Infection and Immunology Flashcards

1
Q

<p>Define autoimmune hepatitis.</p>

A

<p>Autoimmune hepatitis (AIH) is a chronic inflammatory disease of the liver of unknown aetiology. It is characterised by the presence of circulating auto-antibodies with a high serum globulin concentration, inflammatory changes on liver histology, and a favourable response to immunosuppressive treatment.</p>

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2
Q

<p>Explain the aetiology/risk factors of autoimmune hepatitis.</p>

A

<p>Female gender<br></br>Genetic predisposition<br></br>Immune dysregulation</p>

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3
Q

<p>Summarise the epidemiology of autoimmune hepatitis.</p>

A

<p>All ethnicities are susceptible to the disease, but prevalence is greatest among people with northern European ancestry who have a high frequency of human leukocyte antigen (HLA)-DR3 and HLA-DR4 markers.</p>

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4
Q

<p>Recognise the presenting symptoms of autoimmune hepatitis. Recognise the signs of autoimmune hepatitis on physical examination.<br></br></p>

A

<p>Fatigue/malaise<br></br>Anorexia<br></br>Abdominal discomfort<br></br>Hepatomegaly<br></br>Jaundice<br></br>Pruritus<br></br>Arthralgia<br></br>Nausea<br></br>Fever<br></br>Spider angiomata<br></br>Splenomegaly</p>

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5
Q

<p>Identify appropriate investigations for autoimmune hepatitis and interpret the results.</p>

A

<p>Aspartate transaminase<br></br>Alanine transaminase<br></br>Bilirubin<br></br>Gamma-GT<br></br>Alkaline phosphatase<br></br>Serum globulin<br></br>Serum albumin<br></br>Prothrombin time</p>

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6
Q

<p>Generate a management plan for autoimmune hepatitis.</p>

A

<p>Observation and monitoring<br></br>Corticosteroid monotherapy e.g. prednisolone</p>

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7
Q

<p>Identify the possible complications of autoimmune hepatitis and its management.</p>

A

<p>Osteoporosis, diabetes mellitus, hypertension, truncal obesity, cataracts due to corticosteroid therapy.<br></br>Hepatocellular carcinoma, end-stage liver disease due to progression of AIH.<br></br>Bone marrow suppression, cholestatic hepatitis, pancreatitis, skin rash due to azathioprine therapy.</p>

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8
Q

<p>Summarise the prognosis for patients with autoimmune hepatitis.</p>

A

<p>The natural history of AIH reveals that untreated AIH has a poor prognosis with a 5-year survival rate of 50% and 10-year survival rate of 10%. Immunosuppressive therapy significantly improves survival.</p>

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9
Q

<p>Define Behçet’s disease.</p>

A

<p>A systemic vasculitis which can cause skin and mucosal lesions, uveitis, major arterial and venous vessel disease, and GI and neurological manifestations.</p>

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10
Q

<p>Explain the aetiology/risk factors of Behçet’s disease.</p>

A

<p>Age 20 to 40 years<br></br>Family history of Behçet’s syndrome<br></br>Genetic predisposition</p>

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11
Q

<p>Summarise the epidemiology of Behçet’s disease.</p>

A

<p>Patients are most commonly from the Middle East, the Mediterranean region, and eastern Asia, with Japan and South Korea leading the list. Behçet’s syndrome is rare in northern Europe and Africa. The prevalence in Turkey is 1 in 250 of the adult population.</p>

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12
Q

<p>Recognise the signs of Behçet’s disease on physical examination. Recognise the presenting symptoms of Behçet’s disease.</p>

A

<p>Increased predisposition in certain ethnic/geographic groups<br></br>Oral ulcers<br></br>Genital ulcers<br></br>Uveitis<br></br>Acne lesions<br></br>Erythema nodosum</p>

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13
Q

<p>Identify appropriate investigations for Behçet’s disease and interpret the results.</p>

A

<p>Pathergy testing<br></br>RF<br></br>ANA<br></br>Anti-neutrophil cytoplasmic antibodies<br></br>HLA-B51<br></br>MRI brain with contrast<br></br>Colonoscopy<br></br>Upper GI endoscopy<br></br>High-resolution chest CT<br></br>CT angiography of chest<br></br>Pulmonary angiography</p>

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14
Q

<p>Define candidiasis.</p>

A

<p>Oral candidiasis involves an infection of oral tissues by yeasts of the genus Candida, mostly C albicans. It is the most common oral fungal infection and is commonly seen in infants and older adults, and also with states of local and systemic immunological suppression.</p>

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15
Q

<p>Explain the aetiology/risk factors of candidiasis.</p>

A

<p>Hyposalivation/xerostomia<br></br>Poor oral hygiene, especially among denture wearers<br></br>Malabsorption and malnutrition<br></br>Advanced malignancy<br></br>Cancer chemotherapy and radiotherapy<br></br>HIV infection<br></br>Endocrine disturbance (e.g., diabetes mellitus, hypoparathyroidism, pregnancy, hypoadrenalism)<br></br>Immunosuppressive agents (e.g., systemic corticosteroid therapy)<br></br>Current or recent past use of broad-spectrum or multiple narrow-spectrum antibiotics</p>

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16
Q

<p>Summarise the epidemiology of candidiasis.</p>

A

<p>Oral candidal colonisation has been reported to range from approximately 40% to 70% of healthy children and adults, with higher rates observed among children with carious teeth and older adults wearing dentures.</p>

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17
Q

<p>Recognise the presenting symptoms of candidiasis. Recognise the signs of candidiasis on physical examination.</p>

