Infection & Immunology Flashcards

1
Q

Define an abscess.

A

A mass of necrotic tissue, with dead and viable neutrophils suspended in tissue breakdown products (pus), surrounded by a layer of inflammatory exudate.

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2
Q

Explain the aetiology / risk factors of an abscess.

A

The disruption of a tissue barrier through a penetrating injury, local infection or the migration of normal flora to the sterile areas of the body becomes walled off in an attempt to limit further spread of the infection.

Common Bacteria:

  • Staphyloccocus
  • Streptococci
  • Enteric organisms - e.g. E.coli
  • Coliforms and anaerobes - e.g. Bacteroides spp.

TB - cold abscesses.

Risk factors:

  • Local - tissue necrosis, an under-perfused space or foreign body that provides a focus for infection - e.g. a tooth or root fragment, splinters, mesh of hernia repair or embedded hair
  • Systemic - diabetes, immunosuppression (although may interfere with pus formation)

PATHOLOGY
- Bacteria incidte intense acute inflammatory response
- Formation of pus - collection of cellular debris and bacteria
- Becomes surrounded by fibrinous exudate and granulation tissue - macrophages and fibroblasts
- Collagen deposition and walling off
= Abscess

Cold Abscess

  • Collections of caseating necrosis
  • Conatining myobacterium
  • Cold = not associated acute inflammatory response
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3
Q

Summarise the epidemiology of an abscess.

A

Common in all ages.

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4
Q

Recognise the presenting symptoms of an abscess.

A

Local effects:

  • Pain
  • Swelling
  • Heat
  • Redness
  • Impaired function of the area
  • Dolor
  • Tumour
  • Calor
  • Rubor
  • Functionalaesa
  • Celsian features of acute inflammation

Systemic:

  • Fever
  • Feeling unwell
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5
Q

Recognise the signs of an abscess on physical examination.

A

Within an organ

  • No localizing signs
  • Swinging pyrexia - caused by periodic release of microbes or inflammatory mediators into the systemic circulation

Old Adage
= If pus is somewhere and the pus is nowhere, then pus is under the diaphragm
= SUBPHRENIC ABSCESS

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6
Q

Identify appropriate investigations for an abscess and interpret the results.

A

Bloods

  • FBC - high neutrophils
  • Imaging - US, CT or MRI
  • Imaging - 67-Ga white cell scanning to search for site
  • Aspiration - low in glucose, acidic
  • Culture of pus for organisms and sensitivity to antibiotics
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7
Q

Generate a management plan for an abscess.

A

PREVENTION

  • Prophylactic antibiotics - e.g. operations
  • Given early during an infection
  • Often not effective once abscess has formed

GENERAL

  • Drainage of pus
  • Removal of necrotic and foreign material
  • Anti-microbial cover
  • Correction of predisposing cause

SURGERY

  • Drainage of pus by incision and drainage
  • Debridement of cavity
  • Free drainage by packing of cavity (if superficial) or by drains (if deep)

IR
- US or CT guidance to localise and aspirate contents

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8
Q

Identify the possible complications of an abscess and its management.

A
  • Cellulitis - skin
  • Bacteraemia
  • Systemic sepsis
  • Chronic abscess
  • DIscharging sinus
  • Fistula
  • Sterile collection
  • Antibioma
  • Pressure necrosis of surrounding tissues
  • Destruction of normal functioning tissue
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9
Q

Summarise the prognosis for patients with an abscess.

A

Good if adequately drained and predisposing factor removed.

If left untreated, abscesses tend to point to the nearest epithelial surface and may spontaneously discharge their contents.

Depp abscesses may become chronic, undergoing dystrophic calcification.

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10
Q

Define candidiasis.

A

Infection with candida, especially as causing oral or vaginal thrush.

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11
Q

Explain the aetiology / risk factors of candidiasis.

A

Dimorphic fungus (yeast) colonizes approx. 30% individuals.

  • Colonization begins shortly after birth and persists throughout life
  • Found in respiratory, GI, genitourinary tracts and the skin and mucous membranes
  • Exists in both yeast (blastospore) phase and hyphal (mycelial) phase, depending on surrounding conditions
  • Immunocompetent individuals provide effective immune surveillance against Candida
  • Any immune defect can lead to infection and visible disease

Risk factors:

  • Antibiotics
  • Corticosteroids
  • Dental prostheses
  • Chemotherapy
  • Radiation treatment
  • HIV
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12
Q

Summarise the epidemiology of candidiasis.

A

Rise in Candida infections - due to diabetes, malignancy, chemotherapy, human immunodeficiency virus

200 species - most common C. albicans.

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13
Q

Recognise the presenting symptoms of candidiasis.

A
  • Areas of heat and humidity and maceration
  • Burning
  • Itching
  • Irritation
  • Redness and swelling
  • Pain and soreness
  • Rash
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14
Q

Recognise the signs of candidiasis on physical examination.

A

Cutaneous

  • Under breasts
  • In gluteal and inguinal folds
  • Diaper area
  • Under pannus
  • Armpit
  • Erythema with satellite papules
  • Overlying white plaques - intertrigo

Oral

  • Thrush
  • Infants and elderly
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15
Q

Identify appropriate investigations for candidiasis and interpret the results.

A
  • Superficial scraping
  • Add saline - see pseudohyphae and yeast under microscope
  • KOH added to nail or skin specimens to help dissolve the keratin and visualise the yeast
  • Calcolfluor white - rapid diagnosis with a fluorescent microscope
  • Culture and sensitivities
    Skin biopsy with periodic acid-Schiff (PAS) staining
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16
Q

Define cellulitis and erysipelas.

A

Cellulitis - an acute spreading infection of the skin with visually indistinct borders that principally involves the dermis and subcutaneous tissue, characterised by redness, swelling, heat and tenderness and usually occurs in an extremity.

Erysipelas - a distinct form of superficial cellulitis with notable lymphatic involvement, that is raised and sharply demarcated from uninvolved skin.

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17
Q

Explain the aetiology / risk factors of cellulitis and erysipelas.

A

Often results from penetrating injury (e.g. IV cannulation), local lesions (e.g. insect bites, sebaceous cysts, surgery) or fissuring (e.g. in anal fissured, toe web spaces), which allows pathogenic bacteria to enter the skin.

In rare cases of septicaemia, it can arise spontaneously from blood-borne sources.

Most common organisms: Streptococcus pyogenes, Staphylococcus aureus. (MRSA not uncommon)

If occuring in orbit, Haemophilus influenzae is most common cause, arising from adjacent sinuses.

Risk Factors:

  • Diabetes
  • Venous insufficiency
  • Eczema
  • Oedema
  • Lymphoedema
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18
Q

Summarise the epidemiology of cellulitis and erysipelas.

A

Very common.

Main risk factors - skin break poor hygiene, poor vascularization of tissue (e.g. DM)

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19
Q

Recognise the presenting symptoms of cellulitis and erysipelas.

A

History of cut, scratch or injury.

Periorbital:
- Painful swollen red skin around eye

Orbital cellulitis:

  • Painful or limited eye movements
  • Visual impairment
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20
Q

Recognize the signs of cellulitis and erysipelas on physical examination.

A

Cellulitis - acute onset of red, painful, hot, swollen skin

Erysipelas - well-demarcated, bright-red raised skin

Lesion:

  • Erythema
  • Oedema
  • Warm tender indistinct margins
  • Pyrexia (may indicate systemic spread)
  • Orange-peel appearance
  • Bistering & bleeding

Exclude Abscess:

  • Test for fluid thrill or fluctuation
  • Aspirate if pus suspected

Periorbital:

  • Swollen eyelids
  • Conjunctival injection

Orbital Cellulitis:

  • Proptsis - protrusion of the eyeball
  • Impaired acuity and eye movement
  • Test for relative afferent pupillary defect, visual acuity and colour vision (to monitor optic nerve function)
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21
Q

Identify appropriate investigations for cellulitis and erysipelas and interpret the results.

A

Bloods

  • WCC / CRP / ESR
  • U&E
  • Blood culture

Discharge

  • Culture & sensitivity
  • Skin swab and biopsy

Aspiration
- Often non-purulent, not usually necessary

CT/MRI Scan
- When orbital cellulitis is suspected - to assess the posterior spread of infection

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22
Q

Generate a management plan for cellulitis and erysipelas.

A

Medical:

  • Oral penicillins - e.g. flucloxacillin, benzylpenicillin, coamoxiclav (community)
  • Tetracyclines (community)
  • Hospital - treat empirically using local microbiological guidelines but change depending on sensitivity of any cultured organisms
  • IV use may be necessary

Surgical
- Orbital decompression if orbital cellulitis (emergency)

Abscess
- Can be aspirated, incised and drained or excised completely

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23
Q

Identify the possible complications of cellulitis and erysipelas and its management.

A
  • Sloughing of overlying skin
  • Localised tissue damage
  • Orbital cellulitis - permanent vision loss, spread to brain, abscess formation, meningitis, carvenous sinus thrombosis
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24
Q

Summarise the prognosis for patients with cellulitis and erysipelas.

