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Year 3 - Diseases > Infection and Immunology > Flashcards

Infection and Immunology Flashcards

1
Q

Define cellulitis and erysipelas

A
  • Cellulitis is an acute bacterial infection of the dermis and subcutaneous tissue.
  • Erysipelas is a superficial form, affecting the dermis. It is well demaracated, and sepsis is less likely
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2
Q

List risk factors of cellulitis

A
  • Trauma, leg ulceration, maceration or eczema (break in the skin)
  • Insect bites
  • Lymphoedema
  • Leg oedema
  • Venous insufficiency and history of venous surgery
  • Obesity
  • Pregnancy
  • Chicken pox
  • Conditions that predispose infection (eg. diabetes)
  • Neuropathy
  • Alcohol misuse
  • Recurrent - elderly, previous cellulitis, chronic lymphoedema
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3
Q

List common causative agents of cellulitis

A
  • Strep pyogenes

- Staph aureus

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4
Q

Describe prevalence of cellulitis

A
  • 0.2 per 1000 person years to 24.6 per 1000 person years

- Recurrence common

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5
Q

List symptoms of cellulitis

A
  • Acute onset of red, painful, hot, swollen skin
  • Spreads rapidly
  • Fever, malaise, nausea, shivering, rigors
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6
Q

List signs of cellulitis

A
  • Tender skin
  • Obvious break in the skin where an organism may have entered
  • Diffuse redness, well demarcated edge
  • Blisters and bullae
  • Inflamed lymph nodes or lymphangitis (presence of red, linear streaks spreading proximally from the area of cellulitis, peau d’orange appearance)
  • Ulceration
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7
Q

Describe classification of cellulitis

A
  • Class I — there are no signs of systemic toxicity and the person has no uncontrolled comorbidities.
  • Class II — the person is either systemically unwell or systemically well but with a comorbidity (for example peripheral arterial disease, chronic venous insufficiency, or morbid obesity) which may complicate or delay resolution of infection.
  • Class III — the person has significant systemic upset, such as acute confusion, tachycardia, tachypnoea, hypotension, or unstable comorbidities that may interfere with a response to treatment, or a limb-threatening infection due to vascular compromize.
  • Class IV — the person has sepsis or a severe life-threatening infection, such as necrotizing fasciitis.
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8
Q

Describe investigations performed in cellulitis

A
  • Swab for culture
  • Ultrasonography (abscess, drainable fluid collection)
  • Skin biopsy
  • WBC, ESR, CRP
  • If orbital, CT/MRI
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9
Q

Describe management of cellulitis

A
  • Draw around the lesion and monitor
  • Antibiotics (oral amox if possible, review IV after 48 hours to switch to oral, if MRSA trimethoprim-sulfamethoxazole)
  • Hospital admission if class IV or III, rapidly deteriorating, young, immunocompromised, facial, or significant lymphoedema
  • Referral if severely unwell, infection near eyes or nose, uncommon pathogen, lymphangitis, cannot take oral antibiotics, not responding to oral antibiotics)
  • Recurrent episodes refer
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10
Q

List complications of cellulitis

A

Acute

  • Necrotizing fasciitis (rapidly progressive, extensive gangrene and necrosis of skin and underlying structures)
  • Myositis
  • Sepsis
  • Subcutaneous abscesses
  • Post streptococcal nephritis

Chronic complications

  • Persistent leg ulceration
  • Lymphoedema
  • Recurrent cellulitis
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11
Q

Describe prognosis of cellulitis

A
  • Most cases resolve with treatment
  • After 12 months, 29.4% of patients had at least 1 recurrence
  • Length of hospitalization increases with each subsequent recurrence
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12
Q

Define anaphylaxis

A

A severe, generalised or systemic hypersensitivity reaction, characterised by rapidly developing life-threatening airway and/or breathing and/or circulation problems usually associated with skin and mucosal changes

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13
Q

Describe epidemiology of anaphylaxis

A
  • Risen by 70% in the last 5 years
  • Most commonly food allergic reactions in young children
  • Affects both sexes equally
  • 1/3 is food related
  • Medicines are common causes in adults
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14
Q

List risk factors of anaphylaxis

A
  • Less than 30 at risk of food and exercise related
  • Atopy/ asthma
  • History of anaphylaxis
  • Exposure to a common sensitiser (eg. latex)
  • Adults at risk of food, insect venom and medicine related
  • Female sex more at risk of food-associated and exercise associated
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15
Q

List symptoms of anaphylaxis

A
  • Acute onset
  • Angiooedema (airway swelling, tongue)
  • SOB
  • Respiratory arrest
  • Confusion
  • Hives
  • Pruritis
  • Nausea, vomiting, diarrhoea, incontinence
  • Abdominal cramps and pain
  • Agitation, anxiety, sense of impending doom
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16
Q

List signs of anaphylaxis

A
  • Inspiratory stridor and hoarse voice
  • Chest hyperinflation, accessory muscle use, wheeze
  • Cyanosis
  • Pale clammy skin
  • Hypotension
  • Tachycardia
  • Respiratory arrest
  • Bradycardia
  • Urticaria
  • Erythema
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17
Q

List investigations for anaphylaxis

A
  • Mast cell tryptase (16 years or over during or soon after resusitation, one as soon as possible, one 1-2 hours after symptoms, one 24 hours. May be elevated)
  • Plasma histamine
  • ECG (non-specific ST changes)
  • Urea and electrolytes (normal)
  • ABG (elevated lactate)
  • CXR (hyperinflation, interstitial fluid)
  • Allergy testing follow up
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18
Q

Describe management of anaphylaxis

A
  • CPR and ALS if arrested
  • ABCDE
  • IM adrenaline 0.5ml 1:1000
  • Airway + high flow oxygen, legs in the air
  • IV fluids, chlorphenamine and hydrocortisone
  • Cardioresp assess
  • Consider nebulised adrenaline, SABA, atropine, glucagon

After initial treatment

  • Antihistamine (chlorphenamine)
  • Corticosteroid (hydrocortisone sodium succinate)
  • Monitor for biphasic reaction
  • Review by senior clinician and observation
  • Give patient adrenaline auto-injector (eg. Epipen)
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19
Q

List complications of anaphylaxis

A
  • MI

- Recurrence

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20
Q

Describe prognosis of anaphylaxis

A
  • Severity of previous reaction does not predict severity of subsequent events, treatment does
  • Serious sequelae of inadequate brain perfusion may occur, prognosis of MI depends on comorbidities and patient age
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21
Q

Which skin condition is aspirin linked to?