A

<p>Creamy white or yellowish plaques, fairly adherent to oral mucosa<br></br>Cracks, ulcers, or crusted fissures radiating from angles of the mouth<br></br>Lesions on any part of the oral mucosa<br></br>Atrophic, fiery red, flat lesions on the palate<br></br>Patchy areas of loss of filiform papillae on the dorsum of the tongue<br></br>Spotty red areas on the buccal mucosa<br></br>Lesions confined to the outline of a dental prosthesis<br></br>Burning oral pain</p>

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18
Q

<p>Identify appropriate investigations for candidiasis and interpret the results.</p>

A

<p>Superficial smear of lesion for microscopy</p>

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19
Q

<p>Define encephalitis.</p>

A

<p>Encephalitis is defined as inflammation of the brain parenchyma associated with neurological dysfunction such as altered state of consciousness, seizures, personality changes, cranial nerve palsies, speech problems, and motor and sensory deficits.</p>

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20
Q

<p>Explain the aetiology/risk factors of encephalitis.</p>

A

<p>Age <1 or >65 years<br></br>Immunodeficiency<br></br>Post-infection<br></br>Blood/body fluid exposure<br></br>Organ transplantation<br></br>Animal or insect bites<br></br>Location<br></br>Season<br></br>Swimming or diving in warm freshwater or nasal/sinus irrigation</p>

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21
Q

<p>Summarise the epidemiology of encephalitis.</p>

A

<p>Around 2500 cases of encephalitis occur in England each year. Globally, the incidence of encephalitis is around 7 per 100,000 population per year.</p>

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22
Q

<p>Recognise the presenting symptoms of encephalitis. Recognise the signs of encephalitis on physical examination.</p>

A

<p>Fever<br></br>Rash<br></br>Altered mental state<br></br>Focal neurological deficit<br></br>Meningismus<br></br>Parotitis<br></br>Lymphadenopathy<br></br>Optic neuritis<br></br>Acute flaccid paralysis<br></br>Movement disorder<br></br>Cough<br></br>Gastrointestinal infection<br></br>Seizures</p>

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23
Q

<p>Identify appropriate investigations for encephalitis and interpret the results.</p>

A

<p>FBC<br></br>Peripheral blood smear<br></br>Serum electrolytes<br></br>Liver function tests<br></br>Blood cultures<br></br>Throat swab<br></br>Nasopharyngeal aspirate<br></br>Sputum culture<br></br>Chest radiography<br></br>CT brain<br></br>MRI brain<br></br>Electroencephalogram (EEG)<br></br>Cerebrospinal fluid (CSF) analysis, culture, serology andpolymerase chain reaction (PCR)</p>

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24
Q

<p>Define human immunodeficiency virus (HIV).</p>

A

<p>HIV is caused by a retrovirus that infects and replicates in human lymphocytes and macrophages, eroding the integrity of the human immune system over a number of years, culminating in immune deficiency and a susceptibility to a series of opportunistic and other infections as well as the development of certain malignancies.</p>

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25
Q

<p>Explain the aetiology/risk factors of human immunodeficiency virus (HIV).</p>

A

<p>Needle sharing with intravenous drug use<br></br>Unprotected receptive anal intercourse<br></br>Unprotected receptive penile-vaginal sexual intercourse<br></br>Percutaneous needle stick injury<br></br>High maternal viral load (mother to child transmission)</p>

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26
Q

<p>Summarise the epidemiology of human immunodeficiency virus (HIV).</p>

A

<p>Globally, there were 37.9 million people living with HIV worldwide at the end of 2018, with approximately 1.7 million becoming newly infected in 2018. Approximately 70% of people living with HIV are in sub-Saharan Africa.</p>

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27
Q

<p>Recognise the presenting symptoms of human immunodeficiency virus (HIV). Recognise the signs of human immunodeficiency virus (HIV) on physical examination.</p>

A

<p>Fevers and night sweats<br></br>Weight loss<br></br>Skin rashes and post-inflammatory scars<br></br>Oral ulcers, angular cheilitis, oral thrush, or oral hairy leukoplakia<br></br>Diarrhoea<br></br>Wasting syndrome<br></br>Changes in mental status or neuropsychiatric function<br></br>Recent hospital admissions<br></br>Tuberculosis (TB)<br></br>Generalised lymphadenopathy<br></br>Kaposi's sarcoma<br></br>Genital STIs<br></br>Chronic vaginal candidiasis<br></br>Shingles</p>

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28
Q

<p>Identify appropriate investigations for human immunodeficiency virus (HIV) and interpret the results.</p>

A

<p>Serum HIV enzyme-linked immunosorbent assay (ELISA)<br></br>Serum HIV rapid test<br></br>HIV non-invasive tests<br></br>Serum Western blot<br></br>Serum p24 antigen<br></br>Serum HIV DNA polymerase chain reaction (PCR)<br></br>CD4 count<br></br>Serum viral load (HIV RNA)<br></br>Serum hepatitis B serology<br></br>Serum hepatitis C serology<br></br>Serum electrolytes<br></br>Serum creatinine<br></br>Urinalysis</p>

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29
Q

<p>Define malaria.</p>

A

<p>Malaria is a parasitic infection caused by protozoa of the genus <em>Plasmodium</em>. Five species are known to infect humans; <em>Plasmodium falciparum</em> is the most life-threatening.</p>

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30
Q

<p>Explain the aetiology/risk factors of malaria.</p>

A

<p>Travel to endemic area<br></br>Inadequate or absent chemoprophylaxis<br></br>Insecticide-treated bed net not used in endemic area<br></br>Settled migrants returning from travel to endemic area of origin<br></br>Low host immunity<br></br>Pregnancy<br></br>Age <5 years<br></br>Immunocompromised<br></br>Older age</p>