A

Good with treatment

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25
Define Behcet's disease.
A systemic vasculitis. Can cause skin and mucosal lesions, uveitis, major arterial and venous vessel disease, and gastrointestinal and neurological manifestations.
26
Identify appropriate investigations for Behcet's disease and interpret the results.
1st Line: - Pathergy testing - induration with or without formation of a pustule within 48 hours - Rheumatoid factor - negative - Anti-nuclear antibodies - negative - Anti-neutrophil cytoplasmic antibodies - negative - HLA-B51 - present - Lumbar puncture - hypercellularity, lymphocytosis, polymorphonuclear cells or pleocytosis - MRI - white matter changes involving midbrain, brainstem and basal ganglia - Colonoscopy - inflammation and apthous-type ulcers, vasculitis on biopsy - Upper GI endoscopy - inflammation and apthous-type ulcers, vasculitis on biopsy - CT chest - haemorrhage, pulmonary aneurysm - CT chest angiography - haemorrhage, pulmonary aneurysm - CTPA - pulmonary aneurysm Emerging: - Anti-Saccharomyces cervisiae antibodies - may be elevated when GI symptoms are present
27
Recognise the signs of Behcet's disease on phyiscal examination.
Common: - Increased predisposition in certain ethnic / geographic groups - Oral ulcers - Genital ulcers - Uveitis - Acne lesions - Erythema nodosum - Limitated duration of symptoms - Superficial thrombophlebitis - Hypopyon - inflammatory cells in the anterior chamber of eye Uncommon: - Stroke - Eye pain, blurry vision, photophobia or photosensitivity - Memory loss - Headache, confusion or fever - Haemoptysis, cough, shortness of breath or chest pain - Eye redness or tearing - Impaired speech, balance or movement - Cramping abdominal pain, diarrhoea or GI ulceration
28
Recognise the presenting symptoms of Behcet's disease.
Common: - Increased predisposition in certain ethnic / geographic groups - Oral ulcers - Genital ulcers - Uveitis - Acne lesions - Erythema nodosum - Limitated duration of symptoms - Superficial thrombophlebitis - Hypopyon - inflammatory cells in the anterior chamber of eye Uncommon: - Stroke - Eye pain, blurry vision, photophobia or photosensitivity - Memory loss - Headache, confusion or fever - Haemoptysis, cough, shortness of breath or chest pain - Eye redness or tearing - Impaired speech, balance or movement - Cramping abdominal pain, diarrhoea or GI ulceration
29
Summarise the epidemiology of Behcet's disease.
Most commonly seen in Turkey, Israel, the Mediterranean basin and eastern Asia - where Japan and South Korea report the most cases. Most commonly seen in young people aged 20-30 years. More active and severe in males.
30
Explain the aetiology / risk factors of Behcet's disease.
In many patients, disease activity decreases with time and this natural course can affect treatment decisions about the type and duration of medical therapy. Presents in various combinations and sequences in patients over time. Risk factors: - Age 20-40 years - Family history - Genetic predisposition - evidence for genetic anticipation
31
Define anaphylaxis.
A severe, generalized 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.
32
Explain the aetiology / risk factors of anaphylaxis.
A systemic response is caused by the release of immune and inflammatory mediators from basophils and mast cells. Most frequently caused by allergies to food, medication and venoms. Non-immunological anaphylaxis - similar symptoms (anaphylactoid reaction). Risk factors: - <30 years old - food associated, exercise induced - Atopy / asthma - History of anaphylaxis - Exposure to a common sensitiser - e.g. latex - Adult age - food, insect venom, medicine related - Female sex
33
Summarise the epidemiology of anaphylaxis.
The lifetime prevalence of anaphylaxis is currently estimated at 0.05-2 % in the USA and ~3 % in Europe. Several population-specific studies have noted a rise in the incidence, particularly in the hospitalizations and ER visits due to anaphylaxis.
34
Recognise the presenting symptoms of anaphylaxis.
- Acute onset - Shortness of breath - Confusion or disorientation - Hives (urticaria) - Nausea - Vomiting - Diarrhoea - Incontinence - Abdominal cramps and pain - Agitation - Anxiety - Sense of impending doom = angor animi
35
Recognise the signs of anaphylaxis on phyiscal examination.
- Airway swelling - angio-oedema - Inspiratory stridor - Hoarse voice - Chest hyperinflation - Wheezing - Accessory muscle use - Cyanosis - Respiratory arrest - Pale clammy skin - Hypotension - Tachycardia or bradycardia - Cardiac arrest - Erythema - Pruritus - Rhinits - Bilateral conjunctivitis
36
Identify appropriate investigations for anaphylaxis and interpret the results.
1st Line: - Mast cell tryptase - may be elevated, normally undetectable - 12-lead ECG - myocardial ischaemia, non-specific ST ECG changes post-adrenaline and with anaphylaxis - U&E - normal in initial phase of anaphylaxis unless comorbidity present - ABG - elevated lactate, metabolic acidosis Consider: - CXR - may show hyperinflation if bronchoconstriction, interstitial fluid (After time-critical interventions have been administered)
37
Generate a management plan for anaphylaxis.
IN CARDIORESPIRATORY ARREST - CPR and ALS - Do not give IM adrenaline after cardiac arrest has occurred as circulation to the muscle is inadequate NOT IN CARDIORESPIRATORY ARREST - ABCDE - Position patient and remove trigger - Adrenaline - IM 150ug adrenaline into anterolateral aspect of middle third of thigh, repeat if no improvement after 5 minutes - Establish airway plus high-flow oxygen - 94-96% target sats - IV fluids - rapid IV fluid challenge (500-1000mL, kids 20mL/kg) over <15 mins with crystalloid that has sodium concentration 130-154 mmol/L to counteract fluid shifts associated with vasodilation and/or capillaries - Serial CR assessments - pulse oximeter, ECG monitor, non-invasive blood pressure monitor - Nebulised adrenaline - Nebulised short-acting beta-2-agonist - e.g. salbutamol 5mg every 20-30 mins (adult) - IV atropine - IV glucagon AFTER TREATMENT - Antihistamine - e.g. chlorphenamine - 10mg IM/IV single dose, may be repeated up to 4 doses per day - Corticosteroid - e.g. hydrocortisone sodium succinate 200mg IM/IV - Monitor for biphasic reactions (incidence 1-20%) - Review by a senior clinician and observation POST-ANAPHYLAXIS - Adrenaline autoinjector - Antihistamine - e.g. chlorphenamine 4mg orally every 4-6 hours, max 24mg / day - Corticosteroid - e.g. prednisolone NB: Length of needle - 25 mm (blue 23G or orange 25G) needle is best and suitable for all ages - 16 mm (orange 25G) needle is appropriate for preterm or small infants - 38 mm (green 21G) needle may be needed in some adults. Injection technique - Stretch the skin and give the injection with the needle at a 90° angle to the skin.
38
Identify the possible complications of anaphylaxis and its management.
- Brain damage - Kidney failure - Cardiogenic shock - Arrhythmias - Heart attacks - Death
39
Summarise the prognosis for patients with anaphylaxis.
With prompt treatment, the overall prognosis of anaphylaxis is good, with a case fatality ratio of less than 1% reported in most population-based studies [Resuscitation Council (UK), 2012].
40
Define infective endocarditis.
Infection of intracardiac endocardial structures - mainly heart valves.
41
Explain the aetiology / risk factors of infective endocarditis.
Vegetations form as a result of lodging of the organisms on the heart valves during a period of bacteraemia. - Made of platelets, fibrin, infective organisms - Poorly penetrated by immune system - Destroy valve leaflets - Invade myocardium - Invade aortic wall - Abscess cavities form - Activation of immune system also causes formation of immune complexes --> cutaneous vasculitis, glomerulonephritis, arthritis Endocardium can be colonized by virtually any organism, but most common are: 1) Streptococci (40%) - mainly alpha-haemolytic Streptococcus viridans or bovis 2) Staphylococci (35%) - aureus or epidermidis (IVDU) 3) Enterococci (20%) - faecalis 4) Others - e.g. Coxiella burnetti, histoplasma, HACEK - Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella Risk Factors: - Abnormal valves - e.g. congenital, post-rheumatic, calcification, degeneration - Prosthetic heart valves - Turbulant flow - e.g. patent ductus arteriosus or VSD - Recent dental work - Bacteraemia - S.bovis --> GI Malignancy
42
Summarise the epidemiology of infective endocarditis.
16-22 per million per year (UK)
43
Recognise the presenting symptoms of infective endocarditis.
- Fever - Sweats - Chills - Malaise - Arthralgia - Myalgia - Confusion - Skin lesions - Ask about recent dental surgery or IV drug use
44
Recognise the signs of infective endocarditis on physical examination.
- Pyrexia - Tachycardia - Signs of anaemia - Clubbing - if long-standing - New regurgitant murmur - Muffled heart sounds - Splenomegay NB: Right-sided lesions may imply IV drug use. Frequency: Mitral > Aortic > Tricuspid > Pulmonary Vasculitic Lesions: - Roth's spots - petechiae on retina - Petechiae (especially on pharyngeal and conjunctival mucosa) - Janeway lesions - painless palmar macules that blanch on pressure - Osler's nodes - tender nodules on finger / toe pads - Splinter haemorrhages - nail-bed haemorrhage
45
Identify appropriate investigations for infective endocarditis and interpret the results.
1) Bloods 2) Urinalysis 3) Blood culture 4) Echocardiography 5) Others Bloods - FBC - high neutrophils, normocytic anaemia - High ESR and CRP - U&E - Rheumatoid factor positive Urinalysis - Microscopic haematuria - Proteinuria Blood Culture - 3 sets 1 hour apart - Culture and sensitivity vital but start empirical treatment first - Culture negative 2-5% Echocardiography (Transthoracic) - Transoesophageal echocardiography more sensitive for endocarditis - Useful for detection of vegetations, valve abscess, diagnosis of prosthetic valve endocarditis, assessment of embolic risk Others: - ECG - conduction changes - CXR - septic pulmonary emboli : focal lung infiltrates, central cavitation - e.g. tricuspid valve endocarditis Duke's Classification (2 major, 1 major + 3 minor, all minor): - MAJOR - positive blood culture in 2 separate samples, positive echocardiogram - MINOR - high grade pyrexia >38 degrees, risk factors, positive blood culture (no major criteria), positive echocardiogram (not major), vascular signs +ve echocardiogram = vegetation, abscess, prosthetic valve dehiscence, new valve regurgitation Risk factors: - Abnormal valves - IV drug use - Dental surgery