A

Urticaria

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22
Q

What specific inflammatory marker is raised in sepsis?

A

TNFa

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23
Q

Compare sepsis, septic shock and SIRS

A
  • SIRS consists of changes in clinical signs including an abnormal body temperature, increased heart rate, increased respiratory rate, an abnormal white cell count (either decreased or elevated), or an increase in band neutrophils due to a severe inflammatory response resulting in organ dysfunction
  • Sepsis is SIRS with an infectious cause. Life threatening organ dysfunction caused by dysregulated host response to infection
  • Septic shock is lactate over 2mmol/l despite good fluid resucitation, or patient requiring vasopressers to maintain MAP over 65
  • Septicaemia is an infection in the bloodstream
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24
Q

Define SLE

A

A chronic multi-system disorder that most commonly affects women during their reproductive years. It is characterised by the presence of antinuclear antibodies

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25
Q

Describe epidemiology of SLE

A
  • Age 15-45 most commonly
  • 9 times more common in females
  • Over age 45, 2 times more common in females
  • 97 per 100000 prevalence UK
  • More common and more severe in those of African descent
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26
Q

Describe aetiology of SLE

A
  • Genetic factors (familial aggregation, higher concordance in twin studies, more common if compliment deficiency). 95% ANA +ve, anti-dsDNA more specific. Associated with HLA B8, DR2 and DR3
  • IRF5 gene polymorphisms
  • Environmental factors (non-infectious like drugs, and infectious like epstein barr, smoking)
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27
Q

List symptoms and signs of SLE

A
  • Malar (butterfly rash)
  • Photosensitivie rash
  • Discoid rash
  • Fatigue
  • Weight loss
  • Fever
  • Oral ulcers
  • Alopecia
  • Arthralgia/arthritis
  • Fibromyalgia
  • Raynauds
  • Chest pain SOB
  • Venous or arterial thrombosis
  • Hypertension
  • Signs of nephrosis
  • Lymphadenopathy
  • Abdo pain, vomiting, diarrhoea
  • Nose ulcers, poorly localised proximal limb inflammatory pain with weakness
  • Dysrhythmias, conduction defects, or unexplained cardiomegaly
  • CNS signs (psychosis, seizures)
  • Dysphagia
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28
Q

List risk factors for SLE

A
  • Female sex
  • Age 15 to 45 years
  • African/Asian descent
  • Drugs (procainamide, minocycline, phenytoin, carbamasepine)
  • Sun exposure
  • Family history (DR3 and 4)
  • Tobacco smoking
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29
Q

Describe investigations of SLE

A
  • FBC (anaemia, leukopenia, thrombocytopenia)
  • aPTT (may be prolonged)
  • U and E (urea and creatinine raised)
  • ESR and CRP (raised, CRP normally lower or even normal)
  • ANA, dsDNA, smith antigen (positive, smith and dsDNA very specific for SLE)
  • Urinalysis (haematuria, casts, proteinuria)
  • CXR (pleural effusion, infiltrates, cardiomegaly)
  • ECG
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30
Q

Define vasculitide

A
  • Heterogeneous group of autoimmune disease characterised by inflammation of blood vessels (vasculitis) and subsequent ischaemia and damage to the organs supplied by these vessels
  • Primary is idiopathic
  • Secondary has an underlying cause
  • May be small vessel, medium vessel or large vessel
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31
Q

Describe aetiology of vasculitides

A
  • Primary is idiopathic

- Secondary may include response to hep B, hep C, myeloma or autoimmune disease

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32
Q

Define eosinophilic granulomatosis with polyangiitis

A

A multisystem disease characterised by necrotizing granulomatous vasculitis with eosinophilia. Most commonly affects the lungs and skin but can affect the renal, CV, GI, central and peripheral nervous system. Also called Churg Strauss syndrome

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33
Q

Describe epidemiology of eosinophilic granulomatosis with polyangiitis

A
  • 1-3 cases per million people.
  • 67 per million in asthma patients
  • Typically diagnosed in middle age
  • Male predominance
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34
Q

List risk factors for eosinophilic granulomatosis with polyangiitis

A
  • Asthma, allergic rhinitis or sinusitis

- Use of some medications (macrolide antibiotics and quinidine)

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35
Q

List symptoms of eosinophilic granulomatosis with polyangitis

A
  • Focal numbness or weakness
  • Nasal discharge or stuffiness or facial pain
  • Haemoptysis
  • Fatigue, arthralgias, myalgias
  • SOB/cough
  • Abdo pain
  • Orthopnoea
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36
Q

List signs of eosinophilic granulomatosis with polyangiitis

A
  • Palpable purpura and petechiae
  • Wheeze
  • Skin nodules
  • Sensory or motor deficit
  • Tachypnoea
  • Rales
  • Peripheral oedema
  • Hepatojugular reflux
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37
Q

List investigations for eosinophilic granulomatosis with polyangiitis

A
  • FBC (raised eosinophils)
  • Serum anti-neutrophil cytoplasmic antibodies (+ve pANCA)
  • CRP (raised)
  • ESR (raised)
  • U and E, urinalysis (glomerulonephritis)
  • Pulmonary function test (reversible airway obstruction
  • CXR
  • ECG (left ventriular wall abnormalities, intracardiac thrombus, pericardial effusion)
  • Flow cytometry of peripheral blood (normal)
  • Mutation testing
  • IgE (raised)
  • Stool sample
  • CT chest (may show pulmonary nodules)
  • Electromyogram
  • BAL/broncoscopy
  • Biopsy affected tissue
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38
Q

Define granulomatosis with polyangiitis

A

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. Also called Wegners Granulomatosis.

