the joints become inflamed

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14
Q

What are some examples of bursitis?

A
  1. Greater trochanteric pain syndrome (trochanteric bursitis)
  2. Knees:
    a. Infrapatellar bursitis (Clergyman’s knee): Associated with kneeling
    b. Prepatellar bursitis (Housemaid’s knee): Associated with more upright kneeling
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15
Q

What are the features of bursitis?

A
  1. Pain: usually a dull, achy pain
    tender or warmer than surrounding skin
  2. Swollen
  3. More painful when on movement or pressed on
  4. May also be erythema
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16
Q

What is the conservative management for bursitis?

A
  1. Rest: avoid activities that put pressure on the joint
  2. Use ice: 10 minutes at a time
  3. Analgesia
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17
Q

What are the investigations for bursitis?

A
  1. Usually clinical
  2. If suspecting a hot swollen joint:
    a. Bloods: inflammatory markers
    b. Aspiration for microscopy (gout) and culture (septic arthritis)
    c. Refer to secondary care?
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18
Q

What is the medical management of bursitis?

A
  1. Antibiotics: usually taken for 7 days if caused by an infection
  2. Steroid injection: to reduce swelling
  3. Rarely may need to be drained
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19
Q

What advice can be given to patients to prevent bursitis?

A
  1. Maintain a healthy weight
  2. Warm up properly before exercising
  3. Use padding when putting a lot of pressure on joints e.g. kneeling
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20
Q

What is Greater trochanteric bursitis?

A
  1. Due to repeated movement of the fibroelastic iliotibial band
  2. Most common in women aged 50-70 years
  3. Features:
    a. Pain over the lateral side of hip/thigh
    b. Tenderness on palpation of the greater trochanter
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21
Q

What is cytomegalovirus?

A
  1. One of the herpes viruses
  2. Thought that around 50% of people have been exposed to the CMV virus although it only usually causes disease in the immunocompromised, e.g. people with HIV or those on immunosuppressants following organ transplantation
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22
Q

What is the pathophysiology of CMV?

A

Infected cells have a ‘Owl’s eye’ appearance due to intranuclear inclusion bodies

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23
Q

What are the different types of CMV infection?

A
  1. Congenital
  2. Mononucleosis
  3. Retinitis
  4. Encephalopathy
  5. Pneumonitis
  6. Colitis
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24
Q

What are the features of congenital CMV infection?

A
  1. Growth retardation
  2. Pinpoint petechial ‘blueberry muffin’ skin lesions
  3. Microcephaly
  4. Sensorineural deafness
  5. Encephalitis (seizures)
  6. Hepatosplenomegaly
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25
Q

What is CMV mononucleosis?

A
  1. Infectious mononucelosis-like illness
  2. May develop in immunocompetent individuals
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26
Q

What is CMV retintis?

A
  1. Common in HIV patients with a low CD4 count (< 50)
  2. Presents with visual impairment e.g. ‘blurred vision’.
  3. Fundoscopy shows retinal haemorrhages and necrosis, often called ‘pizza’ retina
  4. IV ganciclovir is the treatment of choice
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27
Q

What is the most common treatment for CMV?

A

IV ganciclovir

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28
Q

What is Human immunodeficiency virus (HIV)?

A
  1. Caused by a retrovirus that infects and replicates in human lymphocytes and macrophage
  2. Erodes the integrity of the human immune system over a number of years
  3. This results in immune deficiency and a susceptibility to a series of opportunistic and other infections as well as the development of certain malignancies
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29
Q

What is the aetiology of Human immunodeficiency virus (HIV)?

A
  1. HIV is retrovirus that infects and replicates primarily in human CD4+ T cells and macrophages
  2. It can be transmitted via blood, blood products, sexual fluids, other fluids containing blood, and breast milk
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30
Q

How is HIV transmitted?

A
  1. Sexual contact (most common)
  2. Before birth or during delivery
  3. During breastfeeding
  4. When sharing contaminated needles and syringes (intravenous drug users)
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31
Q

What is the epidemiology of Human immunodeficiency virus (HIV)?

A

Globally, the HIV incidence rate is believed to have peaked in the late 1990s and to have stabilised subsequently

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32
Q

What are the three phases of Human immunodeficiency virus (HIV)?

A
  1. Seroconversion: (4–8 weeks post-infection)
  2. Early/asymptomatic: (18 months to 15 +years)
  3. AIDS: Syndrome of secondary diseases reflecting severe immuno deficiency or direct effect
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33
Q

What is HIV seroconversion?

A
  1. Typically occurs 3-12 weeks after infection
  2. Presents as a glandular fever type illness
  3. Symptomatic in 60-80% of patients
  4. Increased symptomatic severity is associated with poorer long term prognosis
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34
Q

What are the features of HIV seroconversion?

A
  1. Sore throat
  2. Lymphadenopathy
  3. Malaise, myalgia, arthralgia
    diarrhoea
  4. Maculopapular rash
  5. Mouth ulcers
  6. Rarely meningoencephalitis
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35
Q

What is involved in HIV testing?

A
  1. After discussion and consent)
  2. Serum HIV enzyme linked immunosorbent assay: positive/Serum HIV rapid test
  3. HIV antibodies (usually positive by 12 weeks after exposure)
  4. p24 antigen: viral core protein
  5. PCR for viral RNA or incorporated proviral DNA
  6. Monitor CD4+ count and viral load
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36
Q

What is the standard HIV test?

A

Combination tests (HIV p24 antigen and HIV antibody):
1. For both diagnosis and screening of HIV
2. If the combined test is positive it should be repeated to confirm the diagnosis
3. Some centres may also test the viral load (HIV RNA levels) at the same time

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37
Q

What is the HIV testing protocol for asymptomatic patients?

A
  1. Should be done at 4 weeks after possible exposure
  2. After an initial negative result when testing for HIV in an asymptomatic patient, offer a repeat test at 12 weeks
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38
Q

What are the early symptoms of HIV?

A
  1. Can be asymptomatic for years
  2. Apparently well
  3. Some patients may have persistent lymphadenopathy (>1 cm nodes, at 2 + extrainguinal sites for >3 months)
  4. Progressive minor symptoms, e.g. rash, oral thrush, weight loss, malaise
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39
Q

What is the third stage of HIV and how does this present?

A
  1. AIDS: acquired immune deficiency syndrome
  2. Presents as symptoms of opportunistic infections (linked to CD4 count)
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40
Q

What are the opportunistic infections in a patient with HIV and a CD4 count of 200-500 cells/mm3?