46
Generate a management plan for infective endocarditis.
Antibiotics for 4-6 weeks (at least 6 weeks for prosthetic valve endocarditis). On clinical suspicion: - Benzylpenicillin + Gentamycin - Gentamycin - dose adjusted for peak serum level of 3-4ug/ml, trough <1ug/ml STREPTOCOCCI - Continue Benzylpenicillin + Gentamycin - Alt - Ceftriaxone, Vancomycin STAPHYLOCOCCI - Flucloxacillin / Vancomycin + Gentamycin - Prosthetic - Vancomycin + Gentamicin + Rifampin ENTEROCOCCI - Ampicillin + Gentamycin HACEK - Ampicillin or Ceftriaxone + Gentamycin Culture Negative - Vancomycin + Gentamycin Surgery - If poor response or deterioration = urgent valve replacement - Replacement of prosthees - Kissing mitral valve vegetations - may be able to salvage Prophylaxis - If history of infective endocarditis + undergoing high risk procedures - High risk procedures - e.g. dental, incision or biopsy of respiratory mucosa, procedures in patients with GI/GU tract infection, procedures on infected skin or musculoskeletal tissue, prosthetic heart valve placement - Dental - 2g oral amoxicillin 30-60 mins before procedure
47
Identify the possible complications of infective endocarditis and its management.
- Valve incompetence - Intracardiac fistulae or abscesses - Aneurysm formation - Heart failure - Renal failure - Glomerulonephritis - Arterial emboli from vegetations (brain, kidney, lungs, spleen)
48
Summarise the prognosis for patients with infective endocarditis.
Fatal if untreated. | When treated, 15-30% mortality.
49
Define infectious mononucleosis.
A clinical syndrome most commonly caused by Epstein-Barr virus (EBV) infection in 80-90% of cases. Mononucleosis syndrome used when the syndrome is caused by a non-EBV aetiology.
50
Explain the aetiology / risk factors of infectious mononucleosis.
Risk factors: - Kissing - Sexual behaviour
51
Summarise the epidemiology of infectious mononucleosis.
More than 90 percent of adults worldwide show serologic evidence of Epstein Barr virus infection. Most common time to develop clinical infectious mononucleosis: Freshman year in college. Incubation period: 4-8 weeks.
52
Recognise the presenting symptoms of infectious mononucleosis.
- Adolescents and young adults - Febrile illness - Sore throat - Enlarged lymph nodes - Malaise
53
Recognise the signs of infectious mononucleosis on physical examination.
TRIAD: Fever, Pharyngitis & Lymphadenopathy + atypical lymphocytosis + positive heterophile antibodies test + positive serological test for antibodies against EBV Other Rarer Signs: - Splenomegaly - Rash - Signs of hepatitis - hepatomegaly, jaundice - Myalgia
54
Identify appropriate investigations for infectious mononucleosis and interpret the results.
TRIAD: Fever, Pharyngitis & Lymphadenopathy + atypical lymphocytosis + positive heterophile antibodies test + positive serological test for antibodies against EBV 1st Line: - FBC - lymphocytosis, atypical lymphocytosis - Heterophile antibodies - positive - EBV-specific antibodies - positive for VCA-IgM, VCA-IgG, EA, EBV, EBNA - LFTs - elevated transaminases (transient, mild) 2nd Line: - Real-time PCR - EBV DNA detection - Abdominal US Scan - Splenomegaly - CT Abdo - Splenic rupture (haemodynamically stable patient when rupture is suspected)
55
Generate a management plan for infectious mononucleosis.
- Supportive care - paracetamol, ibuprofen, hydration, anti-pyretics, analgesics - Add Corticosteroid if upper airway obstruction or haemolytic anaemia - Prednisolone
56
Identify the possible complications of infectious mononucleosis and its management.
- Upper airway obstruction - Splenic rupture - Fulminant hepatitis - Encephalitis - Severe thrombocytopaenia - Haemolytic anaemia - Long-term fatigue & lethargy
57
Summarise the prognosis for patients with infectious mononucleosis.
Most people with mono recover completely with no long-term problems. The fatigue associated with the condition may persist for a few months after the fever and other symptoms have resolved. Severe complications as described above are very rare.
58
Define gastroenteritis and infectious colitis.
Acute inflammation of the lining of the GI tract, manifested by nausea, vomiting, diarrhoea and abdominal discomfort.
59
Explain the aetiology / risk factors of gastroenteritis and infectious colitis.
Caused by viruses, bacteria, protozoa or toxins in contaminated food or water. Virus - e.g. rotavirus, adenovirus, astrovirus, calcivirus, Norwalk virus, small round structured viruses Bacteria - e.g. Campylobacter jejuni, E.coli 0157, Salmonella, Shigella, Vibrio cholerae, Listeria, Yersinia enterocolitica Protozoal - e.g. Entamoeba histolytica, Cryptosporidium parvum, Giardia lamblia Toxins - e.g. from Staphylococcus aureus, Cryptosporidium parvum, Giardia lamblia ``` Commonly contaminated foods - Improperly cooked meat - e.g. S.aureus, C.perfringens - Old rice - e.g. B.cereus, S.aureus - Eggs & poultry - e.g. Salmonella - Milk and cheeses - e.g. Listeria, Campylobacter - Canned food - e.g. botulism ``` Non-inflammatory mechanisms - e.g. V. cholerae, enterotoxigenic E.coli (enterotoxins causing enterocytes to release water and electrolytes) Inflammatory mechanisms - e.g. Shigella, enteroinvasive E.coli (release cytokines, invade, damage epithelium), Salmonella typhi (greater invasion and bacteraemia)
60
Summarise the epidemiology of gastroenteritis and infectious colitis.
Common Under-reported Morbidity & mortality in developing world
61
Recognise the presenting symptoms of gastroenteritis and infectious colitis.
- Sudden onset nausea - Vomiting - Anorexia - Diarrhoea - bloody or watery - Abdominal pain / discomfort - Fever - Malaise NB: Enquire about recent travel, antibiotic use and recent food intake - how cooked, source, anyone else ill. Time of onset: - Toxins - early, 1-24h - Bacterial/Viral/Protozoal - 12h or later Effect of toxin: - Botulinum - paralysis - Mushrooms - fits, renal or liver failure
62
Recognise the signs of gastroenteritis and infectious colitis on physical examination.
- Diffuse abdominal tenderness - Abdominal distension - Increased bowel sounds Severe: - Pyrexia - Dehydration - Hypotension - Peripheral shutdown
63
Identify appropriate investigations for gastroenteritis and infectious colitis and interpret the results.
1. Blood 2. Stool 3. AXR or US 4. Sigmoidoscopy Blood - FBC, blood culture (bacteraemia), U&Es (dehydration) Stool - Faecal microscopy for polymorphs, parasites, oocytes, culture, EM (viraL) - Analyse for toxins, pseudomembranous colitis - e.g. Clostridium difficile toxin AXR or US - Exclude other causes of abdominal pain Sigmoidoscopy - IBD exclusion
64
Generate a management plan for gastroenteritis and infectious colitis.
- Bed rest - Fluids - Electrolyte replacement - Oral rehydration solution - glucose, salt - IV rehydration if severe vomiting - Antibiotic treatment if severe or infective agent identified - e.g. ciprofloxacin against Salmonella, Shigella, Campylobacter - Educate on basic hygiene and cooking NB: Botulism - Botulinum anti-toxin IM and manage in ITU
65
Identify the possible complications of gastroenteritis and infectious colitis and its management.
- Dehydration - Electrolyte imbalance - Pre-renal failure - Secondary lactose intolerance (infants) - Sepsis & shock (Salmonella, Shigella) - Haemolytic uraemic syndrome (E.coli 0157) - Guillian-Barré syndrome in weeks after Campylobacter gastroenteritis Botulism - respiratory muscle weakness, paralysis
66
Summarise the prognosis for patients with gastroenteritis and infectious colitis.
Majority of cases self-limiting
67
Define conjunctivitis.
The inflammation of the lining of the eyelids and eyeball caused by bacteria, viruses, allergic or immunological reactins, mechanical irritation, or medicines.
68
Explain the aetiology / risk factors of conjunctivitis.
Risk Factors: - Exposure to infected person - Infection in one eye - Environmental irritants - Allergen exposure - Camps, swimming pools, military bases - Asian or Mediterranean young male - Atopy - Contact lens use - Ocular prosthesis - Mechanical irritation
69
Summarise the epidemiology of conjunctivitis.
The incidence of bacterial conjunctivitis was estimated to be 135 in 10 000 in one study.
70
Recognise the signs of conjunctivitis on physical examination.
- Watery discharge - Ropy, mucoid discharge - Purulent discharge - Itching predominant symptom - Eyelids stuck together in morning - Tender, pre-auricular lymphadenopathy - Conjunctival follicles - Superficial punctate keratopathy - Unilateral disease - Corneal subepithelial infiltrates - Corneal pannus - Vesicular skin rash
71
Identify appropriate investigations for conjunctivitis and interpret the results.
- Rapid adenovirus immunoassay - Cell culture - Gram stain - Polymerase chain reaction - Ocular pH
72
Define encephalitis.
Inflammation of the brain parenchyma.
73
Explain the aetiology / risk factors of encephalitis.
Causes: - VIRAL - e.g. HSV, herpes zoster, mumps, adenovirus, coxsackie, echovirus, enteroviruses, measles, EBV, HIV, rabies (Asia), Nipah (Malasia), arboviruses transmitted by mosquitos (Jap B encephalitis - Asia, St Louis and West Nile encephalitis - USA) - NON-VIRAL - e.g. syphillis, Staphylococcus aureus - IMMUNOCOMPROMISED - e.g. CMV, toxoplasmosis, Listeria - AUTOIMMUNE OR PARANEOPLASTIC - associated with antibodies - e.g. anti-NMDA or anti-VGKC
74
Summarise the epidemiology of encephalitis.
7.4 in 100,000 in UK
75
Recognise the presenting symptoms of encephalitis.