C disease- curvy nose, cANCA, chronic sinusitis

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39
Q

Describe epidemiology of granulomatosis with polyangiitis

A
  • In the US 3 per 100,000
  • In Sweden 160 per million
  • Can occur at any age (mean age 40-60)
  • Equal gender distribution
  • Most common in white people
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40
Q

List risk factors/aetiology for granulomatosis with polyangiitis

A
  • Genetic predisposition
  • Infection
  • Environmental factors (silica, heavy metals, other chemicals)
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41
Q

List signs and symptoms of granulmatosis with polyangiitis

A
  • Upper respiratory tract (otorrhoea, pain in ears, sinus pain, nasal discharge, epistaxis, hoarseness, stridor, ulcers, mucosal bleeding, sinus tenderness)
  • Saddle nose
  • Lowe respiratory tract (SOB, cough, heamoptysis, chest pain, dyspnoea, dullness on percussion, crackles)
  • Renal involvement (oedema, hypertension)

Non-triad:

  • Non specific symptoms eg. fatigue, malaise, weight loss, night sweats, anorexia
  • Ocular manifestations (eg. redness, visual loss and pain)
  • Cutaneous manifestations (purpura or petichea, ulcerative lesions)
  • Musculoskeletal manifestations (myalgia/artralgia)
  • Neurological manifestations (mononeuritis multiplex)
  • Thromboembolism
  • GI involvement (abdo pain, vomiting, diarrhoea, blood or mucus in stool)
  • Cardiac involvement (pericarditis, myocarditis - chest pain, fatigue cough wheeze oedema)
  • Breast mass
  • Lower GU tract (dysuria/pelvic pain)
  • Endocrine involvement
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42
Q

List investigations for granulomatosis with polyangiitis

A
  • Urinalysis and microscopy (haematuria, proteinurea, RBC casts, dysmorphic red blood cells)
  • CT chest/CXR (lung cavitations)
  • Anti-neutrophil cytoplasmic antibody (ANCA - positive sufficient for diagnosis with otorhinolarygeal, lung and renal involvement. cANCA 80% or pANCA 15%)
  • FBC (anaemia)
  • Serum creatinine (raised)
  • Erythrocyte sedimentation rate (ESR- raised)
  • Tissue biopsy (granulomatous inflammation, necrosis and vasculitis, minimal immune deposits)
  • Pulmonary function testing
  • Bronchoscopy
  • Electromyography/nerve conduction studies
  • Upper airway endoscopy
  • CT sinuses
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43
Q

Define microscopic polyangiitis

A

Necrotising vasculitis of small vessels typically with renal, pulmonary and skin involvement. Nasopharynx not affected

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44
Q

List common signs and symptoms of microscopic polyangiitis

A
  • Renal (90%) pauci-immune glomerulonephritis with hypertension
  • Lungs (50%) pulmonary vasculitis with haemoptysis - no URT
  • Skin (40%) palpable purpura, nodules, necrosis
  • Tiredness, anorexia, joint and muscle aches
  • Mononeuritis multiplex
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45
Q

Describe investigations for microscopic polyangiitis

A
  • Biopsy of involved organ (fibrinoid necrosis with infiltration of neutrophils, no granulomas)
  • MPO-ANCA/pANCA, U and E, Creatinine
  • Urinalysis for haematuria and proteinuria
  • CXR showing cavitating lesions
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46
Q

Describe epidemiology of microscopic polyangiitis

A
  • Commonest in middle aged people

- Affects both men and women

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47
Q

Define polyarteritis nodosa

A

Necrotising inflammation of medium-sized or small arteries without glomerulonephritis or vasculitis in arterioles, capillaries, or venules

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48
Q

Describe epidemiology of polyarteritis nodosa

A
  • Progressively becoming less common
  • 2 - 9 per million/year in Europe and US
  • 31 - 33 per million in western europe
  • Higher where HBV is endemic
  • 40-60 most common
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49
Q

Describe aetiology of polyarteritis nodosa

A
  • Hepatitis B implicated very commonly
  • Deposition of immune complexes
  • Genetic, infectious and environmental agents may be important
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50
Q

List risk factors for polyarteritis nodosa

A
  • Hepatitis B virus (HBV) infection
  • Age 40 to 60 years
  • Hairy cell leukaemia
  • Blood transfusion at a time before routine screening for HBV
  • Hepatitis C virus (HCV) infection
  • Male sex
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51
Q

List symptoms of polyarteritis nodosa

A
  • Fever
  • Weight loss
  • Myalgia or arthralgia
  • Paraesthesia
  • Muscle tenderness
  • Abdominal pain
  • Testicular pain
  • Seizure
  • GI bleeding
  • Peritonitis (ischaemic bowel- pain)
  • Monocular blindness
  • Chest pain (ischaemic)
  • Congestive cardiac failure
  • Tender breast lumps
  • Skin: livedo retiularis
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52
Q

List signs of polyarteritis nodosa

A
  • Skin manifestations (peripheral neuropathy)
  • Diastolic blood pressure >90 mmHg
  • Mononeuritis multiplex
  • Upper motor neuron weakness
  • Peritonitis (tender rigid abdomen, patient immobile)
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53
Q