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31
Q

<p>Summarise the epidemiology of malaria.</p>

A

<p>There were an estimated 219 million malaria cases worldwide (in 87 countries) in 2017, resulting in an estimated 435,000 deaths. Approximately 92% of all malaria cases and 93% of all malaria deaths occurred in the African region, and the majority of deaths were due to <em>Plasmodium falciparum</em> infection.</p>

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32
Q

<p>Recognise the presenting symptoms of malaria. Recognise the signs of malaria on physical examination.</p>

A

<p>Fever<br></br>Headache<br></br>Myalgia<br></br>Arthralgia<br></br>Diarrhoea<br></br>Nausea and vomiting<br></br>Abdominal pain<br></br>Pallor<br></br>Hepatosplenomegaly, jaundice<br></br>Altered level of consciousness<br></br>Hypotension<br></br>Anuria/oliguria</p>

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33
Q

<p>Identify appropriate investigations for malaria and interpret the results.</p>

A

<p>Giemsa-stained thick and thin blood smears<br></br>Rapid diagnostic tests (RDTs)<br></br>FBC<br></br>Serum electrolytes, urea and creatinine<br></br>Serum LFTs<br></br>Serum blood glucose<br></br>Urinalysis<br></br>Arterial blood gas</p>

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34
Q

<p>Define mastitis and breast abscesses.</p>

A

<p>Mastitis is inflammation of the breast with or without infection. Mastitis with infection may be lactational (puerperal) or non-lactational (e.g., duct ectasia). A breast abscess is a localised area of infection with a walled-off collection of pus. It may or may not be associated with mastitis.</p>

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35
Q

<p>Explain the aetiology/risk factors of mastitis and breast abscesses.</p>

A

<p>Female sex<br></br>Women aged >30 years<br></br>Poor breastfeeding technique<br></br>Lactation<br></br>Milk stasis<br></br>Nipple injury<br></br>Shaving or plucking areola hair<br></br>Anatomical breast defect, mammoplasty, or scar<br></br>Other underlying breast condition<br></br>Staphylococcus aureus carrier<br></br>Immunosuppression</p>

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36
Q

<p>Summarise the epidemiology of mastitis and breast abscesses.</p>

A

<p>The global prevalence of mastitis in lactating women is approximately 1% to 10% but may be higher. Breast abscess develops in 3% to 11% of women with mastitis with a reported incidence of 0.1% to 3.0% in breastfeeding women.</p>

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37
Q

<p>Recognise the presenting symptoms of mastitis and breast abscesses. Recognise the signs of mastitis and breast abscesses on physical examination.</p>

A

<p>Flu-like symptoms, malaise, and myalgia<br></br>Fever<br></br>Breast pain<br></br>Decreased milk outflow<br></br>Breast warmth, tenderness, erythema and swelling<br></br>Breast firmness<br></br>Breast mass<br></br>Nipple discharge<br></br>Nipple inversion/retraction</p>

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38
Q

<p>Identify appropriate investigations for mastitis and breast abscesses and interpret the results.</p>

A

<p>Breast ultrasound<br></br>Diagnostic needle aspiration drainage<br></br>Cytology of nipple discharge or sample from fine-needle aspiration<br></br>Milk, aspirate, discharge, or biopsy tissue for culture and sensitivity<br></br>Histopathological examination of biopsy tissue</p>

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39
Q

<p>Generate a management plan for mastitis and breast abscesses.</p>

A

<p>Antibiotic therapy e.g. Flucloxacillin<br></br>Effective milk removal and supportive care e.g. paracetamol</p>

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40
Q

<p>Identify the possible complications of mastitis and breast abscesses and its management.</p>

A

<p>Cessation of breastfeeding<br></br>Abscess (complicating mastitis)<br></br>Sepsis<br></br>Scarring<br></br>Functional mastectomy<br></br>Breast hypoplasia<br></br>Necrotising fasciitis</p>

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41
Q

<p>Summarise the prognosis for patients with mastitis and breast abscesses.</p>

A

<p>When treated promptly and appropriately, most breast infections, including abscess, will resolve without serious complications. Resolution of mastitis after 2-3 days of appropriate antibiotic therapy is expected among most patients.</p>

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42
Q

<p>Define necrotising fasciitis.</p>

A

<p>Necrotising fasciitis is a life-threatening subcutaneous soft-tissue infection that may extend to the deep fascia, but not into the underlying muscle.</p>

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43
Q

<p>Explain the aetiology/risk factors of necrotising fasciitis.</p>

A

<p>Inpatient contact with index case<br></br>Varicella zoster infection<br></br>Cutaneous injury, surgery, trauma<br></br>Non-traumatic skin lesions<br></br>Intravenous drug use</p>

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44
Q

<p>Summarise the epidemiology of necrotising fasciitis.</p>

A

<p>Absolute data for the incidence and prevalence of necrotising fasciitis are lacking. There is no trend towards an increase or decrease in the prevalence or incidence of necrotising fasciitis, or evidence of global differences in epidemiology.</p>

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45
Q

<p>Recognise the presenting symptoms of necrotising fasciitis. Recognise the signs of necrotising fasciitis on physical examination.</p>

A

<p>Anaesthesia or severe pain over site of cellulitis<br></br>Fever<br></br>Palpitations, tachycardia, tachypnoea, hypotension, and lightheadedness<br></br>Nausea and vomiting<br></br>Delirium<br></br>Crepitus<br></br>Vesicles or bullae<br></br>Grey discoloration of skin<br></br>Oedema or induration</p>