- Can be mild and self-limiting - Subacute onset (hours to days) - Headache - Fever - Vomiting - Neck stiffness - Photophobia - i.e. symptoms of meningism (meningoencephalitis) - Behavioural changes - Drowsiness - Confusion - History of seizures - Focal neurological symptoms - e.g. dysphagia, hemiplegia - DETAILED TRAVEL HISTORY
76
Recognise the signs of encephalitis on physical examination.
- Reduced level of consciousness with deteriorating GCS - Seizures - Pyrexia - Neck stiffness - Photophobia - Kernig's test positive - Hypertension - Bradycardia - Papilloedema - Focal neurological signs - e.g. dysphagia, hemiplegia - Minimental examination may reveal cognitive or psychiatric disturbances NB: Raised intracranial signs and meningism signs.
77
Identify appropriate investigations for encephalitis and interpret the results.
1. Bloods 2. MRI / CT 3. Lumbar Puncture 4. EEG 5. Brain Biopsy Bloods - FBC - high lymphocytes - U&E - SIADH may occur - Glucose - compare with CSF glucose - Viral serology - ABG MRI / CT - Excludes mass lesion - HSV produces characteristic oedema of the temporal lobe on MRI Lumbar Puncture - High lymphocytes - High monocytes - High protein - Glucose usually normal - CSF culture difficult - Viral PCR now first line EEG - Epileptiform activity - E.g. spiking activity in temporal lobes Brain Biopsy - Rarely performed
78
Define herpes simplex virus.
Includes HSV1 and HSV2.
79
Explain the aetiology / risk factors of herpes simplex virus.
Alpha-herpes virus with double-stranded deoxyribonucleic acid (dsDNA). Transmitted via close contact with an individual shedding the virus (e.g. kissing, sexual intercourse). Multiply in epithelial cells of mucosal surface. Produces vesicles or ulcers. Lifelong latent infection when virus enters sensory neurons at infection site. Can then reactivate, replicate and infect surrounding tissue - occurs in response to physical, emotional stresses or immunosuppression.
80
Summarise the epidemiology of herpes simplex virus.
HSV1 - infection in 2/3 of world's population (approx 3.7 billion <50 years) HSV2 - infection in 11% of world's population ( approx 400 million) 90% adults seropositive for HSV1 by 30 years. 35% adults >60 years seropositive for HSV2. 1/3rd population recurrent HSV infections.
81
Recognise the presenting symptoms of herpes simplex virus.
HSV1 Primary Infection: - Asymptomatic - Pharyngitis - Gingivostomatitis - may make eating very painful - Herpetic whitlow - inoculation of virus into a finger Recurrent infection / reactivation: - Prodrome (6h) peri-oral tingling and burning - Vesicles appear (48h), ulcerate and crust over - Complete healing 8-10 days HSV2 - Very painful blisters and rash in genital, perigenital and anal area - Dysuria - Fever - Malaise HSV Keratoconjunctivitis: - Epiphoria - watering eyes - Photophobia
82
Recognise the signs of herpes simplex virus on physical examination.
Primary Infection: - Subclinical or sensory nerve prodrome (tingling) - Vesicles - Shallow ulcers Systemic Symptoms: - Fever - Malaise - Tender cervical lymphadenopathy - Heals 8-12 days Reactivation: - Usually less severe unless immunosuppressed Herpes Labialis: - Cold sore lesion at lip border, predominantly HSV1 Genital Herpes: - Predominantly HSV2 Gingivostomatitis: - Fever - Sore throat - Tender oropharyngeal vesicles - Yellow slough filled ulcers Keratoconjunctivitis: - Corneal dendritic ulcers - Avoid steroids Herpetic Whitlow: - Painful vesicles on distal phalanx due to inoculation through a break in the skin Herpes Encephalitis: - Most common treatable viral encephalitis - Transfer of virus from peripheral site to brain via neuronal transmission - Prodrome - fever, malaise, headache, nausea - Encephalopathy - general/ focal signs of cerebral dysfunction including psychiatric symptoms, seizure, focal neurology (temporal involvement in 60%), memory loss (HSV1 in immunocompetent patients)
83
Identify appropriate investigations for herpes simplex virus and interpret the results.
- Clinical diagnosis - Confirmation required in encephalitis, keratoconjunctivitis or immunosuppression - Viral PCR of CSF, swab or vesicle scraping - Culture - Immunofluorescence - Serology
84
Define incision and drainage of an abscess.
A time-honored method of draining abscesses to relieve pain and speed healing. Routine cultures and antibiotics are usually unnecessary if an abscess is properly drained.
85
Summarise the indications for incision and drainage of an abscess.
- Palpable fluctuant abscess - An abscess that does not resolve despite conservative measures - Large abscess >5mm
86
Identify the possible complications of incision and drainage of an abscess.
- Inadequate anaesthesia - Pain during and after the procedure - Bleeding - Reoccurrence of abscess formation - Septic thrombophlebitis - Necrotizing fasciitis - Fistula formation - Damage to nerves and vessels - Scarring
87
Define epididymitis and orchitis.
Epididymitis - inflammation of the epididymis Orchitis - inflammation of one or both testicles Acute epididymitis - inflammation of the epididymis characterized by scrotal pain and swelling of less than 6 weeks' duration. Acute Epididymo-orchitis - if concurrent inflammation of the testis is present.
88
Explain the aetiology / risk factors of epididymitis and orchitis.
Sexually active men - most commonly caused by: - Chlamydia trachomatis - Neisseria gonorrhoea - Mycoplasma genitalium Older men - most commonly caused by enteric pathogens: - Bladder outlet obstruction - Recent instrumentation of the urinary tract - Systemic illness RISK FACTORS: - Unprotected sexual intercourse - Bladder outflow obstruction - Instrumentation of urinary tract - Immunosuppression - Vasculitis - Amiodarone - Mumps - Exposure to TB
89
Summarise the epidemiology of epididymitis and orchitis.
Usually unilateral.
90
Recognise the presenting symptoms of epididymitis and orchitis.
- Irritative lower urinary tract symptoms - Urethral discharge (purulent) - Fever Common - Presence of risk factors - Age >19 years - Gradual onset - Symptoms <6 weeks' duration - Frequent and painful micturition
91
Recognise the signs of epididymitis and orchitis on physical examination.
Common - Unilateral scrotal pain - Tenderness - Hot - Erythematous - Swollen hemiscrotum Uncommon - Pyrexia - Fluctuant swelling or induration of scrotal tissue - Enlarged or tender prostate
92
Identify appropriate investigations for epididymitis and orchitis and interpret the results.
1st line: - Gram stain of urethral secretions - >5 WBC per oil immersion field, intracellular gram-negative diplococci - Urine dipstick test - positive leukocyte esterase tests shown as colour change on the reagent strip - Urine microscopy - >10 WBC per high-power field - Urine culture - Isolate of causative organism - NAAT (nucleic acid amplification test) of urethral secretions or first-void urine - Chalmydia trachomatis, Neisseria gonorrhoea, Mycoplasma genitalium DNA / RNA detected - Culture of urethral secretions - positive culture for N.gonorrhoea Consider: - Colour duplex US - epididymis is enlarged, hyperaemic, low-resistance monophasic arterial waveform pattern, good for localising areas of inflammation - Surgical exploration - oedematous epididymis with vascular congestion and evidence of surrounding inflammatory reaction, with no evidence of testicular torsion - 3 early morning urine samples for acid-fast bacilli staining, culture and NAAT - may be positive - HIV test - may be positive - Syphilis test - may be positive
93
Generate a mangement plan for epididymitis and orchitis.
BACTERIAL INFECTION - Abx - Supportive measures - paracetamol or naproxen or ibuprofen NB: Abx Gonorrhoea / Chlamydia suspected - ceftriaxone and doxycycline Gonorrhoea / Chlamydia suspected, Gonorrhoea likely - ceftriaxone, doxycycline and azithromycin Gonorrhoea / Chlamydia / Enteric organisms suspected - ceftriaxone, ofloxacin / levofloxacin Enteric organisms suspected - ofloxacin or levofloxacin M Genitalium suspected - moxifloxacin AMIODARONE-INDUCED - Discontinuation or dose reduction - Supportive measures - paracetamol or naproxen or ibuprofen UNDERLYING VASCULITIS - Specialist referral to rheumatologist - can be due to Behcet's Syndrome or Henoch-Schonlein purpura - Supportive measures - paracetamol or naproxen or ibuprofen IDIOPATHIC OR VIRAL - Supportive measures - paracetamol or naproxen or ibuprofen TB - Anti-TB antibiotics - guidelines! - Specialist referral - Supportive measures - paracetamol or naproxen or ibuprofen
94
Identify the possible complications of epididymitis and orchitis and its management.
- Scrotal abscess and pyocele - Testicular infarction - Fertility problems - Testicular atrophy - Cutaneous fistulization from rupture of abscess through tunica vaginalis - Recurrence, chronic epididymitis and orchialgia
95
Summarise the prognosis for patients with epididymitis and orchitis.
Most epididymitis cases clear up within 3 months. However, more invasive treatment may be needed in some cases. If an abscess has formed on the testicles, your doctor can drain the pus using a needle or with surgery. Surgery is another option if no other treatments have been successful.
96
Define HIV.
A pandemic infectious disease whose impact on societies is without precedent. AIDS - develops over 10-15 years.
97
Explain the aetiology / risk factors of HIV.
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 malignancies. Most people are infected through sexual contact, before birth or during delivery, during breastfeeding, or when sharing contaminated needles and syringes. Risk Factors: - Needle sharing with IV drug use - Unprotected receptive anal intercourse - Unprotected receptive penile-vaginal sexual intercourse - Percutaneous needle stick injury - High maternal viral load - mother to child transmission - Use of progestin-only injectable contraceptives - HSV-2 infection
98
Summarise the epidemiology of HIV.
1.7 million people were newly infected in 2018.
99
Recognise the presenting symptoms of HIV.