List investigations for polyarteritis nodosa

A
  • CRP (raised), ESR (raised), FBC (normocytic anaemia, rasied WBC and platelets), LFT, complement (reduced), creatinine
  • Midstream urine analysis
  • HBV + HCV serology
  • Cryoglobulins (no- HCV)
  • Blood culture
  • Creatine kinase
  • ANCA, ANA, anti-dsDNA, rheumatoid factor, anti-CCP antibodies, lupus anticoagulant, IgG antiphospholipid antibodies (negative)
  • B2 glycoprotein
  • Fibrinogen
  • Conventional digital subtraction angiography (microaneurysms, vessel ectasia, or focal occlusive lesions in medium-sized vessels)
  • Echocardiography
  • Magnetic resonance angiography (MRA) rosary sign
  • CT angiography ROSARY SIGN (bead like appearance on angiogram)
  • Biopsy of affected tissue
  • HIV serology
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54
Q

Define takayasu arteritis

A
  • A chronic granulomatous vasculitis affecting large arteries: primarily the aorta and its main branches.
  • Vascular inflammation can cause stenosis, occlusion, and aneurysm formation.
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55
Q

Describe epidemiology of takayasu arteritis

A
  • US 2.6 cases per million
  • In Japan 1 in every 3000 autopsies
  • Women affected 8 times more in japan, but men and women affected equally in India
  • The peak incidence is usually in the third decade of life, although among Japanese people it typically presents between the ages of 15 and 25. In European people the mean age at diagnosis is 41.
  • Patients in the US are more likely than those in Japanto have constitutional and musculoskeletal symptoms, claudication, and visual changes
  • More common in women
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56
Q

Describe aetiology of takayasu arteritis

A
  • Environmental and genetic factors are thought to play roles in the development of the disease.
  • Cell-mediated immune mechanisms have been implicated.
  • Genetic screening has shown polymorphisms in IL-12, IL-6, and IL-2 genes
  • HLA-Bw5 and HLA-B39.2 are reportedly increased in frequency in some populations.
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57
Q

List risk factors for takayasu arteritis

A
  • Genetic predisposition
  • Female sex
  • Age <40
  • Asian ethnicity
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58
Q

List symptoms of takayasu arteritis

A
  • Upper or lower limb claudication
  • Transient ischaemic attack (TIA)
  • Myalgia
  • Arthralgia
  • Weight loss
  • Fatigue
  • Dizziness on upper-limb exertion
  • Stroke
  • Chest pain
  • Abdominal pain
  • Diarrhoea
  • Shortness of breath
  • Haemoptysis
  • Night sweats
  • Vertigo
  • Syncope
  • Headache
  • Visual symptoms
59
Q

List signs of takayasu artertis

A
  • Hypertension
  • Absent pulse(s)
  • Unequal blood pressures
  • Vascular bruits
  • Low-grade fever
  • Heart murmur
  • Erythema nodosum
  • Pyoderma gangrenosum (a rare, inflammatory skin disease where painful pustules or nodules become ulcers that progressively grow)
60
Q

List investigations for takayasu arteritis

A
  • ESR (high)
  • CRP (high)
  • Computerised tomography angiography (segmental narrowing or occlusion, occasionally dilation, of affected vessels; aortic aneurysms may be seen; thickening of vessel walls)
  • Magnetic resonance imaging angiography (same as above)
  • Catheter angiogram (same as above)
  • Doppler ultrasound (same as above)
  • Positron emission tomography with radiolabelled fluorodeoxyglucose (PET-FDG - increased uptake in actively inflamed areas)
61
Q

List sepsis 6

A
  • Give high flow oxygen
  • Give IV fluid challenge
  • Give antibiotics
  • Take blood for culture
  • Take lactate measurement
  • Take measurement of urine output
62
Q

List the human herpes viruses, their transmission route and clinical presentation

A

HHV1 (HSV1)

  • Respiratory/saliva
  • Gingivostomatitis, keratoconjunctivitis, herpes labialis, temporal lobe encephalitis

HHV2 (HSV2)

  • Sexual contact, perinatal
  • Genital herpes, neonatal herpes

HHV3 (VZV)

  • Respiratory
  • Chicken pox and shingles

HHV4 (EBV)

  • Saliva (kissing disease)
  • Mononucleosis

HHV5 (CMV)

  • Congenital, sexual, saliva
  • Mononucleosis in the immunocompromised

HHV6&7

  • Saliva
  • Roseola infantum

HHV8

  • Sexual contact
  • Kaposi sarcoma
63
Q

Define herpes simplex virus

A

Disease resulting from HSV1 or 2 infection

64
Q

Describe epidemiology of herpes simplex virus

A
  • Very common, 90% of adults are seropositive for HSV1 by 30 years
  • HSV1 2/3 population
  • HSV2 11% population
65
Q

Describe aetiology of HSV

A
  • Dominant in primary infection (trigeminal/sacral root ganglia)
  • Reactivation occurs in response to physical or emotional stress, or immunosuppression
  • Latent phase is asymptomatic, lytic phase is transport of virus to skin
66
Q

Describe signs and symptoms of HSV1

A
  • Gingivostomatitis, cold sores (herpes labialis - ulcers filled with yellow slough near the mouth)
  • Herpetic whitlow (on finger)
  • Eczema herpeticum
  • Systemic infection (fever, sore throat, lympadenopathy, pneumonitis, hepatitis)
  • Herpes simplex meningitis, encephalitis
  • Keratoconjunctivitis
67
Q

Describe signs and symptoms of HSV2

A
  • Genital herpes (flu like prodrome, vesicles/papules around genitals/anus which are painful)
  • Shallow ulcers
  • Urethral discharge
  • Dysuria
  • Fever and malaise
68
Q

Describe investigations for HSV

A
  • Clinical diagnosis

- Viral culture and HSV PCR (CSF, swab) in encephalitis, keratoconjunctivitis or immunosuppression

69
Q

List risks for HSV

A
  • HIV infection (risk factor for clinical disease)
  • Immunosuppressive medications (risk factor for clinical disease)
  • High-risk sexual behaviour (risk factor for seropositivity)
  • Female sex (risk factor for seropositivity)
  • Black race (risk factor for seropositivity)
  • Increasing age (risk factor for seropositivity)
  • Lack of condom use (risk factor for seropositivity)
70
Q

Define varicella zoster virus

A
  • Primary infection is called varicella (chickenpox).