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46
Q

<p>Identify appropriate investigations for necrotising fasciitis and interpret the results.</p>

A

<p>Full blood count and differential<br></br>Serum electrolytes<br></br>Serum urea and creatinine<br></br>CRP<br></br>CK<br></br>Serum lactate<br></br>Blood and tissue cultures<br></br>Gram stain<br></br>ABG<br></br>CT/MRI<br></br>Surgical exploration</p>

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47
Q

<p>Define neutropenic sepsis.</p>

A

<p>Neutropenic sepsis is a potentially life-threatening complication of neutropenia (low neutrophil count). It is defined as a temperature of greater than 38°C or any symptoms and/or signs of sepsis, in a person with an absolute neutrophil count of 0.5 x 10^9/L or lower.</p>

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48
Q

<p>Explain the aetiology/risk factors of neutropenic sepsis.</p>

A

<p>Characteristics of neutropenia<br></br>Rapid rate of decline of the neutrophil count increases infection risk<br></br>Age (infants and >60)<br></br>Chemotherapy<br></br>Corticosteroids<br></br>Antibiotics<br></br>Advanced malignancy<br></br>History of previous febrile neutropenia<br></br>Prolonged hospital admission<br></br>Previous surgery<br></br>Comorbidities</p>

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49
Q

<p>Summarise the epidemiology of neutropenic sepsis.</p>

A

<p>The incidence of neutropenic sepsis is increasing over time, possibly reflecting the increasing use of anticancer and other immunosuppressive drug therapies The incidence of neutropenic sepsis among people with cancer ranges from three cases a month in general hospitals in the UK to over 20 cases a month in specialist haematology/oncology units.</p>

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50
Q

<p>Recognise the presenting symptoms of neutropenic sepsis. Recognise the signs of neutropenic sepsis on physical examination.</p>

A

<p>Dysuria<br></br>Diarrhoea<br></br>Productive cough<br></br>Rapid decline<br></br>Chills, shivers, rigors<br></br>Febrile >38°C (may also present with hypothermia)</p>

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51
Q

<p>Identify appropriate investigations for neutropenic sepsis and interpret the results.</p>

A

<p>FBC<br></br>CRP<br></br>Temperature<br></br>Urinalysis<br></br>Blood culture<br></br>Lactate</p>

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52
Q

<p>Define osteomyelitis.</p>

A

<p>Osteomyelitis is an inflammatory condition of bone caused by an infecting organism, most commonly <em>Staphylococcus aureus</em>. It usually involves a single bone but may rarely affect multiple sites.</p>

53
Q

<p>Explain the aetiology/risk factors of osteomyelitis.</p>

A

<p>Penetrating injuries<br></br>Surgical contamination<br></br>Intravenous drug misuse<br></br>Diabetes mellitus<br></br>Periodontitis</p>

54
Q

<p>Summarise the epidemiology of osteomyelitis.</p>

A

<p>A study in the US showed that the overall age- and sex-adjusted annual incidence of osteomyelitis was 21.8 cases per 100,000 person-years between 1969 and 2009. The annual incidence was higher for men than for women and increased with age.</p>

55
Q

<p>Recognise the presenting symptoms of osteomyelitis. Recognise the signs of osteomyelitis on physical examination.</p>

A

<p>Non-specific pain at site of infection<br></br>Malaise and fatigue<br></br>Local inflammation, erythema, or swelling<br></br>Low-grade fever<br></br>Wound drainage<br></br>Scars, previous flaps<br></br>Reduced range of movement<br></br>Reduced sensation in diabetic foot ulcer</p>

56
Q

<p>Identify appropriate investigations for osteomyelitis and interpret the results.</p>

A

<p>WBC count<br></br>ESR<br></br>CRP<br></br>Plain x-rays of affected area</p>

57
Q

<p>Define pneumonia.</p>

A

<p>Pneumonia is inflammation of the lungs with consolidation or interstitial lung infiltrates, most often categorised according to the causative organism.</p>

58
Q

<p>Explain the aetiology/risk factors of pneumonia.</p>

A

<p>Age >65 years<br></br>Residence in a healthcare setting<br></br>COPD<br></br>Exposure to cigarette smoke<br></br>Alcohol abuse<br></br>Poor oral hygiene<br></br>Use of acid-reducing drugs, inhaled corticosteroids, antipsychotics, antidiabetic drugs<br></br>Contact with children<br></br>HIV infection<br></br>Aspiration risk</p>

59
Q

<p>Summarise the epidemiology of pneumonia.</p>

A

<p>The global burden of diseases, injuries, and risk factors (GDB) study showed that lower respiratory tract infections affected over 336 million people all over the world. HAP and ventilator-associated pneumonia (VAP) are now the most common nosocomial infections (accounting for 22% of the total). In the UK, between 0.5% and 1% of adults will have CAP every year.</p>

60
Q

<p>Recognise the presenting symptoms of pneumonia. Recognise the signs of pneumonia on physical examination.</p>

A

<p>Dyspnoea<br></br>Productive cough<br></br>Fever<br></br>Chest pain<br></br>Asymmetrical expansion of the chest<br></br>Diminished resonance</p>

61
Q

<p>Identify appropriate investigations for pneumonia and interpret the results.</p>

A

<p>Chest x-ray<br></br>FBC<br></br>Serum electrolytes, urea<br></br>Liver function tests<br></br>Blood glucose<br></br>Arterial blood gases/oximetry<br></br>Blood culture<br></br>Sputum culture</p>

62
Q

<p>Generate a management plan for pneumonia.</p>

A

<p>Oral antibiotics e.g. amoxicillin, doxycycline, macrolide<br></br>Supportive care</p>