- Presence of risk factors - Fevers - Night sweats - Weight loss - Skin rashes - Post-inflammatory scars - Oral ulcers - Angular cheilitis - Oral thrush - Oral hairy leukoplakia - Diarrhoea - Wasting syndrome - Changes in mental status or neuropsychiatric function - Recent hospital admissions - TB - Medical comorbidities - Sexual activity - Generalised lymphadenopathy - Kaposi's sarcoma - Genital STIs - Chronic vaginal candidiasis - Shingles - Headaches - Periodontal disease - Retinal lesions on fundoscopy - SOB - Cyanosis - Dry cough - Silent chest - Peripheral neuropathy - Hepatomegaly or splenomegaly - Meningeal signs (bacterial or viral meningitis)
100
Recognise the signs of HIV on physical examination.
- Presence of risk factors - Fevers - Night sweats - Weight loss - Skin rashes - Post-inflammatory scars - Oral ulcers - Angular cheilitis - Oral thrush - Oral hairy leukoplakia - Diarrhoea - Wasting syndrome - Changes in mental status or neuropsychiatric function - Recent hospital admissions - TB - Medical comorbidities - Sexual activity - Generalised lymphadenopathy - Kaposi's sarcoma - Genital STIs - Chronic vaginal candidiasis - Shingles - Headaches - Periodontal disease - Retinal lesions on fundoscopy - SOB - Cyanosis - Dry cough - Silent chest - Peripheral neuropathy - Hepatomegaly or splenomegaly - Meningeal signs (bacterial or viral meningitis)
101
Identify appropriate investigations for HIV and interpret the results.
1st Line: - Serum HIV ELISA - Serum HIV rapid test - HIV non-invasive tests - Serum Western blot - Serum p24 antigen - Serum HIV DNA PCR - CD4 count - CD4 count of >500 cells/mL: patients are usually asymptomatic; CD4 count of <350 cells/mL: implies substantial immune suppression; CD4 count <200 cells/microlitre: defines AIDS and places the patient at high risk of most opportunistic infections - Serum viral load (HIV RNA) - Drug resistance testing - Pregnancy test - Serum hep B serology - Serum hep C serology - Serum venereal disease research lab test - positive if syphilis infection - Treponema pallidum haemagglutination test - positive if syphilis infection - Rapid plasma reagin - positive if syphilis infection - Tuberculin skin test - FBC with differential - anaemia, thrombocytopenia - Serum electrolytes - Serum creatinine - Urinalysis - proteinuria (renal disease), leukocytes and nitriles (UTI) Consider: - CXR - Pneumocystis jirovecii pneumonia: interstitial to extensive alveolar shadowing; TB: many abnormalities possible including apical fibrosis/scarring, pleural effusion, hilar adenopathy, miliary pattern, lobar or patchy opacification; bacterial pneumonia: lobar or patchy opacification - LFTs - Random of fasting lipid profile - ART high levels - Random or fasting plasma glucose - ART high levels - Hep A serology (IgG) - Toxoplasma serology (IgG) - Gonorrhoea and Chalmydia testing - HLA-B*5701 testing
102
Define mastitis / breast abscesses.
Localised infection with pus collection in breast tissue. 2 main forms - puerperal (lactational) and non-puerperal.
103
Explain the aetiology / risk factors of mastitis / breast abscesses.
Lactational: - Milk stasis associated with infection - Most commonly with Staphylococcus aureus, coagulase-negative staphylococci Non-Puerperal: - Staphylococcus aureus and anaerobes - Enterococci or Bacteroides spp. - TB and actinomycosis - more rare - Smoking, mammary duct ectasia / periductal mastitis, associated inflammatory breast cancer excluded - Associated with wound infections after breast surgery, diabetes and steroid therapy
104
Summarise the epidemiology of mastitis / breast abscesses.
Lactational breast abscesses are common and tend to occur soon after starting breast-feeding and on weaning, when incomplete emptying of the breast results in stasis and engorgement. Non-lactational abscesses are more common in those aged 30-60 years and in smokers.
105
Recognise the presenting symptoms of mastitis / breast abscesses.
The patient complains of discomfort and development of a painful swelling in an area of the breast. She may complain of feeling unwell and feverish. Women with a non-puerperal abscess often have a history of previous infections, systemic upset is often less pronounced.
106
Recognise the signs of mastitis / breast abscesses on physical examination.
Local - Area of breast is swollen, warm and tender - Overlying skin inflammation - Cracks or fissures in nipple - Non-puerperal cases - evidence of scars or tissue distortion, or signs of duct ectasia (e.g. nipple retraction) Systemic - Pyrexia - Tachycardia
107
Identify appropriate investigations for mastitis / breast abscesses and interpret the results.
- USS | - Aspiration for microscopy, culture and sensitivity of pus samples
108
Generate a management plan for mastitis / breast abscesses.
Medical - Early, cellulitic phase treated with antibiotics - flucloxacillin for lactational, +metronidazole in non-puerperal - Breast drainage regularly to prevent milk stasis Surgical Lactational - Daily needle aspiration with antibiotic cover - Formal incision and drainage for >5cm - Cosmetically acceptable and ensures full drainage - Loculi explored and broken down - Wound may be packed lightly and left open, with daily packing, or primary closure performed - Breastfeeding should continue from the non-affected breast and the affected side emptied either manually or with a breast pump - Advice on avoided cracked nipples Non-puerperal - Open drainage should be avoided - Carried out through small incision - Definitive treatment carried out once infection has settles by the excision of the involved duct system
109
Identfiy the possible complications of mastitis / breast abscesses and its management.
- Slow wound healing - Difficulties in breastfeeding - Poor cosmetic outcome - Mammary fistula formation - Overlying skin undergoes necrosis
110
Summarise the prognosis for patients with mastitis / breast abscesses.
- Untreated, it will eventually point and spontaneously discharge onto the skin surface - Non-puerperal abscesses tend to recur
111
Define neutropenic sepsis.
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.
112
Explain the aetiology / risk factors of neutropenic sepsis.
Causes: - Cytotoxic chemotherapy - temporary reduction in production of blood cells (5-10 days after chemotherapy neutrophils are at their lowest, recover 5 days later) - Drugs - azathioprine, methotrexate, sulfasalazine, adalimumab, infliximab - Stem cell transplantation - Infections - Bone marrow disorders such as aplastic anaemia and myelodysplastic syndromes - Nutritional deficiencies - Autoimmune Risk factors: - People receiving high-intensity chemotherapy regimens - People undergoing haematopoietic stem cell transplantations - Age - >60yrs - Chemotherapy - Corticosteroids - Antibiotics - Advanced maliganncy - History of previous febrile neutropenia - Prolonged hospital admission - Previous surgery - DM - Liver disease - Renal disease - Poor nutritional status - CV access device - TPN - risk of invasive fungal infection
113
Summarise the epidemiology of neutropenic sepsis.
Rate of increase of deaths is higher for 15-24 year old age group, lower for >80 age group.
114
Recognise the presenting symptoms of neutropenic sepsis.
- Neutrophil count <0.5 x 10^9/L - Temperature >38 degrees - Chills and shvering - Tachycardia - Tachypnoea - Clammy - Cold - Pale or mottled skin - Dizziness - Confusion - Disorientation - Slurred speech - Diarrhoea - N&V
115
Recognise the signs of neutropenic sepsis on physical examination.
- Neutrophil count <0.5 x 10^9/L - Temperature >38 degrees - Chills and shvering - Tachycardia - Tachypnoea - Clammy - Cold - Pale or mottled skin - Dizziness - Confusion - Disorientation - Slurred speech - Diarrhoea - N&V
116
Identify appropriate investigations for neutropenic sepsis and interpret the results.
Take blood tests and microbiology samples including: - Blood gas including glucose and lactate measurement — hypoglycaemia may result from depleted glycogen stores; hyperglycaemia may result from the stress response to sepsis; hyperlactataemia is a non-specific indicator of cellular or metabolic stress and is a marker of illness severity, with a higher level predictive of higher mortality rates. - Blood culture — ideally done before antibiotic administration. - Full blood count — white cell count may be high or low; thrombocytopenia may indicate disseminated intravascular coagulation (DIC), but may also be chemotherapy- or tumour-related. - C-reactive protein (CRP) — may indicate infection and/or inflammation. - Creatinine, urea and electrolytes — may indicate dehydration and/or acute kidney injury. - Liver function tests — increased bilirubin or alanine aminotransferase (ALT) levels may indicate cholestasis or other liver dysfunction, and may be chemotherapy-induced. - Clotting screen — if abnormal may indicate coagulopathy/DIC. - Urine analysis and culture, sputum microscopy and culture, chest X-ray, and additional investigations such as chest CT or bronchoalveolar lavage may be indicated if there is severe or prolonged neutropenia. This may allow identification of the source of infection, pathogen(s) and sensitivities, and subsequent tailoring and/or de-escalation of antibiotic therapy if appropriate. Source control to eliminate a focus of infection may be possible, such as abscess drainage, debridement of infected tissue, removal of infected devices or foreign bodies, or surgery.
117
Define meningitis.
Inflammation of the leptomeningeal (pia mater and arachnoid) coverings of the brain, most commonly caused by infection. Aseptic meningitis - characterised by clinical and laboratory evidence for meningeal inflammation and negative routine bacterial culture Mollaret's meningitis - recurrent benign lymphocytic meningitis
118
Explain the aetiology / risk factors of meningitis.