- Reactivation of the dormant virus in the dorsal root ganglia, causes zoster (shingles).

71
Q

Describe epidemiology of varicella zoster virus

A
  • Chickenpox peak incidence: 4–10 years
  • Shingles peak incidence: >50 years.
  • About 90% of adults are VZV IgG positive.
72
Q

Describe signs and symptoms of chicken pox

A
  • Prodromal malaise
  • Mild pyrexia
  • Generalised pruritic, vesicular rash - face and trunk predominantly
  • Contagious from 48 h before the rash and until all the vesicles have crusted over (within 7–10 days).
73
Q

Describe signs and symptoms of shingles

A
  • May occur due to stress
  • Tingling in a dermatomal distribution
  • Followed by painful skin lesions, pruritic and vesicular again
  • Unilateral
  • Recovery in 10–14 days.
74
Q

Describe aetiology of varicella zoster

A
  • Droplet spread
  • Replicates in lymph nodes
  • Disseminates in mononuclear cells to skin
75
Q

List risks for varicella zoster

A
  • Age 1 to 9 years
  • Exposure to varicella
  • Unimmunised status
  • Occupational exposure
76
Q

Describe investigations for varicella zoster

A
  • Clinical diagnosis

- Consider PCR, viral culture, ELISA,

77
Q

Describe management of varicella zoster

A

Children w/chickenpox

  • Calamine lotion
  • Analgesia
  • Antihistamines

Adults w/chicken pox
- Aciclovir, valaciclovir, famciclovir if within 24h of rash onset

Shingles

  • Valacilovir or famciclovir first line, aciclovir second line
  • Within 72 h appearache of the rash for 7 days

If pregnant or immunosuppressed
- IV aciclovir

78
Q

List complications of varicella zoster virus

A

Acute

  • Bacterial sepsis
  • Pneumonia
  • Encephalitis
  • Haemorrhagic complications

Without rash

  • Meningoencephalitis
  • Myelitis
  • CN palsies
  • Vasculopathy
  • GI ulcers
  • Pancreatitis
  • Hepatitis

15% elderly patients get postherpetic neuralgia

79
Q

Describe prognosis of varicella zoster

A
  • Typically, varicella is a self-limiting disease.
  • After initial infection and clinical syndrome, no follow-up is necessary.
  • In up to one third of infected people, varicella-zoster virus reactivates later in life as shingles or herpes zoster.
80
Q

Define HIV

A
  • A retrovirus (RNA) which infects and replicates in human CD4 T cells and macropages
  • HIV1 and HIV2
  • Leads to progressive immune dysfunction, opportunistic infection and malignancy (acquired immunodeficiency syndrome - AIDS)
81
Q

Describe aetiology/risks of HIV

A
  • Sexual contact
  • Pregnancy, childbirth ad breast feeding
  • Injection drug use
  • Occupational exposure
  • Blood transfusion or organ transplant
82
Q

Describe symptoms of HIV infection

A
  • Flu-like
  • Feeling fine
  • Falling count
  • Final crisis

Three phases:

  1. Seroconversion: (4–8 weeks post-infection), self-limiting – fever, night sweats, generalized lymphadenopathy, sore throat, oral ulcers, erythematous maculopapular rash, myalgia, headache, encephalitis, diarrhoea.
  2. Early/asymptomatic: (18 months to 15 years), apparently well – some patients may have persistent lymphadenopathy (>1 cm nodes, at 2 extrainguinal sites for >3 months). Progressive minor symptoms, e.g. rash, oral thrush, weight loss, malaise.
  3. AIDS: Syndrome of secondary diseases reflecting severe immunodeficiency or direct effect of HIV infection (CD4 cell count <200/mm3).
83
Q

Describe epidemiology of HIV

A
  • 37 million adults and children living with HIV worldwide
  • 1.2 million deaths per year
  • Africa has most of the disease (26 million, 760000 mortality a year and 1% of the worlds wealth)
  • In the UK 100000 living with HIV, 1.9/1000
  • 5% of men who have had sex with men
  • 17% unaware they have HIV
  • HIV1 is seen globally, HIV2 is seen in west africa
84
Q

Describe pathophysiology of HIV

A
  • Binds via GP120 envelope glucoprotein to CD4 receptors on helper T cells, monocytes, and macrophages
  • CD4 cells migrate to lymphoid tissue, virus replicates and makes billions of new virions
  • These are released and infect new CD4 cells
85
Q

Describe prevention of HIV

A
  • Consistent use of condoms
  • Post-exposure prophylaxis (anti-retroviral therapy after exposure, can be given up to 72h after exposure - tenofir and raltegravir)
  • Pre-exposure prophylaxis (for those at risk of HIV)
  • All pregnant women with HIV have ART by 24 weeks gestation. Caesarian delivery indicated if viral load over 50 copies)
86
Q

List common infections in HIV

A

Bacterial:
- Mycobacteria (lungs, GI, skin), staphylococci, Salmonella, capsulated organisms

Viral: CMV, HSV (encephalitis), VZV (recurrent shingles), HPV (warts), papovavirus (progressive multifocal leukoencephalopathy), EBV (oral hairy leukoplakia), JC virus (progressive multifocal leukoencephalopathy)

Fungal: Pneumocystis pneumonia (PCP), Cryptococcus (meningitis), Candida, invasive aspergillosis.

Protozoal: Toxoplasmosis, cryptosporidia and microsporidia (diarrhoea).