A
  1. Oral thrush: Secondary to Candida albicans
  2. Shingles: Secondary to herpes zoster
  3. Hairy leukoplakia: Secondary to EBV
  4. Kaposi sarcoma: Secondary to HHV-8
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41
Q

What is Kaposi sarcoma?

A
  1. Caused by HHV-8 (human herpes virus 8)
  2. Presents as purple papules or plaques on the skin or mucosa (e.g. gastrointestinal and respiratory tract)
  3. Skin lesions may later ulcerate
  4. Respiratory involvement may cause massive haemoptysis and pleural effusion
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42
Q

What is the management of Kaposi sarcoma?

A

Radiotherapy and resection

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43
Q

What are the opportunistic infections in a patient with HIV and a CD4 count of 100-200 cells/mm3?

A
  1. Cryptosporidiosis: The disease is usually self-limiting and similar to that in immunocompetent hosts
  2. Cerebral toxoplasmosis
  3. Progressive multifocal leukoencephalopathy: Secondary to the JC virus
  4. Pneumocystis jirovecii pneumonia
  5. HIV dementia
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44
Q

What is Pneumocystis jiroveci pnuemonia?

A
  1. A unicellular eukaryote, generally classified as a fungus but some authorities consider it a protozoa
  2. PCP is the most common opportunistic infection in AIDS
    all patients with a CD4 count < 200/mm³ should receive PCP prophylaxis
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45
Q

What are the features of Pneumocystis jiroveci pnuemonia?

A
  1. Dyspnoea
  2. Dry cough
  3. Fever
  4. Very few chest signs
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46
Q

What is a common complication of Pneumocystis jiroveci pnuemonia?

A

Pneumothorax

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47
Q

What are the extra-pulmonary features of Pneumocystis jiroveci pnuemonia?

A
  1. Rare (1-2%)
  2. Hepatosplenomegaly
  3. Lymphadenopathy
  4. Choroid lesions
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48
Q

What are the investigations for Pneumocystis jiroveci pnuemonia?

A
  1. CXR:
    a. Typically shows bilateral interstitial pulmonary infiltrates
    b. Can present with other x-ray findings e.g. lobar consolidation
    c. May be normal
  2. Exercise-induced desaturation
  3. Bronchoalveolar lavage (BAL) often needed to demonstrate PCP (silver stain shows characteristic cysts)
    a. Sputum often fails to show PCP
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49
Q

What is the management of Pneumocystis jiroveci pnuemonia?

A
  1. Co-trimoxazole
  2. IV pentamidine in severe cases
  3. Steroids if hypoxic (if pO2 < 9.3kPa then steroids reduce risk of respiratory failure by 50% and death by a third)
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50
Q

What are the opportunistic infections in a patient with HIV and a CD4 count of 50-100 cells/mm3?

A
  1. Aspergillosis: Secondary to Aspergillus fumigatus
  2. Oesophageal candidiasis: Secondary to Candida albicans
  3. Cryptococcal meningitis
  4. Primary CNS lymphoma: Secondary to EBV
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51
Q

What is oesophageal candidiasis in HIV patients?

A
  1. The most common cause of oesophagitis in patients with HIV
  2. It is generally seen in patients with a CD4 count of less than 100
  3. Typical symptoms include dysphagia and odynophagia
  4. Fluconazole and itraconazole are first-line treatments
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52
Q

What are the opportunistic infections in a patient with HIV and a CD4 count of 50-100 cells/mm3?

A
  1. Cytomegalovirus retinitis: Affects around 30-40% of patients with CD4 < 50 cells/mm³
  2. Mycobacterium avium-intracellulare infection
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53
Q

What are the neurocomplications of HIV?

A
  1. Toxoplasmosis (50%)
  2. Primary CNS lymphoma (30%)
  3. TB
  4. Others:
    a. Encephalitis
    b. Cryptococcus
    c. Progressive multifocal leukoencephalopathy
    d. AIDS dementia complex
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54
Q

What is Toxoplasmosis in HIV patients?

A
  1. Opportunistic infection when CD4 count is between 100-200 cells/mm3
  2. Accounts for 50% of cerebral lesions in HIV patients
  3. Features: constitutional symptoms, headache, confusion, drowsiness
  4. On CT: usually single or multiple ring enhancing lesions, mass effect may be seen
  5. Management: sulfadiazine and pyrimethamine
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55
Q

What is primary CNS lymphoma in HIV patients?

A
  1. Secondary to EBV when CD4 count is between 50-100 cells/mm3
  2. Accounts for 30% of cerebral lesions in HIV patients
  3. CT: single or multiple homogenous enhancing lesions
  4. Treatment:
    a. Steroids (may significantly reduce tumour size), chemotherapy (e.g. methotrexate) + with or without whole brain irradiation
    b. Surgical may be considered for lower grade tumours
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56
Q

What are the differences in toxoplasmosis and primary CNS lymphoma in HIV patients?

A
  1. Toxoplasmosis:
    a. Multiple lesions
    b. Ring or nodular enhancement
    c. Thallium SPECT negative
  2. Primary CNS lymphoma:
    a. Single lesion
    b. Solid (homogenous) enhancement
    c. Thallium SPECT positive
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57
Q

How does TB present on CT in patients with HIV?

A
  1. Much lesson common than toxoplasmosis and lymphoma
  2. Single enhancing lesion
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58
Q

What is the most common fungal infection of the CNS (particularly in HIV)?

A

Cryptococcus:
1. Headache, fever, malaise, nausea/vomiting, seizures, focal neurological deficit
2. CSF:
a. high opening pressure
b. elevated protein
c. reduced glucose
d. normally a lymphocyte predominance but in HIV white cell count many be normal
e. India ink test positive
3. CT:
a. meningeal enhancement
b. cerebral oedema
c. meningitis is typical presentation but may occasionally cause a space-occupying lesion

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59
Q

What are the common causes of diarrhoea in HIV patients?

A
  1. May be due to the effects of the virus itself (HIV enteritis) or opportunistic infections
  2. Possible causes:
    a. Cryptosporidium + other protozoa (most common)
    b. Cytomegalovirus
    c. Mycobacterium avium intracellulare
    d. Giardia
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60
Q

What is the management of HIV?

A
  1. Antiretroviral therapy (ART): involves a combination of at least three drugs
  2. Typically two nucleoside reverse transcriptase inhibitors (NRTI) and either a protease inhibitor (PI) or a non-nucleoside reverse transcriptase inhibitor (NNRTI)
  3. This combination both decreases viral replication but also reduces the risk of viral resistance emerging
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61
Q

When should ART be started in HIV patients?

A

As soon as they have been diagnosed with HIV

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62
Q

What are Nucleoside analogue reverse transcriptase inhibitors (NRTIs)?