Bacterial - Neonates - Group B streptococci, Escherichia coli, Listeria monocytogenes - Children - Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae - Adults - Neisseria meningitidis (meningococcus), Streptococcus pneumonia, tuberculosis - Elderly - Streptococcus pneumoniae, Listeria monocytogenes Viral - Enteroviruses - Mumps - HSV - VZV - HIV Fungal - Cryptococcus - associated with HIV infection Aseptic Meningitis - Enterovirus, mycobacteria, fungi, spirochetes - Autoimmune - e.g. Sarcoidosis, Behcet's disease, Systemic lupus erythematosus - Malignancy - lymphoma, leukaemia, metastatic carcinomas - Medication - NSAIDs, trimethoprim, azathioprine Mollaret's Meningitis - 50% exhibit transient neurological manifestations - HSV-2 - Large granular plasma cells on Papnicolaou's stain, PCR for HSV DNA - Treat with acyclovir Risk Factors: - Close communities - e.g. dormitories - Basal skull fractures - Mastoiditis - Sinusitis - Inner ear infections - Alcoholism - Immunodeficiency - Splenectomy - Sickle cell anaemia - CSF shunts - Intracranial surgery
119
Summarise the epidemiology of meningitis.
Variation according to geography, age, social conditions. UK Public Health Laboratory Service receives approx 2500 notifications / year. Recent visitors to Haj (meningococcal serogroup W135). Epidemics occur in the meningitis belt of Africa (meningococcal serogroup A).
120
Recognise the presenting symptoms of meningitis.
- Severe headache - Photophobia - Neck or backache - Irritability - Drowsiness - Vomiting - High-pitched crying or fits (common in children) - Clouding of consciousness - Fever Check travel and exposure history: - Rodents - lymphocytic choriomeningitis virus - Ticks - Lyme borrelia, Rocky Mountain spotted fever - Mosquitoes - West Nile virus, St. Louis encephalitis virus - Sexual activity - HSV-2, HIV, syphilis - Travel - C.immitis, A.cantonensis - Contact with other individuals with vrial exanthems - enteroviruses
121
Recognise the signs of meningitis on physical examination.
Signs of Meningism: - Photophobia - Neck stiffness - Kernig's sign - with hips flexed, pain / resistance on passive knee extension - Brudzinski's sign - flexion of hips on neck flexion Signs of Infection - Fever - Tachycardia - Hypotension - Skin rash - petechiae with meningococcal septicaemia - Altered mental state
122
Identify appropriate investigations for meningitis and interpret the results.
1. Bloods 2. Imaging 3. Lumbar Punctre 4. viral 5. TB Bloods - 2 sets of blood cultures - do not delay antibiotics Imaging - CT scan to exclude a mass lesion or raised intracranial pressure before LP - LP may lead to cerebral herniation due to subsequent CSF removal - CT head before LP in patents with immunodeficiency, history of CNS disease, reduced consciousness, fit, focal nerologic deficit, papilloedema LP - Note opening CSF pressure - Send for microscopy with culture, sensitivity, Gram staining, biochemistry, cytology - Streptococcus pneumoniae - Gram-positive diplococcic - Neisseria Meningitidis - gram-negative diplococcic Bacterial - Cloudy CSF - Increased neutrophils - Increased protein - Reduced glucose - CSF serum glucose ratio of <0.5 Virus - Increased lymphocytes - Increased protein - Normal glucose TB - Fibrinous CSF - Increased lymphocytes - Increased protein - Reduced glucose Staining of petechiae scrapings may detect meningococcus in 70%. Additional studies - e.g. viral PCR, staining / culture for mycobacteria and fungi, HIV test depending on the clinical presentation / CSF findings.
123
Generate a management plan for meningitis.
1. IMMEDIATE ANTIBIOTICS IV or IM - If meningitis suspected before lumbar puncture or CT - 3rd generation cephalosporin - cefotaxime 2g QDS or ceftriaxone 2g BD - Benzylpenicillin - initial blind therapy, sensitive meningococci and pneumococci - Listeria = amoxicillin + gentamicin - Penicillin & Cephalosporin resistant pneumococci = + vancomycin + rifampicin - History of anaphylaxis to penicillin or cephalosporins = chloramphenicol - Patients treated with benzylpenicillin or chloramphenicol = 2 days rifampicin (eliminate nasopharyngeal carriage) 2. DEXAMETHASONE IV - 10mg QDS for 4 days - Given shortly before or with first dose of antibiotics - Continue in pneumococcal or H. influenzae meningitis - reduce complications of death (pneumococcal) and hearing loss (H.influenzae) - Avoid dexamethasone if HIV suspected 3. RESUSCITATION - ITU 4. PREVENTION - Notify public health services - Consult a consultant in communicable disease control for advice regarding chemoprophylaxis - e.g. rifampicin for 2 days - Vaccination for close contacts - Vaccination against meningococcal serogroups A and C (none for B)
124
Identify the possible complications of meningitis and its management.
- Septicaemia - Shock - DIC - Renal failure - Fits - Peripheral gangrene - Cerebral oedema - Cranial nerve lesions - Cerebral venous thrombosis - Hydrocephalus - Water house - Friderichsen Syndrome - bilateral adrenal haemorrhage
125
Summarise the prognosis for patients with meningitis.
Bacterial meningitis mortality at 10-40% with meningococcal sepsis. In developing countries - higher mortality rate Viral meningitis - self-limiting
126
Define myocarditis.
Acute inflammation and necrosis of cardiac muscle = myocardium.
127
Explain the aetiology / risk factors of myocarditis.
Infection: - Viruses - e.g. Coxackie B, echovirus, EBV, CMV, adenovirus, influenza - Bacterial - e.g. post-streptococcal, tuberculosis, diptheria, Lyme disease - Fungal - e.g. candidiasis - Protozoal - e.g. trypanosomiasis (Chagas disease) - Helminths - e.g. thrichinosis Non-infective: - Systemic disorders - e.g. SLE, sarcoidosis, polymyositis - Hypersensitivity myocarditis - e.g. sulphonamides Drugs: - Chemotherapy agents - e.g. doxorubicin, streptomyocin - Cocaine abuse - Heavy metals - Radiation
128
Summarise the epidemiology of myocarditis.
Unknown. Many cases not detected at time of acute illness. Europe & USA - Coxsackie B virus SA - Chagas disease.
129
Recognise the presenting symptoms of myocarditis.
- Prodromal 'flu-like' illness - Fever - Malaise - Fatigue - Lethargy - Breathlessness - pericardial effusion, myocardial dysfunction - Sharp chest pain - suggesting associated pericarditis
130
Recognise the signs of myocarditis on physical examination.
Signs of concurrent pericarditis or complications - e.g. heart failure, arrhythmia.
131
Identify appropriate investigations for myocarditis and interpret the results.
1) Blood 2) ECG 3) CXR 4) Pericardial fluid drainage 5) Echocardiography 6) Myocardial biopsy Bloods - FBC - high WCC in infective causes - U&E - High ESR or CRP - Cardiac enzymes high - Antistreptolysin O titre, ANA, serum ACE, TFT - viral or bacterial serology ECG - Non-specific T wave and ST changes - Widespread saddle-shaped ST elevation in pericarditis CXR - Normal - Cardiomegaly - Pulmonary oedema Pericardial fluid drainage - Glucose - Protein - Cytology - Culture - Sensitivity Echocardiography - Systolic / diastolic function - Wall motion abnormalities - Pericardial effusion Myocardial Biopsy - Rarely required - Result does not influence management
132
Define malaria.
A parasitic infection caused by protozoa of the genus Plasmodium.
133
Explain the aetiology / risk factors of malaria.
5 species infect humans. - Plasmodium falciparum (or P. falciparum) - Plasmodium malariae (or P. malariae) - Plasmodium vivax (or P. vivax) - Plasmodium ovale (or P. ovale) - Plasmodium knowlesi (or P. knowlesi) Naturally transmitted to humans through a bite by an infected female Anopheles mosquito, potentially transmitted by blood transfusion or organ transplantation. Widely distributed throughout tropical and subtropical regions. Travellers account for the majority of disease in Western countries. Risk factors: - Travel to endemic area - Inadequate or absent chemoprophylaxis - Insecticide-treated bed net not used in endemic area - Settled migrants returning from travel to endemic area of origin - Iron administration (children) Risk factors for SEVERE DISEASE: - Low host immunity - Pregnancy - Age < 5 years - Immunocompromise - Older age
134
Summarise the epidemiology of malaria.
Malaria is a major health problem in Africa, Asia, Central America, Oceania, and South America. About 40% of the world's population lives in areas where malaria is common. Approximately 300-500 million cases of malaria occur every year, and 1-2 million deaths occur, most of them in young children.
135
Recognise the presenting symptoms of malaria.
- Presence of risk factors for acquiring malaria - Presence of risk factors for severe disease - Fever or history of fever - Headache - Weakness - Myalgia - Arthalgia - Anorexia - Diarrhoea - Seizures - N&V - Abdominal pain - Pallor - Hepatosplenomegaly - Jaundice - Altered level of consciousness - Hypotension - Anuria / oliguria - Influenza-like respiratory symptoms
136
Recognise the signs of malaria on physical examination.
- Presence of risk factors for acquiring malaria - Presence of risk factors for severe disease - Fever or history of fever - Headache - Weakness - Myalgia - Arthalgia - Anorexia - Diarrhoea - Seizures - N&V - Abdominal pain - Pallor - Hepatosplenomegaly - Jaundice - Altered level of consciousness - Hypotension - Anuria / oliguria - Influenza-like respiratory symptoms
137
Identify appropriate investigations for malaria and interpret the results.
1st Line: - Giemsa-stained thick and thin blood smears - detection of asexual or sexual forms of parasites inside erythrocytes - Rapid diagnostic tests (RDTs) - detection of parasite antigen or enzymes - FBC - thrombocytopenia, anaemia, variable WCC - Clotting profile - PT prolonged - Serum electrolytes, urea and creatinine - normal or mildly impaired, renal failure in severe infection - Serum LFTs - elevated bilirubin, elevated aminotransferases - Serum blood glucose - hypoglycaemia, hyperglycaemia - Urinalysis - moderate protein, urobilinogen, conjugated bilirubin - ABG - metabolic acidosis or lactic acidosis (severe) Consider: - PCR blood for malaria - detection of parasites at very low levels - CXR - pneumonia, pulmonary oedema, ARDS - Blood culture - no abnormal growth (search for other causes) - Urine culture - no abnormal growth (search for other causes) - Sputum culture - no abnormal growth (search for other causes ) - Lumbar puncture - exclude bacterial meningitis, sometimes CSF lactate elevated - HIV test - may be positive (more severe malaria in presence of HIV) - PCRT nasopharyngeal swabs for influenza - negative in malaria - CT head - usually normal - Loop-mediated isothermal amplification - detection of parasites at very low levels