87
Q

Define hairy luekoplakia and its cause

A
  • Irregular, white, painless plaques on lateral tongue that cannot be scraped off
  • EBV mediated, occurs in HIV positive patients and organ transplant recipients
88
Q

List HIV associated tumours

A
  • Kaposi sarcoma (pink or purple atch on the skin or mouth caused by HHV8)
  • SCC (especially cervical or anal due to HPV)
  • Lymphoma
89
Q

Describe investigations for HIV

A
  • Elisa confirmed with western blot
  • Serum HIV rapid test
  • Serum HIV DNA PCR in infants
  • CD4 count (immune status, staging process)
  • Serum viral load (millions of copies/mL)
  • Test or drug resistance, hep B and C, t. pallidum, tuberculin skin test, FBC, U+E, LFT
90
Q

Define candidiasis

A
  • Fungal infection caused by candida species (thrush)
91
Q

Describe epidemiology of candidiasis

A
  • Oral colonisation from 40-70% of healthy children and adults
  • Higher rates among children with carious teeth and older adults with dentures
92
Q

Describe aetiology of candidiasis

A
  • Dimorphic fungus
  • Oral Candidiasis and Oesophageal thrush (Immunocompromised)
  • Vulvovaginitis (diabetes, use of antibiotics)
  • Diaper rash
  • Infective Endocarditis (IV drug users)
  • Disseminated candidiasis (especially in neutropenic patients)
93
Q

List signs and symptoms of candidiasis

A
  • Oral and oesophageal dysphagia (creamy white plaques which can be scraped off to reveal an erythematous base, dysphagia)
  • Vulvovaginitis/balanitis (thick discharge, itching, soreness, redness)
  • Diaper rash
  • Endocarditis
  • Disseminated candidiasis (fever, hypotension, leykocytosis)
94
Q

List risk factors for candidiasis

A
  • Hyposalivation/xerostomia
  • Poor oral hygiene, especially among denture wearers
  • Malabsorption and malnutrition
  • Advanced malignancy
  • Cancer chemotherapy and radiotherapy
  • HIV infection
  • Endocrine disturbance (e.g., diabetes mellitus, hypoparathyroidism, pregnancy, hypoadrenalism)
  • Immunosuppressive agents (e.g., systemic corticosteroid therapy)
  • Current or recent past use of broad-spectrum or multiple narrow-spectrum antibiotics
  • Age >60 years
  • Female sex
  • Inhaled corticosteroid
95
Q

Describe investigations of candidiasis

A
  • Swabs are not routinely done (as candida generally found in healthy people), but may do swab, biopsy, sputum culture.
  • Urinalysis for UTI
  • Blood glucose for diabetes
  • HIV antibody test
  • Vaginal pH test
96
Q

Describe aetiology of tonsillitis

A

Viral

  • Most common: rhinovirus, coronavirus, adenovirus
  • Associated with IM infection

Bacterial
- Group A streptococci
Mycoplasma pneumoniae,
- Neisseria gonorrhoea

97
Q

Define abscess

A

Collection of pus that has built up within a tissue, organ or confined space walled off by fibrosis

98
Q

Describe aetiology of abscess

A
  • Usually caused by bacterial infection
  • Rarely parasites or foreign substances
  • Defensive reaction forming WBC and a capsule of healthy cells to prevent pus infecting neighbouring structures
99
Q

List common locations of abscesses

A

Skin (cutaneous of subcut - usually staph aureus)

Internal

  • Lungs
  • Brain
  • Teeth
  • Kidneys
  • Tonsils
  • Perianal absess (common in IBD, diabetes)
  • Incisional
100
Q

List signs and symptoms of abscesses

A

External

  • Erythema
  • Hot
  • Oedema
  • Pain
  • Loss of function

Internal

  • Systemically unwell
  • Pain
  • Fever
101
Q

Describe investigations for abscess

A
  • Clinical diagnosis

- Ultrasound can aid diagnosis in some cases

102
Q

Describe management of abscess

A

Uncomplicated skin:

  • Aspiration
  • Incision and drainage

Severe/multiple sites/ cellulitis/sepsis

  • Antibiotics
  • Incision and drainage
  • Excision in severe cases
103
Q

List consequences of taking steroids on FBC and glucose

A
  • Raised glucose

- Leukocytosis (due to decreased adhesion to wall)

104
Q

Define malaria

A
  • Parasitic infection caused by Plasmodium. Most common in humans is Plasmodium falciparum, this is also the most life-threatening (causes RBCs to adhere to the blood vessel lumen)
  • P ovale can reactivate
105
Q

Describe epidemiology of malaria

A
  • 219 mill cases worldwide in 2017
  • 435000 deaths
  • Over 90% cases in Africa, majority of deaths due to falciparum.
  • Most common tropical disease imported to the UK, around 2000 cases a year
  • Plasmodium vivax is dominant outside of sub-saharan africa
106
Q

Describe aetiology/risks of Malaria

A
  • Plasmodium. Anopheles mosquitos transmit the virus via blood
  • Infection can occur with contact with infected blood
  • Travel to an endemic area, lack of appropriate prophylaxis, and absence of an insecticide treated bed net are all risks
  • Severe infection risks include low immunity, pregnancy, age under 5, immunocompromise, and older age
107
Q

List symptoms of malaria

A
  • Fever
  • Headache
  • Weakness
  • Myalgia
  • Arthralgia
  • Anorexia
  • Diarrhoea
  • Seizures (falciperum)
  • Nausea nad vomiting
  • Abdo pain
  • Resp symptoms
108
Q

List signs of malaria

A
  • Pallor
  • Hepatosplenomegaly
  • Jaundice
  • Fever
109
Q

Describe investigations for malaria

A
  • Giemsa-stained thick and thin blood smears
  • Rapid diagnostic tests
  • FBC (thrombocytopenia, anaemia)
  • Clotting profile
  • U and E
  • Serum LFT
  • Serum blood glucose
  • Urinalysis (haemoglobin)
  • Arterial blood gas
110
Q

List history clues for causative agent for diarrhoea

A
  • C diff - antibiotics
  • Staph aureus - food, 1-6 hours after eating, short lived
  • Vibro cholera - rice water diarrhoea, poor sanitation, shock
  • E coli - leafy veg
  • Bacillus cereus - reheated rice, can cause cerebral abscess
  • Salmonella - eggs, poultry, may present with constipation
  • Campylobacter - uncooked poultry
  • Entamobea histolytica - poor sanitation, tropical places, MSM
  • Shigella - person to person contact, poor sanitation, MSM
111
Q

Describe epidemiology of abscesses

A

Skin abscesses are common and have become more common in recent years. Risk factors include intravenous drug use, with rates reported as high as 65% among users.