63
Q

<p>Identify the possible complications of pneumonia and its management.</p>

A

<p>Septic shock<br></br>Acute respiratory distress syndrome (ARDS)<br></br>Antibiotic-associated Clostridium difficile colitis<br></br>Heart failure<br></br>Acute coronary syndrome<br></br>Cardiac arrhythmias<br></br>Necrotising pneumonia<br></br>Pleural effusion<br></br>Lung abscess</p>

64
Q

<p>Summarise the prognosis for patients with pneumonia.</p>

A

<p>Prognosis is determined by 3 major factors: age of the patient, general state of health (presence of comorbidities), and the setting where antibiotic treatment is given.</p>

<p>The all-cause mortality for HAP is 30% to 70%, while the attributable mortality is approximately 10%. Many people with HAP die of their underlying cause. Readmission rates in patients with CAP range from 7% to 12%.</p>

65
Q

<p>Define septic arthritis.</p>

A

<p>Septic arthritis is defined as the infection of 1 or more joints caused by pathogenic inoculation of microbes. It occurs either by direct inoculation or via haematogenous spread.</p>

66
Q

<p>Explain the aetiology/risk factors of septic arthritis.</p>

A

<p>Underlying joint disease<br></br>Joint prostheses<br></br>Intravenous drug abuse<br></br>Diabetes<br></br>Presence of cutaneous ulcers</p>

67
Q

<p>Summarise the epidemiology of septic arthritis.</p>

A

<p>The estimated incidence of septic arthritis in developed countries is 6 cases per 100,000 population per year. In patients with underlying joint disease or with prosthetic joints the incidence increases approximately 10-fold, to 70 cases per 100,000 of the population.</p>

68
Q

<p>Recognise the presenting symptoms of septic arthritis. Recognise the signs of septic arthritis on physical examination.</p>

A

<p>Hot, swollen, tender, restricted joint<br></br>Fever</p>

69
Q

<p>Identify appropriate investigations for septic arthritis and interpret the results.</p>

A

<p>Synovial fluid Gram stain and culture<br></br>Synovial fluid white cell count<br></br>Blood culture<br></br>White cell count<br></br>Erythrocyte sedimentation rate<br></br>CRP<br></br>Plain radiograph<br></br>Ultrasound</p>

70
Q

<p>Define Sjögren's syndrome.</p>

A

<p>Sjögren's syndrome is a systemic auto-immune disorder characterised by the presence of dry eyes (keratoconjunctivitis sicca) and dry mouth (xerostomia) as a consequence of lymphocytic infiltration into the lacrimal and salivary glands.</p>

71
Q

<p>Explain the aetiology/risk factors of Sjögren's syndrome.</p>

A

<p>Female<br></br>Systemic lupus erythematosus (SLE)<br></br>Rheumatoid arthritis<br></br>Systemic sclerosis (scleroderma)<br></br>HLA class II markers<br></br>Age peaks in 20s to 30s and after the menopause</p>

72
Q

<p>Summarise the epidemiology of Sjögren's syndrome.</p>

A

<p>Possibly the most common of all systemic auto-immune rheumatic diseases, Sjögren's syndrome is a systemic auto-immune disorder with a female-to-male ratio of 9:1 and a population prevalence of between 0.5% and 1.56%, depending on the diagnostic criteria used.</p>

73
Q

<p>Recognise the presenting symptoms of Sjögren's syndrome. Recognise the signs of Sjögren's syndrome on physical examination.</p>

A

<p>Fatigue<br></br>Dry eyes<br></br>Dry mouth<br></br>Vasculitis<br></br>Dental caries<br></br>Increased oral fungal and bacterial infections<br></br>Arthralgia<br></br>Myalgia</p>

74
Q

<p>Identify appropriate investigations for Sjögren's syndrome and interpret the results.</p>

A

<p>Schirmer's test<br></br>Anti-60 kD (SS-A) Ro and anti-La (SS-B)</p>

75
Q

<p>What is Schirmer's Test?</p>

A

<p>Quantitatively measures tears. A filter paper is placed in the lower conjunctival sac. The test is positive if less than 5 mm of paper is wetted after 5 minutes.</p>

76
Q

<p>Define spontaneous bacterial peritonitis.</p>

A

<p>Spontaneous bacterial peritonitis (SBP) is an infection of ascitic fluid that cannot be attributed to any intra-abdominal, ongoing inflammatory, or surgically correctable condition. It is one of the most frequently encountered bacterial infections in patients with cirrhosis.</p>

77
Q

<p>Explain the aetiology/risk factors of spontaneous bacterial peritonitis.</p>

A

<p>Decompensated hepatic state (usually cirrhosis)<br></br>Low ascitic protein/complement<br></br>GI bleeding<br></br>Sclerosis of oesophageal varices</p>

78
Q

<p>Summarise the epidemiology of spontaneous bacterial peritonitis.</p>

A

<p>Studies have demonstrated a SBP prevalence of 12% in patients with ascites admitted for decompensated cirrhosis, 18% in those admitted for hepatic encephalopathy, and 10% to 14% in those admitted with acute GI haemorrhage.</p>

79
Q

<p>Recognise the presenting symptoms of spontaneous bacterial peritonitis. Recognise the signs of spontaneous bacterial peritonitis on physical examination.</p>

A

<p>Abdominal pain or tenderness<br></br>Signs of ascites<br></br>Fever<br></br>Nausea/vomiting<br></br>Diarrhoea<br></br>Altered mental status<br></br>GI bleed<br></br>Hypothermia<br></br>Hypotension<br></br>Tachycardia</p>