A
  1. E.g. zidovudine (AZT), abacavir, lamivudine, zalcitabine, tenofovir
  2. General NRTI side-effects: peripheral neuropathy
  3. Tenofovir: (recommended regime of two NRTIs), adverse effects include renal impairment and ostesoporosis
  4. Zidovudine: anaemia, myopathy, black nails
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63
Q

What is the third drug involved in ART for HIV management (after 2 NRTIs)?

A
  1. Non-nucleoside reverse transcriptase inhibitors (NNRTI):
    a. e.g. nevirapine, efavirenz, b. P450 enzyme interaction (nevirapine induces), rashes
  2. Protease inhibitors (PI):
    a. e.g. indinavir, nelfinavir, ritonavir, saquinavir
    b. SEs: diabetes, hyperlipidaemia, buffalo hump, central obesity, P450 enzyme inhibition, renal stones
  3. Integrase inhibitors:
    a. block the action of integrase, a viral enzyme that inserts the viral genome into the DNA of the host cell
    b. e.g. raltegravir, elvitegravir, dolutegravir
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64
Q

What is Infective Endocarditis?

A

Infection involving the endocardial surface of the heart, including the valvular structures, the chordae tendineae, sites of septal defects, or the mural endocardium

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65
Q

What is the most common cause of infective endocarditis?

A

Staphylococcus aureus (particularly in the acute presentation and IVDU)

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66
Q

What is the aetiology of Infective Endocarditis?

A

The endocardium can be colonized by virtually any organism, but the most common are:
1. Streptococci: Mainly a-haemolytic
2.Staphylococci: Staphylococcus aureus (most common)
3. Enterococci (20%)
4. Historical sources of bacteraemia should be considered, such as indwelling vascular catheters, recent dental work, and intravenous drug use

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67
Q

What are the different causative organisms of infective endocarditis associated with?

A
  1. Staphylococcus aureus: IVDU (and acute presentatin)
  2. Streptococcus viridans: found in the mouth, poor dental hygiene or following a dental procedure
  3. Staphylococcus epidermidis: commonly colonize indwelling lines, most common in prosthetic valves (< 2 months, after which returns to Staph A)
  4. Streptococcus bovis: associated with colorectal cancer
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68
Q

What are the non-infective causes of infective endocarditis?

A
  1. Systemic lupus erythematosus (Libman-Sacks)
  2. Malignancy: marantic endocarditis
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69
Q

What are the risk factors for infective endocarditis?

A
  1. Previously normal valves (50%, typically acute presentation), the mitral valve is most commonly affected
  2. Rheumatic valve disease (30%)
  3. Prosthetic valves
  4. Congenital heart defects
  5. Intravenous drug users (IVDUs) e.g. typically causing tricuspid lesion)
  6. Others: recent piercings
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70
Q

What are the presenting symptoms of Infective Endocarditis?

A
  1. Fever with sweats/chills/rigors (may be relapsing and remitting)
  2. Malaise
  3. Fatigue
  4. Weight loss
  5. Headache
  6. Arthralgia
  7. Myalgia
  8. Dyspnoea
  9. Confusion (particularly in elderly)
  10. Skin lesions
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71
Q

What are the signs of infective endocarditis on examination?

A
  1. Petechiae particularly on retinae (Roth’s spots)
  2. Pharyngeal and conjunctival mucosa vasculitic lesions
  3. Janeway lesions (painless palmar macules, which blanch on pressure)
  4. Osler’s nodes (tender nodules on finger/toe pads)
  5. Splinter haemorrhages (nail-bed haemorrhages)
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72
Q

What are the investigations for Infective Endocarditis?

A
  1. Bloods:
    a. FBC (leukocytosis, normocytic anaemia)
    b. Raised ESR and CRP
    c. U&Es: mildly elevated urea
    d. Rheumatoid factors: may be positive (minor criteria for diagnosis)
    e. Complement levels: decreased
  2. Blood culture: At least three sets 1h apart: bacteraemia or fungaemia
  3. ECG: progression of the infection may lead to conduction system disease
  4. Echocardiography:
    a. Should be performed in all cases of suspected IE
    b. Detection of vegetations and valve abscess
    c. Diagnosis of prosthetic valve endocarditis and assessment of embolic risk
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73
Q

What is the criteria for the diagnosis of Infective Endocarditis?

A
  1. Pathological criteria positive, or
  2. 2 major criteria, or
  3. 1 major and 3 minor criteria, or
  4. 5 minor criteria
    Also known as Modified Duke criteria
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74
Q

What is the pathological criteria for the diagnosis of Infective Endocarditis?

A
  1. Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery
  2. E.g. valve tissue, vegetations, embolic fragments or intracardiac abscess content
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75
Q

What is the Major Modified Duke criteria for Infective Endocarditis?

A
  1. Positive blood cultures
  2. Evidence of endocardial involvement e.g. positive echocardiogram or new valvular regurgitation
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76
Q

What is the criteria regarding positive blood cultures for infective endocarditis diagnosis?

A
  1. Persistent bacteraemia from two blood cultures taken > 12 hours apart or
  2. Three or more positive blood cultures where the pathogen is less specific such as Staph aureus and Staph epidermidis
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77
Q

What is the Minor Modified Duke criteria for Infective Endocarditis?

A
  1. Predisposing heart condition or IVDU
  2. Microbiological evidence does not meet major criteria
  3. Fever > 38ºC
  4. Vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
  5. Immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots
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78
Q

What is the management for infective endocarditis whilst blood cultures have not come back?

A
  1. Native valve: amoxicillin, consider adding low-dose gentamicin
  2. If penicillin allergic, MRSA or severe sepsis: vancomycin + low-dose gentamicin
  3. If prosthetic valve: vancomycin + rifampicin + low-dose gentamicin
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79
Q

What is the management of Infective Endocarditis caused by staphylococci?

A
  1. Native valve:
    a. Flucloxacillin
    b. If pen allergic or MRSA: vancomycin + rifampicin
  2. Prosthetic valve:
    a. Flucloxacillin + rifampicin + low-dose gentamicin
    b. If pen allergic or MRSA: vancomycin + rifampicin + low-dose gentamicin
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80
Q

What is the management of Infective Endocarditis cause by streptococci (e.g. viridans)?

A
  1. Fully sensitive:
    a. Benzylpenicillin
    b. If penallergic: vancomycin + low-dose gentamicin
  2. If less sensitive:
    a. Benzylpenicillin + low-dose gentamicin
    b. If pen allergic: vancomycin + low-dose gentamicin
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81
Q

What are the indications for surgical management of Infective Endocarditis?