112
Q

Describe prognosis of abscesses

A
  • Skin abscesses rarely result in death, as they naturally break through skin
  • Brain abscesses are fatal if untreated, with 5-10% mortality if treated
  • Higher mortality wher the abscess ruptures
113
Q

List complications of abscess

A
  • Endocarditis
  • Sepsis
  • Gangrene
  • Toxic shock syndrome
114
Q

List cephalosporins used by different doctors

A
  • Ceftriaxone used by medics
  • Cefotaxime used by surgeons
  • Cefuroxime used in neonates
115
Q

Describe management of MRSA

A
  • Vancomycin

- Monitor renal function and trough vancomycin levels (15-20 aim)

116
Q

Define systemic sclerosis

A
  • A chronic condition caused by abnormal growth of connective tissue, leading to thickening of the skin and inner organs.
  • May be limited or diffuse
117
Q

Describe epidemiology of systemic sclerosis

A
  • 5:1 female to male
  • Higher incidence in African Americans
  • Peak incidence 30-50 years
118
Q

Describe aetiology/risks of systemic sclerosis

A
  • Unknown
  • Genetic - polymorphisms
  • Immunology - 90% positive ANA. May also have anti-topoisomerase I (20%, associated with ILD), anti-RNA polymerase III (20%, renal crises), anticentromere antibodies (20-25%, better prognosis)
  • 40% no specific antibody
  • Environmental - silica, solvents?
119
Q

Compare limited and diffuse systemic sclerosis

A

Limited

  • Begins with fingers, hands face then progresses to center of body
  • Associated with CREST (calcinosis cutis, raynaud, oesophageal dysmotility, sclerodactyly, telangiectasia)
  • Pulmonary hypertension often present
  • 70-80% anticentromere antibodies

Diffuse

  • More aggressive but less common
  • Early organ involvement, affecting lung, heart, GI and kidneys
  • Antitopoisomerase 1 40%, anti-RNA polymerase 20%
120
Q

List symptoms and signs of systemic sclerosis

A
  • THickening and hardening of the skin (smooth, shiny, puffy)
  • Sclerodactyly (thicking of skin on fingers and hands, limited range of motion and discolouration)
  • Multiple painful ischaemic digital ulcers
  • Pitting (hyperkeratotic scarring, affecting fingertips)
  • Lesions on the proximal nail fold
  • Depigmentation of the skin with sparing of perifollicular pigmentation
  • Face: Loss of expression, no wrinkles, short frenulum, microstomia
  • Raynaud (precedes limited and coincides with diffuse), thomboembolism
  • Fatigue/weakness, joint stiffness/pain
  • CREST
  • Dysphagia, arthralgia, reflux, constipation and cramping
  • Pulmonary hypertension and interstitial lung disease
  • Fibrosis myocardititis pericarditis
  • Renal - renal crisis in 10-15% diffuse patints
121
Q

Describe diagnosis of systemic sclerosis

A
  • ANA, anticentromere antibodies (limited)
  • Anti topoisomerase 1 (Scl-70), anti-RNA polymerase 1 (diffuse)
  • Serum protein electrophoresis shows increased gamma globulins
  • CXR for pulmonary
  • FBC for anaemia/renal crisis
  • U and E
  • ESR and CRP
  • Pulmonary function tests (spirometry, restrictive pattern)
  • ECG
  • Echo
  • Barium swallow
122
Q

Define thyroiditis

A
  • A group of disorders characterised by thyroid inflammation
  • Acute suppurative thyroiditis is due to bacterial infection
  • Subacute is due to viral infection
  • Chronic is usually autoimmune
123
Q

Describe epidemiology of thyroiditis

A
  • 1.2% in individuals age 11-18
  • 25% of adults with T1DM have thyroiditis
  • Chronic is the most common type (Hashimotos - women age 30-50)
  • 10% children with T1DM have antithyroidantibodies
  • Subacute (De Quervains - most common age 20-50 women)
124
Q

Describe aetiology of thyroiditis

A
  • Subacute - Viral infection or post-viral inflammatory process, associated with HLA-B35. Mumps/flu
  • Infectious (acute) thyroiditis - acute gram pos or neg organisms, often immunocompromised patients. Most commonly staph and strep. Others fungal, mycobacterial and pneumocystic
  • Radiation (graves disease treatment)
  • Palpation or trauma induced
  • Autoimmune
  • Postpartum
  • Drug induced, lithium, amiodarone, interferon alpha
  • Fibrous (macrophage and eosinophil infiltration)
125
Q

List signs and symptoms of thyroiditis

A

Acute

  • Fever
  • Acute illness
  • Neck tenderness, tender thyroid, swelling and tenderness unilateral, erythemas, lymphademopathy

Subacute

  • Low grade fever or weakness
  • Hyperthyroidism signs for the first few days, often settles then underactive thyroid gland for a few weeks/months before complete recovery
  • Enlarged and tender thyroid gland

Chronic

  • Initally enlarged, bumpy non-tender.
  • Then hypothyroidism
  • Occasionally early hyperthyroidism signs occur

Postpartum/ painless

  • Initial hypothyroidism
  • Then transient raise in TFTs.
  • Resolves itself within 12-18 months
126
Q