80
Q

<p>Identify appropriate investigations for spontaneous bacterial peritonitis and interpret the results.</p>

A

<p>FBC<br></br>Serum creatinine<br></br>Ascitic fluid appearance<br></br>Ascitic fluid absolute neutrophil count (ANC)<br></br>Ascitic fluid Gram stain<br></br>Ascitic fluid culture<br></br>Highly-sensitive leukocyte esterase reagent strip testing of ascitic fluid (Periscreen)<br></br>Bedside (standard urine) leukocyte esterase reagent strip testing of ascitic fluid<br></br>Blood cultures<br></br>LFT<br></br>PT/INR<br></br>Ascitic fluid pH and arterial blood pH</p>

81
Q

<p>Generate a management plan for spontaneous bacterial peritonitis.</p>

A

<p>Antibiotics<br></br>Antibiotic and beta-blocker prophylaxis</p>

82
Q

<p>Identify the possible complications of spontaneous bacterial peritonitis and its management.</p>

A

<p>Sepsis/septic shock<br></br>Tense ascites<br></br>Bleeding after paracentesis<br></br>Bowel perforation after paracentesis<br></br>Leakage from paracentesis puncture site<br></br>Renal failure</p>

83
Q

<p>Summarise the prognosis for patients with spontaneous bacterial peritonitis.</p>

A

<p>One-year SBP recurrence rates as high as 69% have been reported. Randomised controlled trials comparing antibiotic regimens have described an in-hospital mortality rate of 10% to 28%.</p>

84
Q

<p>Define systemic lupus erythematosus (SLE).</p>

A

<p>Systemic lupus erythematosus (SLE) is a chronic multisystem disorder that most commonly affects women during their reproductive years. It is characterised by the presence of antinuclear antibodies.</p>

85
Q

<p>Explain the aetiology/risk factors of systemic lupus erythematosus (SLE).</p>

A

<p>Female sex<br></br>Age 15 to 45 years<br></br>African/Asian descent in Europe and US<br></br>Drugs</p>

86
Q

<p>Summarise the epidemiology of systemic lupus erythematosus (SLE).</p>

A

<p>Methods applied to study the epidemiology of SLE have limitations. Common to all studies is that the disease occurs most frequently between the ages of 15 and 45 years, when it is 12 times more common in females than in males.</p>

87
Q

<p>Recognise the presenting symptoms of systemic lupus erythematosus (SLE). Recognise the signs of systemic lupus erythematosus (SLE) on physical examination.</p>

A

<p>Malar (butterfly) rash<br></br>Photosensitive rash<br></br>Discoid rash<br></br>Fatigue<br></br>Weight loss<br></br>Fever<br></br>Oral ulcers<br></br>Alopecia<br></br>Arthralgia/arthritis<br></br>Fibromyalgia<br></br>Raynaud's phenomenon</p>

88
Q

<p>Identify appropriate investigations for systemic lupus erythematosus (SLE) and interpret the results.</p>

A

<p>Anti-DSDNA<br></br>ANA<br></br>FBC and differential<br></br>Activated PTT<br></br>Urea and electrolytes<br></br>Erythrocyte sedimentation rate (ESR) and CRP<br></br>Urinalysis<br></br>Chest x-ray<br></br>ECG</p>

89
Q

<p>Define systemic sclerosis.</p>

A

<p>Systemic sclerosis (SSc), also known as scleroderma, is a multi-system, autoimmune disease, characterised by functional and structural abnormalities of small blood vessels, fibrosis of skin and internal organs, and production of auto-antibodies.</p>

90
Q

<p>Explain the aetiology/risk factors of systemic sclerosis.</p>

A

<p>FHx of scleroderma<br></br>Immune dysregulation (e.g., positive ANA)</p>

91
Q

<p>Summarise the epidemiology of systemic sclerosis.</p>

A

<p>There are different prevalence estimates for scleroderma among different world populations, with higher population estimates in the US than in Europe or Asia. The prevalence of scleroderma is estimated at 88 per million in England.</p>

92
Q

<p>Recognise the presenting symptoms of systemic sclerosis. Recognise the signs of systemic sclerosis on physical examination.</p>

A

<p>Raynaud's phenomenon<br></br>Digital pits or ulcers<br></br>Swelling of the hands and feet<br></br>Skin thickening<br></br>Loss of function of hands<br></br>Sclerodactyly<br></br>Heartburn, reflux, and dysphagia<br></br>Bloating<br></br>Faecal incontinence<br></br>Arthralgias and myalgias</p>

93
Q

<p>Identify appropriate investigations for systemic sclerosis and interpret the results.</p>

A

<p>Serum auto-antibodies<br></br>FBC<br></br>Urea and serum creatinine<br></br>ESR<br></br>C-reactive protein (CRP)<br></br>Urine microscopy<br></br>Complete PFTs (spirometry, lung volumes, and diffusing capacity measurement)<br></br>ECG<br></br>Echocardiogra<br></br>CXR<br></br>Barium swallow</p>

94
Q

<p>Define tonsillitis.</p>

A

<p>Acute tonsillitis is an acute infection of the parenchyma of the palatine tonsils. The clinical distinction between tonsillitis and pharyngitis is unclear in the literature, and the condition is often referred to simply as 'acute sore throat'.</p>

95
Q

<p>Explain the aetiology/risk factors of tonsillitis.</p>

A

<p>Age between 5 and 15 years<br></br>Contact with infected people in enclosed spaces (e.g., child care centres, schools, prison)</p>