A
  1. Severe valvular incompetence
  2. Aortic abscess (often indicated by a lengthening PR interval)
  3. Infections resistant to antibiotics/fungal infections
  4. Cardiac failure refractory to standard medical treatment
  5. Recurrent emboli after antibiotic therapy
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82
Q

What are the poor prognostic factors for Infective Endocarditis?

A
  1. Staphylococcus aureus infection
  2. Prosthetic valve (especially ‘early’, acquired during surgery)
  3. Culture negative endocarditis
  4. Low complement levels
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83
Q

What are the causes of culture negative Infective Endocarditis?

A
  1. Prior antibiotic therapy
  2. Coxiella burnetii
  3. Bartonella
  4. Brucella
  5. HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
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84
Q

What is the mortality of Infective Endocarditis based on causative organism?

A
  1. Staphylococci - 30%
  2. Bowel organisms - 15%
  3. Streptococci - 5%
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85
Q

What are the complications of Infective Endocarditis?

A
  1. Valve incompetence
  2. Intracardiac fistulae or abscesses
  3. Aneurysm formation
  4. Heart failure
  5. Renal failure
  6. Glomerulonephritis
  7. Arterial emboli from the vegetations (brain, kidneys, lungs, spleen)
  8. Fatal if untreated
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86
Q

What is Malaria?

A
  1. A parasitic infection caused by protozoa of the genus Plasmodium
  2. Five species are known to infect humans; Plasmodium falciparum is the most life-threatening
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87
Q

What is the aetiology of Malaria?

A
  1. It is naturally transmitted to humans through a bite by an infected female Anopheles mosquito
  2. May potentially be transmitted by blood transfusion or organ transplantation
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88
Q

What are the presenting symptoms of Malaria?

A
  1. High degree of clinical suspicion in any feverish traveller:
    a. incubation up to 1 year, but usually 1–2 weeks
  2. Cyclical symptoms of high fever, flulike symptoms, severe sweating and shivering cold/rigors
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89
Q

What are the signs of Malaria on physical examination?

A
  1. Pyrexia/rigors
  2. Anaemia
  3. Hepatosplenomegaly
90
Q

What are the protective factors against Malaria?

A
  1. Sickle cell anaemia
  2. G6PD deficiency
  3. HLA-B53
91
Q

What is Falciparum malaria?

A

The most common and severe form of Malaria

92
Q

What is the best diagnostic test for Malaria?

A

Thick and thin blood films stained using Field’s or Giemsa’s stain

93
Q

What are the features of severe (falciparum) malaria?

A
  1. Schizonts on a blood film
  2. Parasitaemia > 2%
  3. Hypoglycaemia
  4. Acidosis
  5. Temperature > 39 °C
  6. Severe anaemia
  7. Complications: cerebral malaria, acute renal failure, ARDS, DIC
94
Q

What is the management of malaria?

A

Artemisinin-based combination therapy (ACT) or chloroquine (avoided in pregnant women)

95
Q

What is Myocarditis?

A
  1. Describes inflammation of the myocardium
  2. Acute inflammation and necrosis of cardiac muscle in the absence of the predominant acute or chronic ischaemia characteristic of coronary artery disease
96
Q

What are the causes of myocarditis?

A
  1. Can be idiopathic
  2. Viral: coxsackie B, HIV
  3. Bacteria: diphtheria, clostridia
  4. Spirochaetes: Lyme disease
  5. Protozoa: Chagas’ disease, toxoplasmosis
  6. Autoimmune
  7. Drugs: doxorubicin
97
Q

What are the features of myocarditis?

A
  1. Usually a pro-dromal flu illness
  2. Present acutely as a young patient with chest pain
  3. Dyspnoea
  4. Arrhythmias
  5. Absence of pericarditis features e.g. relived when sitting forward, saddle shape ST elevation
98
Q

What are the investigations for myocarditis?

A
  1. Bloods:
    a. Raised inflammatory markers
    b. Raised cardiac enzymes
    c. Raised BNP
  2. ECG:
    a. Tchycardia
    b. Arrhythmias
    c. ST/T wave changes including ST-segment elevation and T wave inversion
99
Q

What is the management of Myocarditis?

A
  1. Treatment of underlying cause e.g. antibiotics if bacterial cause
  2. Supportive treatment e.g. of heart failure or arrhythmias
100
Q

What are the complications of Myocarditis?

A
  1. Heart failure
  2. Arrhythmia, possibly leading to sudden death
  3. Dilated cardiomyopathy: usually a late complication
101
Q

What is Necrotising fasciitis?

A
  1. A life-threatening subcutaneous soft-tissue infection that may extend to the deep fascia, but not into the underlying muscle
  2. A medical emergency that is difficult to recognise in the early stages
102
Q

What are the different types of Necrotising fasciitis?

A
  1. Type 1: caused by mixed anaerobes and aerobes (often occurs post-surgery in diabetics), the most common type
  2. Type 2: caused by Streptococcus pyogenes
103
Q

What are the risk factors for Necrotising fasciitis?

A
  1. Skin factors: recent trauma, burns or soft tissue infections
  2. Diabetes mellitus:
    a. the most common preexisting medical condition
    b. particularly if the patient is treated with SGLT-2 inhibitors
  3. IVDU
  4. Immunosuppression
104
Q

What is the most commonly affected site in Necrotising fasciitis?

A

Perineum (Fournier’s gangrene)

105
Q

What are the features of Necrotising fasciitis?

A
  1. Acute onset
  2. Pain, swelling, erythema at the affected site
  3. Often presents as rapidly worsening cellulitis with pain out of keeping with physical features
  4. Extremely tender over infected tissue with hypoaesthesia to light touch
  5. Skin necrosis and crepitus/gas gangrene are late signs
  6. Fever and tachycardia may be absent or occur late in the presentation
106
Q

What are the investigations for Necrotising fasciitis?

A
  1. Medical emergency: A to E
  2. Bloods and ABG: hypoxaemia, acidosis, elevated lactate
  3. Blood cultures
  4. Imaging: CT/MRI show oedema extending along fascial plane and/or soft tissue gas
107
Q

What is the management of Necrotising fasciitis?

A
  1. Urgent surgical referral debridement
  2. Intravenous antibiotics
108
Q

What is the prognosis of Necrotising fasciitis?

A

Average mortality of 20%

109
Q

What is osteomyelitis?

A
  1. Infection of the bone
  2. Can be classified into:
    a. Haematogenous (from bacteraemia)
    b. Non-haematogenous (contiguous spread from local tissue)
  3. Most common cause is staphylococcus aureus (but Salmonella in sickle cell patients)
110
Q

What is haematogenous osteomyelitis?