138
Define necrotising fasciitis.
A life-threatening subcutaneous soft-tissue infection that may extend to the deep fascia, but not into the underlying muscle.
139
Explain the aetiology / risk factors of necrotising fasciitis.
Can be aerobic, anaerobic or mixed flora. TYPE 1 - Polymicrobial infection - Anaerobe - e.g. Bacteroides or Peptostreptococcus - Facultative anaerobe - e.g. Enterobacterales, non-group A streptococcus TYPE 2 - Monomicrobial infection - E.g. Streptococcus pyogenes (group A strep) Specific Risk Factors: - Freshwater exposure - Aeromonas hydrophila - Saltwater exposure or consumption of raw oysters - Vibrio vilnificus General Risk Factors: - Inpatient contact with index case - Varicella zoster infection - Cutaneous injury - Surgery - Trauma - Non-traumatic skin lesions - IV drug use - Chronic illness - Immunosuppression - NSAIDs
140
Summarise the epidemiology of necrotising fasciitis.
The number of cases reported for necrotizing fasciitis in adults is 0.40 cases per 100,000 people/year while the incidence in children is reportably higher at 0.08 cases per 100,000 people/year. Necrotizing fasciitis is considered a rare condition, however, the mortality rate remains high.
141
Recognise the presenting symptoms of necrotising fasciitis.
- Presence of risk factors - Anaesthesia or severe pain over site of cellulitis - Fever - Palpitations - Tachycardia - Tachynpnoea - Hypotension - Lightheadedness - N&V - Delirium - Crepitus - Vesicles or bullae - Grey discolouration of skin - Oedema or induration - Location of lesion
142
Recognise the signs of necrotising fasciitis on physical examination.
- Presence of risk factors - Anaesthesia or severe pain over site of cellulitis - Fever - Palpitations - Tachycardia - Tachynpnoea - Hypotension - Lightheadedness - N&V - Delirium - Crepitus - Vesicles or bullae - Grey discolouration of skin - Oedema or induration - Location of lesion
143
Identify appropriate investigations for necrotising fasciitis and interpret the results.
1st Line: - FBC and differential - abnormally high or low WBC count with or without a left shift, high % of polymorphonuclear leukocytes - Serum electrolytes - LOW sodium - Serum urea and creatinine - HIGH - Serum CRP - HIGH - Serum creatinine kinase - HIGH - Serum lactate - HIGH - Blood and tissue cultures - indicates polymicrobial or monomicrobial aetiology - Gram stain - ABG - hypoxaemia, acidosis - Radiography, CT/ MRI, US Scan - oedema extending along fascial plan and/or soft tissue gas - Surgical exploration - necrotising soft-tissue infection
144
Define osteomyelitis.
An inflammatory condition of bone caused by an infecting organism, most commonly Staphylococcus aureus.
145
Explain the aetiology / risk factors of osteomyelitis.
Usually involves single bone, but rarely affects multiple sites. Occurs in peripheral or axial skeleton. Stage on the aetiology of infection, pathogenesis, extent of bone involvement, duration and host factors particular to the individual patients. Either haematogenous or contigous-focus. Risk factors: - Previous osteomyelitis - Penetrating injury - IV drug misuse - Diabetes - HIV infection - Recent surgery - Distant or local infections - Sickle cell anaemia - RA - CKD - Immunocompromising conditions - URTI - Varicella infection
146
Summarise the epidemiology of osteomyelitis.
The annual incidence of osteomyelitis was less than eleven cases per 100,000 person-years until the sixth decade of life. Thereafter, incidence rates increased steeply with age, corresponding to a roughly 50% increase in incidence per decade of life.
147
Recognise the presenting symptoms of osteomyelitis.
- Risk factors - Limp or reluctance to weight-bear - Non-specific pain at site of infection - Malaise and fatigue - Local back pain associated with systemic symptoms - Paravertebral muscle tenderness and spasm - Local inflammation, tenderness, erythema or swelling - Fever - Spinal cord or nerve root compression - Wound drainage, acute or old healed sinuses - Scars, previous flaps, fracture fixation - Reduced range of movement - Reduced sensation in diabetic foot infection - UTI symptoms - Torticollis - Skin or other infections, recent episodes of Staphylococcus aureus bloodstream infection, indwelling catheter - Limb deformity - Tenderness to percussion - Meningitis
148
Recognise the signs of osteomyelitis on physical examination.
- Risk factors - Limp or reluctance to weight-bear - Non-specific pain at site of infection - Malaise and fatigue - Local back pain associated with systemic symptoms - Paravertebral muscle tenderness and spasm - Local inflammation, tenderness, erythema or swelling - Fever - Spinal cord or nerve root compression - Wound drainage, acute or old healed sinuses - Scars, previous flaps, fracture fixation - Reduced range of movement - Reduced sensation in diabetic foot infection - UTI symptoms - Torticollis - Skin or other infections, recent episodes of Staphylococcus aureus bloodstream infection, indwelling catheter - Limb deformity - Tenderness to percussion - Meningitis
149
identify appropriate investigations for osteomyelitis and interpret the results.
1st Line: - FBC - HIGH WCC - ESR - HIGH - CRP - HIGH - Blood culture - may be positive, indicating infecting organism and microbial sensitivities - Plain XR of affected area Results of XR - ACUTE DISEASE - Initially normal - Osteopenia 6-7 days after infection onset - Evidence of bone destruction, cortical breaches and periosteal reaction - Involucra and sequestra sometimes seen - Diffuse osteopenia developing later due to disuse of affected limb - Joint effusion in local joints Results of XR - DISCITIS - Lacteral spin radiographs show late changes at 2-3 weeks into illness - Decreased intervertebral space - Erosion of vertebral plate Results of XR - VERTEBRAL OSTEOMYELITIS: - Localised rarefication (thinning) of vertebral body - Anterior bone destruction later on Results of XR - CHRONIC DISEASE - Intramedullary scalloping - Cavities - Cloacae seen - Fallen leaf sign when a piece of endosteal sequestrum detached and fallen into medullary canal Consider: - Bone samples and bone biopsy - positive, other pathology shown - PCR - MALDI-TOF mass spectrometry - match reference strains - Swabs - Urine microscopy, culture and sensitivities - Histology 0 infecting organisms, acute or chronic inflammatory cells, dead bone, active bone resorption, small sequestra, malignancy - Probe-to-bone test - may reach bone, rule in osteomyelitis in high-risk patient with diabetes - Bone MRI - high signal on T2 images, fat suppression sequences, changes in children within 3-5 days of onset, vertebral bone changes - US - collections, subperiosteal abscesses, adjacent joint infusions - CT scan - bone destruction, sequestra, abscess - Radionuclide scan - increased uptake of radioactive injectate in infected sites - Bone scintigraphy - hot spots of infection, positive 24hrs after onset - Echocardiogram - valvular vegetations - CXR - show primary or reatcive TB - Mantoux test - positive for Mycobacteruim TB
150
Define pericarditis.
Inflammation of the pericardium, may be acute, subacute or chronic.
151
Explain the aetiology / risk factors of pericarditis.
- Idiopathic - Infective - commonly Coxsackie B, echovirus, mumps virus, streptococci, fungi, staphylococci, TB - Connective tissue disease - e.g. sarcoid, SLE, scleroderma - Post-myocardial infarction (24-72h) in up to 20% of patients - Dressler's Syndrome (weeks to months after acute MI) - Malignancy ( lung, breast, lymphoma, leukaemia, melanoma) - Metabolic (myxoedema, uraemia) - Radiotherapy - Thoracic surgery - Drugs - e.g. hydralazine, isoniazid
152
Summarise the epidemiology of pericarditis.
Uncommon Clinical incidence <1 in 100 hospital admissions. More common in males.
153
Recognise the presenting symptoms of pericarditis.
Chest pain: - Sharp - Central - Radiates to neck and shoulders - Aggravated by coughing, deep inspiration, lying flat - Relieved by sitting forward - Dyspnoea - Nausea
154
Recognise the signs of pericarditis on physical examination.
- Fever - Pericardial friction rub - best heard lower left sternal edge, with patient leaning forward in expiration - Heart sounds may be faint in the presence of an effusion Cardiac tamponade: - High JVP (Bell's Triad) - Low BP (^^) - Muffled heart sounds (^^) - Tachycardia - Pulsus paradoxus - Reduced SBP by >10mmHg on inspiration Constrictive Pericarditis (Chronic): - High JVP with inspiration - Kussmaul's sign - Pulsus paradoxus - Hepatomegaly - Ascites - Oedema - Pericardial knock - rapid ventricular filing - AF
155
Identify appropriate investigations for pericarditis and interpret the results.
1) ECG 2) Echocardiogram 3) Bloods 4) CXR ECG - Widespread ST elevation that is saddle shaped Echocardiogram - Assess pericardial effusion and cardiac function Bloods - FBC - U&E - ESR - CRP - Cardiac enzymes - normal - Blood cultures - ASO titres - ANA - Rheumatoid factor - TFT - Mantoux test - Viral serology CXR - Normal - globular heart shadow if 250mL effusion - Pericardial calcification can be seen in constrictive pericarditis - best seen on lateral CXR or CT
156
Generate a management plan for pericarditis.
- Acute - cardiac tamponade treated by emergency pericardiocentesis - Medical - treat underlying cause, NSAIDs for relief of pain and fever - Recurrent - low-dose steroids, immunosuppressants or colchicine - Surgical - excision of pericardium in constrictive pericarditis
157
Identify the possible complications of pericarditis and its management.
- Pericardial effusion - Cardiac tamponade - Cardiac arrhythmia
158
Summarise the prognosis for patients with pericarditis.
Depends on underlying cause Good prognosis in viral cases - recovery within 2 weeks Poor in malignant pericarditis Recurrent - particularly in those caused by thoracic surgery
159
Define rheumatic fever.