96
Q

<p>Summarise the epidemiology of tonsillitis.</p>

A

<p>In UK general practice, recurrent sore throat has an annual incidence of 100 in 1000 population. Acute tonsillitis is more common in children between the ages of 5-15 years.</p>

97
Q

<p>Recognise the presenting symptoms of tonsillitis. Recognise the signs of tonsillitis on physical examination.</p>

A

<p>Pain on swallowing<br></br>Fever (>38°C)<br></br>Tonsillar exudate<br></br>Sudden onset of sore throat<br></br>Headache<br></br>Abdominal pain<br></br>Nausea and vomiting<br></br>Presence of cough or runny nose<br></br>Tonsillar erythema and enlargement<br></br>Enlarged anterior cervical lymph nodes</p>

98
Q

<p>Identify appropriate investigations for tonsillitis and interpret the results.</p>

A

<p>Throat culture<br></br>Rapid streptococcal antigen test</p>

99
Q

<p>Define tuberculosis (extrapulmonary).</p>

A

<p>When TB occurs in organ systems other than the lungs, it is referred to as extrapulmonary TB (EPTB).</p>

100
Q

<p>Explain the aetiology/risk factors of tuberculosis (extrapulmonary).</p>

A

<p>Exposure to TB<br></br>Born in Asia, Latin America, or Africa<br></br>HIV infection<br></br>Immunosuppressive medicines<br></br>Haematological or head/neck malignancy<br></br>End stage renal disease (ESRD)<br></br>Apical fibrosis<br></br>Very young age</p>

101
Q

<p>Summarise the epidemiology of tuberculosis (extrapulmonary).</p>

A

<p>Of the 9272 reported cases of active TB in the US in 2016, 20% had EPTB disease alone. Patients born outside the US accounted for 68.5% of the total cases of TB in 2016.</p>

102
Q

<p>Recognise the presenting symptoms of tuberculosis (extrapulmonary). Recognise the signs of tuberculosis (extrapulmonary) on physical examination.</p>

A

<p>Enlarged lymph node<br></br>Pleuritic chest pain<br></br>Skeletal pain<br></br>Urinary symptoms<br></br>Abdominal swelling<br></br>Abdominal pain<br></br>Cough<br></br>Hepatomegaly<br></br>Fever<br></br>Night sweats</p>

103
Q

<p>Identify appropriate investigations for tuberculosis (extrapulmonary) and interpret the results.</p>

A

<p>Chest x-ray<br></br>Sputum smear<br></br>Sputum culture<br></br>Tuberculin skin testing (TST)<br></br>FBC<br></br>Fine-needle aspiration (FNA)<br></br>Pleural fluid analysis<br></br>Ascitic fluid analysis<br></br>Bone films<br></br>CSF analysis<br></br>Urinalysis<br></br>Nucleic acid amplification test (NAAT)</p>

104
Q

<p>Define tuberculosis (pulmonary).</p>

A

<p>Pulmonary tuberculosis is an infectious disease caused by <em>Mycobacterium tuberculosis</em>. In many cases, <em>M tuberculosis</em> becomes dormant before it progresses to active TB. This is a notifiable disease.</p>

105
Q

<p>Explain the aetiology/risk factors of tuberculosis (pulmonary).</p>

A

<p>Exposure to infection<br></br>Birth in an endemic country<br></br>HIV infection<br></br>Immunosuppressive medicines<br></br>Silicosis<br></br>Apical fibrosis</p>

106
Q

<p>Summarise the epidemiology of tuberculosis (pulmonary).</p>

A

<p>According to WHO data, TB is the ninth leading cause of death worldwide, and is the leading cause of death from a single infectious agent.</p>

107
Q

<p>Recognise the presenting symptoms of tuberculosis (pulmonary). Recognise the signs of tuberculosis (pulmonary) on physical examination.</p>

A

<p>Cough<br></br>Fever<br></br>Anorexia<br></br>Weight loss<br></br>Malaise<br></br>Night sweats<br></br>Pleuritic chest pain<br></br>Haemoptysis</p>

108
Q

<p>Identify appropriate investigations for tuberculosis (pulmonary) and interpret the results.</p>

A

<p>CXR<br></br>Sputum acid-fast bacilli (AFB) smear<br></br>Sputum culture<br></br>FBC<br></br>Nucleic acid amplification tests (NAAT)</p>

109
Q

<p>Define eosinophilic granulomatosis with polyangiitis.</p>

A

<p>Eosinophilic granulomatosis with polyangiitis (EGPA) is a form of primary systemic autoimmune vasculitis characterised by inflammation of blood vessels. In EGPA, vasculitis is associated with asthma and eosinophilia. EGPA is also known as Churg-Strauss syndrome (CSS).</p>

110
Q

<p>Explain the aetiology/risk factors of eosinophilic granulomatosis with polyangiitis.</p>

A

<p>History of asthma, allergic rhinitis, or sinusitis<br></br>Use of certain medications</p>

111
Q

<p>Summarise the epidemiology of eosinophilic granulomatosis with polyangiitis.</p>

A

<p>EGPA is the most rare of the three anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides, with an estimated annual incidence of between 1 and 3 cases per million people. Among asthma patients, the incidence is as high as 67 per million asthma patients.</p>

112
Q

<p>Recognise the presenting symptoms of eosinophilic granulomatosis with polyangiitis. Recognise the signs of eosinophilic granulomatosis with polyangiitis on physical examination.</p>

A

<p>Focal numbness or weakness<br></br>Nasal discharge or stuffiness, or facial pain<br></br>Palpable purpura and petechiae<br></br>Wheeze<br></br>Haemoptysis<br></br>Skin nodules<br></br>Fatigue, arthralgias, myalgias<br></br>Shortness of breath or cough<br></br>Abdominal pain</p>