A
  1. Results from bacteraemia
  2. Usually monomicrobial
  3. Most common form in children
  4. Vertebral osteomyelitis is the most common form of haematogenous osteomyelitis in adults
  5. Risk factors include:
    a. sickle cell anaemia
    b. IVDU
    c. Immunosuppression due to either medication or HIV
    d. Infective endocarditis
111
Q

What is Non-haematogenous osteomyelitis?

A
  1. Results from the contiguous spread of infection from adjacent soft tissues to the bone or from direct injury/trauma to bone
  2. Is often polymicrobial
  3. Most common form in adults
  4. Risk factors include:
    a. Diabetic foot ulcers/pressure sores
    b. Diabetes mellitus
    c. Peripheral arterial disease
112
Q

What is the investigation of choice for osteomyelitis?

A

MRI: imaging modality of choice, with a sensitivity of 90-100%

113
Q

What is the management of osteomyelitis?

A
  1. Flucloxacillin for 6 weeks
  2. Clindamycin if penicillin-allergic
114
Q

What is Rheumatic Fever?

A

Develops following an immunological reaction to a recent (2-4 weeks ago) Streptococcus pyogenes infection

115
Q

What are the presenting symptoms of Rheumatic Fever?

A
  1. 2–5 weeks after GAS infection: recent sore throat
  2. General:
    a. Fever
    b. Malaise
    c. Anorexia
  3. Joints:
    a. Painful, swollen, reduced movement/function
  4. Cardiac:
    a. Breathlessness
    b. Chest pain, palpitations
116
Q

How do the signs of Rheumatic Fever help diagnose it?

A
  1. Major criteria:
    a. Erythema marginatum: transient erythematous rash with raised edges, seen on trunk and proximal limbs (rare in adults)
    b. Sydenham’s chorea: this is often a late feature
    c. Polyarthritis
    d. Carditis and valvulitis (eg, pancarditis)
    e. Subcutaneous nodules
  2. Minor ciriteria:
    a. Raised ESR or CRP
    b. Pyrexia
    c. Arthralgia (not if arthritis a major criteria)
    d. Prolonged PR interval
117
Q

How is Rheumatic Fever diagnosed?

A
  1. Evidence of recent streptococcal infection:
    a. Raised or rising streptococci antibodies
    b. Positive throat swab
    c. Positive rapid group A streptococcal antigen test
  2. Accompanied by:
    a. 2 major criteria or
    b. 1 major with 2 minor criteria
118
Q

What is the the management of Rheumatic Fever?

A
  1. Antibiotics: oral penicillin V
  2. Anti-inflammatories: NSAIDs are first-line
  3. Treatment of any complications that develop e.g. heart failure, mitral stenosis
119
Q

What is the most common cause of mitral stenosis?

A

Rheumatic Fever

120
Q

What is septic arthritis?

A

Joint inflammation resulting from intra-articular (occurring within a joint) infection

121
Q

What is the most common cause of septic arthritis in adults?

A
  1. Most common organism overall: Staphylococcus aureus
    a. In young adults who are sexually active, Neisseria gonorrhoeae
  2. Most common cause is hematogenous spread (may be from distant bacterial infections e.g. abscesses)
122
Q

Where is the most common location for septic arthritis in adults?

123
Q

What are the features of septic arthritis?

A
  1. Acute, swollen joint:
    a. restricted movement in 80% of patients
    b. examination findings: warm to touch/fluctuant
  2. Fever: present in the majority of patients
124
Q

What are the investigations for septic arthritis?

A
  1. Synovial fluid sampling is obligatory:
    a. Should be done prior to the administration of antibiotics if necessary!
    b. May need to be done under radiographic guidance
  2. Blood cultures: the most common cause is hematogenous spread
  3. Joint imaging
125
Q

What is the management of septic arthritis?

A
  1. IV antibiotics which cover Gram-positive cocci are indicated: flucloxacillin or clindamycin if penicillin allergic
  2. Antibiotic treatment is normally be given for several weeks (BNF states 4-6 weeks)
  3. Patients are typically switched to oral antibiotics after 2 weeks
  4. Needle aspiration should be used to decompress the joint
  5. Arthroscopic lavage may be required
126
Q

What is the Kocher criteria for septic arthritis in children?

A
  1. Fever >38.5 degrees C
  2. Non-weight bearing
  3. Raised ESR
  4. Raised WCC
127
Q

What is Sjögren’s syndrome?

A
  1. An autoimmune disorder affecting exocrine glands resulting in dry mucosal surfaces
  2. Particularly dry eyes (keratoconjunctivitis sicca) and dry mouth
128
Q

What is the aetiology of Sjögren’s syndrome?

A

It may be primary (PSS) or secondary to rheumatoid arthritis or other connective tissue disorders, where it usually develops around 10 years after the initial onset

129
Q

What is the epidemiology of Sjögren’s syndrome?

A

Much more common in females (ratio 9:1)

130
Q

What are patients with Sjögren’s syndrome at risk of developing?

A

A marked increased risk of lymphoid malignancy (40-60 fold)

131
Q

What are the features of Sjögren’s syndrome?

A
  1. Dry eyes: keratoconjunctivitis sicca
  2. Dry mouth
  3. Vaginal dryness
  4. Arthralgia
  5. Raynaud’s, myalgia
  6. Sensory polyneuropathy
  7. Recurrent episodes of parotitis
132
Q

What is Raynaud’s phenomenon?

A
  1. An exaggerated vasoconstrictive response of the digital arteries and cutaneous arteriole to the cold or emotional stress
  2. Primary: Raynaud’s disease, young women, bilateral
  3. Secondary: Raynaud’s phenomenon, e.g.:
    a. Scleroderma (most common)
    b. RA
    c. SLE
133
Q

What is the first line management of Raynaud’s?

A

Calcium channel blockers: nifedipine

134
Q

What are the investigations for Sjögren’s syndrome?

A
  1. Bloods, Antibodies:
    a. Rheumatoid factor (RF) positive in nearly 50% of patients
    b. ANA positive in 70%
    c. anti-Ro (SSA) antibodies in 70% of patients with PSS
    d. anti-La (SSB) antibodies in 30% of patients with PSS
  2. Schirmer’s test: filter paper near conjunctival sac to measure tear formation
  3. Histology: focal lymphocytic infiltration
135
Q

What is the management of Sjögren’s syndrome?

A
  1. Artificial saliva and tears
  2. Pilocarpine may stimulate saliva production
136
Q

What is discitis?

A

Inflammation and infection of the vertebra

137
Q

What are the features of discitis?

A

Pain (progressive history) and stiffness

138
Q

What are the investigations for discitis?