List investigations of thyroiditis

A
  • Leukocytosis, raised ESR, normal TFTs in acute
  • Subacute TSH supressed and T4 increased, as disease progresses transient hypothyroidism
  • Chronic TSH increased and low T4 if hypo, may be hyper. Can also be normal. Antithyroid peroxidase levels are higher than normal range
  • Radioactive thryoid scanning - low uptake in hyperthyroidism shows destructive process
  • Thyroid ultrasonongraphy may reveal abscess, and can distinguish between acute and subacute
  • FNA may be used for culture (also subacute shows multinucleated giant cell granulomas)
127
Q

Describe management of thyroiditis

A

Acute

  • Ibuprofen
  • Antibiotics (IV)
  • Operation in children

Subacute

  • B blockers for thyrotoxicosis symptoms
  • Ibuprofen or steroids
  • If it comes back, or hypothyroidism does not resolve, levothyroxine may be taken for a long term basis

Chronic

  • Levothyroxine
  • Rarely surgery (if uncomfortable/cancer is suspected)

Drug induced - stop the drug

128
Q

List prognosis of thyroiditis

A
  • Hashimotos patients need levothyroxine for life
  • Painless + subacute - no permanent long term effects, resolves itself
  • Often rapid diagnosis and treatment is curative for acute, may need surgery
129
Q

List complications of thyroiditis

A
  • Permanent hypothyroidism
  • Long term symptoms
  • Vocal cord paralysis (may be due to surgery)
  • Myxoedema coma
130
Q

Define Behcets disease

A

A systemic vasculitis which causes skin and mucosal lesions, uveitis, arterial and venous disease, and GI and neurological manifestation

131
Q

Describe epidemiology of Behcets disease

A
  • Most common in the Middle East, the Mediterranean and eastern Asia
  • Rare in northern Europe and Africa
  • 80-370 per 100000 population in Turkey
  • 0.6 per 100000 UK
  • Rare before puberty and after 60
  • Most common age 20-40
  • Males more severe symptoms
132
Q

Describe aetiology of Behcet’s syndrome

A
  • Unknown
  • Possibly genetic (anticipation, where next generation gets a more severe form)
  • Inflammation and immunological mechanisms play a role
  • Autoimmune or autoinflammatory
133
Q

List risk factors for behcets disease

A
  • Age 20-40
  • Family history
  • Genetic predisposition (MIddle east, Eastern asia, meditteranian)
134
Q

List symptoms and signs of Behcets disease

A
  • Oral ulcers
  • Genital ulcers (apinful and scar)
  • Uveitis
  • Acne
  • Erythema nodosum
  • Limited duration of symptoms
  • Superficial thrombophlebitis
  • Hypophyon (precipitation of inflammatory cells in the anterior chamber)
  • Stroke
  • Eye pain, blurred vision, photophobia, photosensitivitiy
  • Memory loss
  • Headache, confusion or fever
  • Haemoptysis, cough, SOB, chest pain
  • Eye redness or tearing
  • Impaired speech, balance or movement
  • GI symptoms
135
Q

List investigations for Behcet’s syndrome

A
  • Pathergy testing (positive in 60%, pustule forms when pricking the skin)
  • Rheumatoid factor (-)
  • ANA (-)
  • ANCA (-)
  • HLA-B51 (+)
  • Lumbar puncture (hypercellularity - lymphocytosis)
  • MRI, MR angiography with contrast (Large vessel phlebitis of the CNS- white matter changes)
  • Colonoscopy
  • Upper GI endoscopy
  • High resoltuion chest CT, CT angio of chest, Pulmonary angio (to test haemoptysis - pylomary aneurysm)
136
Q

Describe incision and drainage of an abscess

A
  • Local anaesthetic
  • Cut into the abscess and drain out pus. May take a sample
  • Clean the hole left by the abscess using saline, and leave open with a wound dressing so new pus can drain
  • Gauze is placed inside deep abscesses to keep the wound open so a new abscess does not form
  • If internal, may be percutaneous (through skin with a needle, and a catheter to keep it open) or with surgery
137
Q

List indications for incision and drainage of an abscess

A
  • Palpable fluctuant abscess
  • An abscess that does not resolve despite conservative measures
  • Large abscess (over 5mm)
138
Q

Lis complications of incision and drainage of an abscess

A
  • Inadequate anaesthesia
  • Pain during and after
  • Bleeding
  • Reformation of abscess
  • Septic thrombophlebitis
  • Necrotizing fasciitis
  • Fistula formation
  • Damage to nerves and vessels
  • Scarring
139
Q

List the vasculitides and their buzzwords

A
  • Behcets syndrome uveitis, oral and genital ulcers
  • Churg strauss syndrome (eosinophilic granulomatosis with polyangitis - asthma, pANCA, eosinophilia)
  • Microscopic polyangitis pANCA, glomerulonephritis
  • Polyarteritis nodosa - rosary sign, Hep B
  • Polymyalgia - bilateral hip and shoulder pain
  • Takayasu - asian females
  • Temporal arteritis - Scalp tenderness, headache
  • Wegners (granulomatosis with polyangiitis - cANCA, URT, LRT, GN)
140
Q

List the symptoms of CREST.

A
  • Calcinosis
  • Raynauds
  • Oesophageal dysmotility
  • Sclerodactyly
  • Telangiectasia
141
Q

Describe main difference in appearance of erysipelas and cellulitis

A
  • Erysipelas is WELL DEMARCATED

- Cellutis is not

142
Q

Describe SOAP BRAIN MD for SLE

A 
Serositis – Pleurisy, pericarditis
Oral ulcers
Arthritis
Photosensitivity
Blood disorders (anaemia, leukopenia, thrombocytopenia)
Renal involvement (proteinuria)
Antinuclear antibodies 
Immunologic phenomena (dsDNA)
Neurologic disorder (psychiatric, seizures)
Malar rash
Discoid rash
143
Q

Describe management of necrotising fasciitis

A
  • Clindamycin, penicillin, vancomycin first step regimen
144
Q

Describe management of postherpetic neuralgia

A

Nortriptyline

Year 3 - Diseases (27 decks)

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