113
Q

<p>Identify appropriate investigations for eosinophilic granulomatosis with polyangiitis and interpret the results.</p>

A

<p>FBC with differential<br></br>Serum anti-neutrophil cytoplasmic antibodies (ANCA)<br></br>Serum CRP<br></br>Erythrocyte sedimentation rate<br></br>Serum urea and creatinine<br></br>Urinalysis<br></br>Pulmonary function test<br></br>Chest x-ray<br></br>Echocardiogram</p>

114
Q

<p>Define granulomatosis with polyangiitis.</p>

A

<p>Granulomatosis with polyangiitis (formerly known as Wegener's granulomatosis) is a systemic vasculitis that typically involves small and medium vessels. Although any organ may be targeted, the classic triad consists of upper and lower respiratory tract involvement and pauci-immune glomerulonephritis.</p>

115
Q

<p>Explain the aetiology/risk factors of granulomatosis with polyangiitis.</p>

A

<p>Genetic predisposition<br></br>Infection<br></br>Environmental exposures<br></br>All of these have a weak association, though.</p>

116
Q

<p>Summarise the epidemiology of granulomatosis with polyangiitis.</p>

A

<p>The incidence and prevalence of granulomatosis with polyangiitis (GPA) (formerly known as Wegener's granulomatosis) varies considerably between countries. GPA can occur at any age. The mean age of onset in most series is between 40 and 60 years of age, with an approximately equal gender distribution. It is most commonly seen in white people, but can also occur in other racial and ethnic groups.</p>

117
Q

<p>Recognise the presenting symptoms of granulomatosis with polyangiitis. Recognise the signs of granulomatosis with polyangiitis on physical examination.</p>

A

<p>Upper and lower respiratory tract involvement<br></br>Renal involvement<br></br>Constitutional features<br></br>Ocular manifestations<br></br>Cutaneous manifestations<br></br>Musculoskeletal manifestations<br></br>Neurological manifestations</p>

118
Q

<p>Identify appropriate investigations for granulomatosis with polyangiitis and interpret the results.</p>

A

<p>Urinalysis and microscopy<br></br>CT chest<br></br>Anti-neutrophil cytoplasmic antibody (ANCA)<br></br>FBC and differential<br></br>Serum creatinine<br></br>Erythrocyte sedimentation rate (ESR)</p>

119
Q

<p>Define polyarteritis nodosa.</p>

A

<p>Polyarteritis nodosa (PAN) is a rare disease that results from blood vessel inflammation ("vasculitis") causing injury to organ systems. The areas most commonly affected by PAN include the nerves, intestinal tract, heart, and joints.</p>

120
Q

<p>Explain the aetiology/risk factors of polyarteritis nodosa.</p>

A

<p>Hepatitis B virus (HBV) infection<br></br>Age 40 to 60 years</p>

121
Q

<p>Summarise the epidemiology of polyarteritis nodosa.</p>

A

<p>Over time, polyarteritis nodosa (PAN) has become progressively less common, largely owing to effective hepatitis B virus (HBV) immunisation programmes and improved blood screening for HBV, as well as to major alterations in the definition and classification of vasculitis.</p>

122
Q

<p>Recognise the presenting symptoms of polyarteritis nodosa. Recognise the signs of polyarteritis nodosa on physical examination.</p>

A

<p>Age 40 to 60 years<br></br>Fever<br></br>Weight loss<br></br>Myalgia or arthralgia<br></br>Mononeuritis multiplex<br></br>Paraesthesia<br></br>Muscle tenderness<br></br>Abdominal pain<br></br>Skin manifestations<br></br>Diastolic blood pressure >90 mmHg</p>

123
Q

<p>Identify appropriate investigations for polyarteritis nodosa and interpret the results.</p>

A

<p>CRP<br></br>ESR<br></br>FBC<br></br>Complement<br></br>Serum creatinine<br></br>Midstream urine analysis<br></br>Liver function tests<br></br>HBV serology<br></br>Hepatitis C virus (HCV) serology<br></br>ANCA, ANA, Anti-DSDNA</p>

124
Q

<p>Define Takayasu arteritis.</p>

A

<p>Takayasu arteritis is a chronic granulomatous vasculitis affecting large arteries: primarily the aorta and its main branches. Vascular inflammation can cause stenosis, occlusion, and aneurysm formation.</p>

125
Q

<p>Explain the aetiology/risk factors of Takayasu arteritis.</p>

A

<p>Genetic predisposition<br></br>Female sex<br></br>Age <40<br></br>Asian ethnicity</p>

126
Q

<p>Summarise the epidemiology of Takayasu arteritis.</p>

A

<p>Takayasu arteritis is a rare disease. Its distribution is worldwide, although most cases are reported in Asian populations. Women in Japan affected about 8 times more frequently than men, whereas in India, men and women are equally represented.</p>

127
Q

<p>Recognise the presenting symptoms of Takayasu arteritis. Recognise the signs of Takayasu arteritis on physical examination.</p>

A

<p>Upper or lower limb claudication<br></br>Absent pulse(s)<br></br>Unequal blood pressures<br></br>Vascular bruits<br></br>Low-grade fever<br></br>Transient ischaemic attack (TIA)<br></br>Myalgia/arthralgia<br></br>Weight loss<br></br>Fatigue</p>

128
Q

<p>Identify appropriate investigations for Takayasu arteritis and interpret the results.</p>

A

<p>ESR<br></br>CRP<br></br>Computerised tomography angiography (CTA)<br></br>Magnetic resonance imaging angiography (MRA)</p>