A
  1. Bloods: inflammatory markers
  2. Imaging: radiographs, MRI ± radionuclide scanning
  3. Blood cultures and aspiration of the infected intervertebral disc space
139
Q

What is the management of discitis?

A
  1. Antibiotics specific to cultured organism
  2. Might consider steroids (a complex condition that needs MDT approach)
140
Q

What is Systemic lupus erythematosus (SLE)?

A

A chronic multi-system inflammatory autoimmune disorder that most commonly affects women during their reproductive years

141
Q

What is the aetiology of SLE?

A
  1. Autoimmune: Type 3 hypersensitivity reaction
  2. Associated with HLA B8, DR2, DR3
  3. Thought to be caused by immune system dysregulation leading to immune complex formation
  4. Immune complex deposition can affect any organ including the skin, joints, kidneys and brain
142
Q

What is the epidemiology of SLE?

A
  1. Much more common in females (F:M = 9:1)
  2. More common in Afro-Caribbeans and Asian communities
  3. Onset is usually 20-40 years
  4. Incidence has risen substantially during the past 50 years (3 fold)
143
Q

How can the features of SLE be divided?

A
  1. By system affected by immune complex deposition
  2. General
  3. Skin
  4. MSK
  5. Cardiovascular
  6. Respiratory
  7. Renal
  8. Neuropsychiatry
144
Q

What are the general features of SLE?

A
  1. Fatigue
  2. Fever
  3. Mouth ulcers
  4. Lymphadenopathy
145
Q

What are the skin features of SLE?

A
  1. Malar (butterfly) rash: spares nasolabial folds
  2. Discoid rash: scaly, erythematous, well demarcated rash in sun-exposed areas, lesions may progress to become pigmented and hyperkeratotic before becoming atrophic
  3. Photosensitivity
  4. Raynaud’s phenomenon
  5. Livedo reticularis
  6. Non-scarring alopecia: hair thinning
146
Q

What are the MSK features of SLE?

A
  1. Arthralgia
  2. Non-erosive arthritis
147
Q

What are the cardiovascular and respiratory features of SLE?

A
  1. Cardiovascular:
    a. Pericarditis: the most common cardiac manifestation
    b. Myocarditis
  2. Respiratory:
    a. Pleurisy
    b. Fibrosing alveolitis
148
Q

What are the renal features of SLE?

A
  1. Proteinuria
  2. Glomerulonephritis (diffuse proliferative glomerulonephritis is the most common type)
149
Q

What are the neuropsychiatry features of SLE?

A
  1. Anxiety and depression
  2. Psychosis
  3. Seizures
150
Q

What are the investigations for SLE?

A
  1. Bloods:
    a. inflammatory markers
    b. Complement levels: are low during active disease (formation of complexes leads to consumption of complement)
  2. Antibodies: diagnostic
    a. ANA positive (99%)
    b. anti-dsNSA: highly specific (> 99%), but less sensitive (70%)
    c. anti-Smith: highly specific (> 99%), sensitivity (30%)
    d. Rheumatoid factor (20%)
151
Q

What are the main antibodies in SLE?

A
  1. ANA
  2. Anti-dsDNA
  3. Anti-Smith
  4. Rheumatoid factor (20%)
152
Q

What is the management of SLE?

A
  1. NSAIDs
  2. Suncream for photosensitivity
  3. Hydroxychloroquine: the treatment of choice for SLE
  4. If internal organ involvement e.g. renal, neuro, eye then consider: prednisolone, cyclophosphamide
153
Q

What is the treatment of choice for SLE?

A

Hydroxychloroquine

154
Q

What is systemic sclerosis (scleroderma)?

A

A condition of unknown aetiology characterised by hardened, sclerotic skin and other connective tissues

155
Q

What are the three patterns of disease of systemic sclerosis?

A
  1. Limited cutaneous systemic sclerosis
  2. Diffuse cutaneous systemic sclerosis
  3. Scleroderma: without organ involvement
156
Q

What is the epidemiology of systemic sclerosis?

A
  1. Four times more common in females
  2. Age of onset 30–60 years
157
Q

What is Limited cutaneous systemic sclerosis?

A
  1. Raynaud’s may be the first sign
  2. Affects face and distal limbs predominately
  3. Associated with anti-centromere antibodies
  4. A subtype of limited systemic sclerosis is CREST syndrome:
    a. Calcinosis
    b. Raynaud’s phenomenon
    c. oEsophageal dysmotility
    d. Sclerodactyly
    e. Telangiectasia
158
Q

What is Diffuse cutaneous systemic sclerosis?

A
  1. Affects trunk and proximal limbs predominately
  2. Associated with anti scl-70 antibodies
  3. Most common cause of death is now respiratory involvement, which is seen in around 80%: interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH)
  4. Other complications include renal disease and hypertension
  5. Patients with renal disease should be started on an ACE inhibitor
  6. Poor prognosis
159
Q

What is Scleroderma systemic sclerosis?

A
  1. Without organ involvement
  2. Tightening and fibrosis of skin
  3. May be manifest as plaques (morphoea) or linea
160
Q

What antibodies are associated with limited systemic sclerosis?

A

Anti-centromere

161
Q

What antibodies are associated with diffuse systemic sclerosis?

A

Anti-Scl-70

162
Q

What other antibodies are positive in systemic sclerosis?

A

ANA and Rheumatoid factor

163
Q

What is the management of systemic sclerosis?

A
  1. Pain management through NSAIDs or corticosteroids
  2. Calcium channel blockers for Raynaud’s (limited): nifedipine
  3. ACEi for renal involvement (diffuse)
164
Q

What is threadworm infection?

A
  1. Infestation with threadworms (Enterobius vermicularis, sometimes called pinworms) is extremely common amongst children in the UK
  2. Infestation occurs after swallowing eggs that are present in the environment
165
Q

What are the features of threadworm infection?

A
  1. Asymptomatic in around 90% of cases
  2. Possible features include:
    a. Perianal itching, particularly at night
    b. Girls may have vulval symptoms
166
Q

How is threadworm infection diagnosed?

A
  1. Most patients are treated empirically based on clinical diagnosis
  2. Can also be diagnosed by the applying Sellotape to the perianal area and sending it to the laboratory for microscopy to see the eggs
167
Q

What is the management of threadworm infection?

A
  1. Combination of anthelmintic with hygiene measures for all members of the household
  2. Mebendazole is used first-line for children > 6 months old
  3. A single dose is given unless infestation persists
168
Q

What is Urticaria?

A

A local or generalised superficial swelling of the skin

169
Q

What are the causes of urticaria?

A
  1. Most commonly caused by allergy: drugs e.g. penicillins, and food
170
Q

What is the epidemiology of urticaria?

A
  1. While the majority of these cases are acute and self-limiting events, roughly 30% of people will go on to experience prolonged symptoms
  2. Acute urticaria is more common in children and adolescents than in adults
  3. Chronic urticaria more typically affects adults, women are affected more often than men
171
Q

What are the features of urticaria?

A
  1. Pale, pink raised skin
  2. Variously described as ‘hives’, ‘wheals’, ‘nettle rash’
  3. Pruritic
  4. Generally resolves within 24h
  5. Up to 40% of cases have associated: angio-oedema: swelling of the face, tongue or lips
172
Q

What are the investigations for urticaria?

A
  1. Acutely often diagnosed clinically
  2. Chronic urticaria:
    a. FBC: may provide evidence of occult infection, anaemia, or findings suggestive of chronic illness
    b. Ig-E antibodies
    c. Inflammatory markers
    d. Antithyroid/antinuclear antibodies: exclude thyroid/rheumatic causes of chronic illness
173
Q

What is the management of urticaria?

A
  1. Non-sedating antihistamines are first-line
  2. Prednisolone is used for severe or resistant episodes
174
Q

What vaccines are live attenuated?

A
  1. BCG
  2. measles, mumps, rubella (MMR)
  3. Influenza (intranasal)
  4. Oral rotavirus
  5. Oral polio
  6. Yellow fever
  7. Oral typhoid
175
Q

Which vaccines are inactivated preparations?

A
  1. Rabies
  2. Hepatitis A
  3. Influenza (intramuscular)
176
Q

Which vaccines contain Toxoid (inactivated toxin)?

A
  1. Tetanus
  2. Diphtheria
  3. Pertussis
177
Q

What are the subunit and conjugate vaccines?

A
  1. Pneumococcus (conjugate)
  2. Haemophilus (conjugate)
  3. Meningococcus (conjugate)
  4. Hepatitis B
  5. Human papillomavirus
178
Q

What is Varicella Zoster?

A
  1. Varicella-zoster is the herpes virus that causes chickenpox
  2. Shingles is an acute, unilateral, painful blistering rash caused by reactivation of the varicella-zoster virus (VZV)
179
Q

What is the aetiology of Varicella Zoster?

A
  1. VZV is an herpes ds-DNA virus
  2. Highly contagious, transmission is by aerosol inhalation or direct contact with the vesicular secretions
180
Q

What is the epidemiology of Varicella Zoster?

A
  1. Chickenpox peak incidence occurs at 4–10 years
  2. Shingles peak incidence occurs at >50 years
  3. About 90% of adults are VZV IgG positive (previously infected)
181
Q

What is the aetiology of chickenpox (primary infection of VZV)?

A
  1. Highly infectious
  2. Spread via the respiratory route
  3. Can be caught from someone with shingles (reactivation)
  4. Infectivity = 4 days before rash, until 5 days after the rash first appeared
  5. Incubation period = 10-21 days
182
Q

What are the clinical features of chickenpox?

A
  1. Tends to be more severe in older children/adults
  2. Fever initially
  3. Itchy, rash starting on head/trunk before spreading. 4. Initially macular then papular then vesicular
  4. Systemic upset is usually mild
183
Q

What is the management of chickenpox?

A
  1. Supportive: keep cool, trim nails, calamine lotion
  2. Infectious until all lesions are dry and have crusted over (usually about 5 days after the onset of the rash): school exclusion
  3. IVIG for immunocompromised or pregnant women
184
Q

What is a common complication of chickenpox?

A
  1. Secondary bacterial infection of the lesions
  2. NSAIDs may increase this risk
  3. Whilst this commonly may manifest as a single infected lesion/small area of cellulitis, in a small number of patients invasive group A streptococcal soft tissue infections may occur resulting in necrotizing fasciitis
185
Q

What are the more rarer complications of chickenpox?

A
  1. Pneumonia
  2. Encephalitis (cerebellar involvement may be seen)
  3. Disseminated haemorrhagic chickenpox
  4. Arthritis, nephritis and pancreatitis may very rarely be seen
186
Q

What is Shingles?

A
  1. An acute, unilateral, painful blistering rash caused by reactivation of the varicella-zoster virus (VZV)
  2. Following primary infection with VZV (chickenpox), the virus lies dormant in the dorsal root or cranial nerve ganglia
187
Q

What are the risk factors for shingles?

A
  1. Increasing age
  2. HIV: strong risk factor, 15 times more common
  3. Other immunosuppressive conditions (e.g. steroids, chemotherapy)
188
Q

What are the most common dermatomes affected in shingles?

189
Q

What are the features of shingles?

A
  1. Prodromal period:
    a. Burning pain over the affected dermatome for 2-3 days
    b. Pain may be severe and interfere with sleep
    c. Around 20% of patients will experience fever, headache, lethargy
  2. Rash:
    a. Initially erythematous, macular rash over the affected dermatome
    b. Quickly becomes vesicular
    c. Characteristically is well demarcated by the dermatome and does not cross the midline: however, some ‘bleeding’ into adjacent areas may be seen
190
Q

What is the management of shingles?

A
  1. Analgesia:
    a. Paracetamol and NSAIDs are first-line
    b. If not responding: neuropathic agents (e.g. amitriptyline)
    c. Oral corticosteroids may be considered in the first 2 weeks in immunocompetent adults
  2. Antivirals:
    a. NICE recommendations: antivirals within 72 hours for the majority of patients, unless the patient is < 50 years and has a ‘mild’ truncal rash associated with mild pain and no underlying risk factors
    b. One of the benefits of prescribing antivirals is a reduced incidence of post-herpetic neuralgia, particularly in older people
    c. Aciclovir, famciclovir, or valaciclovir are recommended
191
Q

What should patients with Shingles be reminded of?

A
  1. They are potentially infectious
  2. May need to avoid pregnant women and the immunosuppressed
  3. Should be advised that they are infectious until the vesicles have crusted over, usually 5-7 days following onset
  4. Covering lesions reduces the risk
192
Q

What is post-herpetic neuralgia?

A
  1. most common complication of Shingles
  2. More common in older patients
  3. Affects between 5%-30% of patients depending on age
  4. Most commonly resolves with 6 months but may last longer
193
Q

What are the complications of Shingles?

A
  1. Post-herpetic neuralgia
  2. Herpes zoster ophthalmicus: shingles affecting affecting the ocular division of the trigeminal nerve, is associated with a variety of ocular complications
  3. Herpes zoster oticus (Ramsay Hunt syndrome): may result in ear lesions and facial paralysis
194
Q

What are the large vessel vasculitides?

A
  1. Temporal arteritis
  2. Takayasu’s arteritis
195
Q

What are the medium vessel vasculitides?

A
  1. Polyarteritis nodosa
  2. Kawasaki disease
196
Q

What are the small vessel vasculitides?

A
  1. ANCA-associated:
    a. granulomatosis with polyangiitis (Wegener’s granulomatosis)
    b. eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
    c. microscopic polyangiitis
  2. Immune complex:
    a. Henoch-Schonlein purpura
    b. Goodpasture’s syndrome (anti-glomerular basement membrane disease)
    c. cryoglobulinaemic vasculitis
    hypocomplementemic
    d. urticarial vasculitis (anti-C1q vasculitis)
197
Q

What are the ANCA associated vasculitides (small vessel vasculitis)?

A
  1. Granulomatosis with polyangiitis: Wegener’s granulomatosis
  2. Eosinophilic granulomatosis with polyangiitis: Churg-Strauss syndrome
  3. Microscopic polyangiitis
198
Q

What are the common features of ANCA associated vasculitides?

A
  1. Renal impairment: caused by immune complex glomerulonephritis → raised creatinine, haematuria and proteinuria
  2. Respiratory symptoms:
    a. Dyspnoea
    b. haemoptysis
  3. Systemic symptoms:
    a. Fatigue
    b. Weight loss
    c. Fever
  4. Vasculitic rash: present only in a minority of patients
  5. ENT symptoms: sinusitis
199
Q

What the investigations for ANCA associated vasculitides?

A
  1. Urinalysis for haematuria and proteinuria
  2. Bloods:
    a. urea and creatinine for renal impairment
    b. FBC: normocytic anaemia and thrombocytosis may be seen
    c. CRP: raised
    d. ANCA testing: antibodies
  3. Chest x-ray: nodular, fibrotic or infiltrative lesions may be seen
200
Q

What are the two types of ANCA antibodies?

A
  1. Cytoplasmic (cANCA): Granulomatosis with polyangiitis: Wegener’s granulomatosis
  2. Perinuclear (pANCA): Eosinophilic granulomatosis with polyangiitis: Churg-Strauss syndrome
201
Q

What other conditions are associated with pANCA antibodies?

A
  1. Churg-Strauss syndrome
  2. Ulcerative colitis (70%)
  3. Primary sclerosing cholangitis (70%)
  4. Anti-GBM disease (25%)
  5. Crohn’s disease (20%)
202
Q

What is the general approach to management for ANCA associated vasculitides?

A
  1. Managed by specialist teams (e.g. renal, rheumatology, respiratory) to allow an exact diagnosis to be made
  2. Kidney or lung biopsies may be taken to aid the diagnosis
  3. The mainstay of management is immunosuppressive therapy
203
Q

What is Temporal arteritis?

A
  1. Also known as giant cell arteritis: GCA
  2. A vasculitis of unknown cause that affects medium and large-sized vessels arteries
204
Q

What is temporal arteritis associated with?

A

Polymyalgia rheumatica (PMR): around 50% of patients will have features of PMR

205
Q

What are the features of temporal arteritis?

A
  1. Typically patient > 60 years old
  2. Usually rapid onset (e.g. < 1 month)
  3. Headache (found in 85%)
  4. Jaw claudication (65%)
  5. Tender, palpable temporal artery
  6. Around 50% have features of PMR: aching, morning stiffness in proximal limb muscles (not weakness)
  7. Also lethargy, depression, low-grade fever, anorexia, night sweats
206
Q

What should be initiated as soon as temporal arteritis is suspected?

A

High-dose glucocorticoids (40-60mg prednisolone) should be given as soon as the diagnosis is suspected and before the temporal artery biopsy

207
Q

What is the most feared complication of temporal arteritis?

A

Permanent vision loss: anterior ischemic optic neuropathy

208
Q

What are the investigations for temporal arteritis?

A
  1. Raised inflammatory markers:
    a. ESR > 50 mm/hr (note ESR < 30 in 10% of patients)
    b. CRP may also be elevated
  2. Temporal artery biopsy: skip lesions may be present
  3. Creatine kinase and EMG may be normal
209
Q

What is the management of temporal arteritis?

A
  1. Urgent high-dose glucocorticoids:
    a. Should be given as soon as the diagnosis is suspected
    b. If there is no visual loss: high-dose prednisolone (40-60mg)
    c. If there is evolving visual loss: IV methylprednisolone is usually given prior to starting high-dose prednisolone
    d. There should be a dramatic response, if not the diagnosis should be reconsidered
  2. Urgent ophthalmology review:
    a. Patients with visual symptoms should be seen the same-day by an ophthalmologist
    d. Visual damage is often irreversible
210
Q

What should be given alongside high dose prednisolone in the management of temporal arteritis?

A

Bone protection with bisphosphonates is required as long, tapering course of steroids is required

211
Q

What is Kawasaki disease?

A
  1. A type of vasculitis which is predominately seen in children
  2. Important to recognise as it may cause potentially serious complications, including coronary artery aneurysms
212
Q

What are the features of Kawasaki disease?

A
  1. High-grade fever which lasts for > 5 days (characteristically resistant to antipyretics)
  2. Conjunctivitis
  3. Bright red, cracked lips
  4. Strawberry tongue
  5. Cervical lymphadenopathy
  6. Red palms of the hands and the soles of the feet which later peel
213
Q

What is the management of Kawasaki disease?

A
  1. High-dose aspirin
  2. Intravenous immunoglobulin
214
Q

What is the screening investigation for coronary artery aneurysms in Kawasaki disease?

A

Echocardiogram

215
Q

What is Takayasu’s arteritis?

A
  1. A large vessel vasculitis
  2. It typically causes occlusion of the aorta
  3. Can lead to absent or weak limb pulses
216
Q

What is the epidemiology of Takayasu’s arteritis?

A

More common in younger females (e.g. 10-40 years) and Asian people

217
Q

What are the features of Takayasu’s arteritis?

A
  1. Systemic features of a vasculitis e.g. malaise, headache
  2. Unequal blood pressure in the upper limbs
  3. Carotid bruit and tenderness
  4. Absent or weak peripheral pulses
  5. Upper and lower limb claudication on exertion
  6. Aortic regurgitation (around 20%)
218
Q

What are the associations of Takayasu’s arteritis?

A

Renal artery stenosis

219
Q

What is the investigation for Takayasu’s arteritis?

A
  1. Vascular imaging of the arterial tree: either magnetic resonance angiography (MRA) or CT angiography (CTA)
220
Q

What is the management of Takayasu’s arteritis?

!Final Year (26 decks)

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