An inflammatory multisystem disorder, occurring following group A B-haemolytic streptococci (GAS) infection.
160
Explain the aetiology / risk factors fo rheumatic fever.
Unknown. Streptococcal pharyngeal infection required. Genetic susceptibility. Molecular mimicry - role in the initiation of tissue injury - e.g. antibodies directed against GAS antigens cross-react with host antigens
161
Summarise the epidemiology of rheumatic fever.
5-15 years - peak incidence Far East, Middle East, Easter Europe, South America Mean incidence 19/100,000 . Reduction in incidence in West, non-Western countries incidence is relatively high.
162
Recognize the presenting symptoms of rheumatic fever.
- 2-5 weeks after GAS infection - Fever - Malaise - Anorexia - Painful, swollen joints - Reduced movement and function - Breathlessness - Chest pain - Palpitations
163
Recognise the signs of rheumatic fever on physical examination.
- Duckett Jones Criteria - positive diagnosis if at least 2 major criteria, or one major plus 2 minor criteria Major Criteria: - Arthritis - migratory or fleeting polyarthritis with swelling, redness, tenderness of large joints - Carditis - new murmur (Carey Coombs murmur - mid-diastolic murmur due to mitral valvulitis), pericarditis, pericardial effusion or rub, cardiomegaly, cardiac failure, ECG changes - Chorea - rapid, involuntary, irregular movements with flowing or dancing quality, slurred speech (more common in females) - Nodules - small, firm, painless, subcutaneous nodules on extensor surfaces, joints and tendons - Erythema Marginatum (20%) - transient erythematous rash with raised edges, seen on trunk and proximal limbs (cresent or ring-shaped patches) Minor Criteria - Pyrexia - Previous rheumatic fever - Arthralgia - only if arthritis is not present as major criteria - Recent streptococcal infection - supported by positive throat cultures or high antitreptolysin O titre - High ESR, CRP orWCC - High PR and QT intervals on ECG - if carditis not present as major criteria
164
Identify appropriate investigations for rheumatic fever and interpret the results.
1. Bloods 2. Throat swab 3. ECG 4. Echocardiogram Bloods - FBC - raised WCC - ESR/CRP - raised ESR, CRP - Raised antitreptolysin O titre Throat Swab - Culture for GAS - Rapid streptococcal antigen test ECG - Saddle shaped ST elevation - PR segment depression - Arrhythmias (signs of pericarditis) Echocardiogram - Pericardial effusion - Myocardial thickening or dysfunction - Valvular dysfunction
165
Define peritonitis.
Inflammation of the peritoneum, caused by bacterial infection either via the blood or after rupture of an abdominal organ. E.g. Perforation of peptic ulcer, duodenal ulcer, diverticulum, appendix, bowel, gallbladder Spontaneous bacterial peritonitis - seen in patients with cirrhosis, and is an infection of ascitic fluid that can't be attributed to any intra-abdominal, ongoing inflammatory, or surgically correctable condition
166
Explain the aetiology / risk factors of peritonitis.
Due to bacterial infection Risk factors: - Decompensated hepatic state - Low ascitic protein / complement - GI bleeding - Endoscopic sclerotherapy for oesophageal varices
167
Summarise the epidemiology of peritonitis.
The prevalence of SBP in patients with cirrhosis and ascitis at the time of hospital admission ranges from 10-27%.
168
Recognise the presenting symptoms of peritonitis.
- Prostration - the action of lying stretched out on the ground - Ascites - Fever - Shock - Lying still - +ve cough test - Tenderness- with/without rebound / percussion pain - Board-like abdominal rigidity - Guarding - No bowel sounds - Erect CXR may show gas under the diaphragm - Hypothermia - Hypotension - Tachycardia
169
Recognise the signs of peritonitis on physical examination.
NB: Always check serum amylase as acute pancreatitis also shows these symptoms!
170
Identify appropriate investigations for peritonitis and interpret the results.
NB: Always check serum amylase as acute pancreatitis also shows these symptoms! - Ascitic fluid lab tests - cell count, culture - Urine - look at leukocyte esterase - Defined by ascitic fluid absolute neutrophil count >250cells/mm^3 - Ascitic fluid pH and asterial blood PH - Ascitic fluid protein, glucose, lactate dehydrogenase - Bloos - FBC, creatinine
171
Generate a management plan for peritonitis.
- Antibiotics - beware of local resistance patterns - If sepsis, history of fluoroquinolone prophylaxis, nosocomial-acquired SBP, history of previous infections with resistant organisms --> broader initial empirical coverage - Albumin indicated in renal dysfunction patients - Continuous antibiotic prophylaxis if ascitic fluid protein concentration <15g/L or previous episode of SBP
172
Identify the possible complications of peritonitis and its management.
- Dehydration - Sepsis - Multiple organ infection / failure - Hepatic encephalopathy - Hepatorenal syndrome - liver disease leading to increasing renal failure - Shock - Death
173
Summarise the prognosis for patients with peritonitis.
Depends on underlying cause or how rapidly the patient is effectively treated, especially for infectious bacteria. Ranges from good (appendicitis) to poor (hepatorenal syndrome).
174
Define pneumonia.
Infection of the distal lung parenchyma. Categories: - Community-acquired, hospital-acquired or nosocomial - Aspiration pneumonia, pneumonia in the immunocompromised - Typical and atypical - e.g. Mycoplasma, Chlamydia, Legionella
175
Explain the aetiology / risk factors of pneumonia.
Community-Acquired: - Streptococcus pneumonia (70%) - COPD = Haemophilus influenzae & Morazella catarrhalis - Contract with Birds/Parrots = Chlamydia pneumonia & Chlamydia psittaci - Periodic epidemics = Mycoplasms pneumonia - Anywhere with air con = Legionella - Recent influenza infection, IV drug users = Staphylococcus aureus - Q Fever, rare = Coxiella burnett - TB = may present as pneumonia Hospital-Acquired: - Gram-negative enterobacteria = Pseudomonas, Klebsiella - Anaerobes = aspiration pneumonia Risk Factors: - Age - Smoking - Alcohol - Pre-existing lung disease - Immunodeficiency - Contact with pneumonia
176
Summarise the epidemiology of pneumonia.
Incidence 5-11 in 1000 (25-44 in 1000 in elderly) | Community-acquired causes >60,000 deaths/year in UK
177
Recognise the presenting symptoms of pneumonia.
- Fever - Rigors - Sweating - Malaise - Cough - Sputum (yellow, green or rusty in S pneumoniae) - Breathlessness - Pleuritic chest pain - Confusion - severe cases,elderly, Legionella Atypical Pneumonia: - Headache - Myalgia - Diarrhoea - Abdominal Pain
178
Recognise the signs of pneumonia on physical examination.
- Pyrexia - Respiratory distress - Tachypnoea - Tachycardia - Hypotension - Cyanosis - Reduced chest expansion - Dullness to percussion - Increased tactile vocal fremitus - Bronchial breathing - inspiration phase lasts as long as the expiration phase - Coarse crepitations on the affected side - Chronic suppurative lung disease (e.g. empyema, abscess): Clubbing
179
Identify appropriate investigations for pneumonia and interpret the results.
1. Bloods 2. CXR 3. Sputum 4. Urine 5. Atypical Viral Serology 6. Bronchoscopy & Bronchoalveolar Lavage Bloods - FBC - abnormal WCC - U&E - low Na+, especially with Legionella - LFT - Blood cultures - sensitivity 10-20% - ABG - to assess pulmonary function - Blood film - RBC agglutination by Mycoplasma caused by cold agglutinins CXR - Lobar or patchy shadowing - Pleural effusion - Klebsiella - often seen in upper lobes - Repeat 6-8 weeks - if abnormal suspect underlying pathology Sputum/Pleural Fluid - Microscopy - Culture & sensitivity - Acid-fast bacilli Urine - Pneumococcus antigens - Legionella antigens Atypical Viral Serology - Increased antibody titres between acute and convalescent samples - greater than 2 weeks post onset Bronchoscopy - If Pneumocystis carinii pneumonia is suspected - When pneumonia fails to resolve - When there is clinical progression
180
Generate a management plan for pneumonia.
1. Assess Severity - see prognosis, if >1 feature presents the manage in hospital 2. Start Empirical Antibiotics - Oral amoxicillin (0 markers) - Oral or IV amoxicillin and erythromycin (1 marker) - IV cefuroxime / cefotaxime / co-amoxiclav and erythromycin (>1 marker) - Add metronidazole, if aspiration, lung abscess or empyema suspected - Switch to the appropriate antibiotic as per sensitivity NB: Levofloxacin and moxifloxacin can provide useful alternatives in selected hospitalized patients with community-acquired pneumonia. 3. Supportive Treatment - Oxygen - maintain PO2 > 8kPa, start with 28% O2 in COPD to avoid hypercapnia - Parenteral fluids for dehydration or shock - Analgesia - Chest physiotherapy - CPAP, BiPAP or ITU care for respiratory failure - Surgical drainage may be needed for empyema / abscess 4. Discharge Planning - Presence of two or more features of clinical instability predict a significant chance of re-admission or mortality - Raised temperature, heart rate, respiratory rate - Low BP, oxygen saturation, mental status and oral intake 5. Non-Resolving Pneumonia - Consider other causes Causes of Non-Resolving Pneumonia - Unusual pathogens - e.g. Chlamydia psittaci, C.burnetti, Mycobacterium tuberculosis, Nocardia, Actinomyces israeli, fungi (Aspergillus, histoplasmosis, coccidioidomycosis, blastomycosis) - PE - Malignancy - e.g. bronchogenic carcinoma, bronchoalveolar cell carcinoma, lymphoma - Inflammatory - e.g. vasculitis, Wegener's granulomatosis, sarcoidosis, systemic lupus erythematosus - Congestive heart failure - Drug toxicity - Diffuse alveolar hemorrhage - Bronchiolitis obliterans-organizing pneumonia - Eosinophilic pneumonia - Acute interstital pneumonia - Pulmonary alveolar proteinosis 6. Prevention - Pneumococcal & H.influenzae type B vaccination in vulnerable groups - E.g. elderly, splenectomized
181
Identify the possible complications of pneumonia and its management.
- Pleural effusion - Empyema (pus in the pleural cavity) - Localized superation leading to lung abscess - seen by Staphyloccoal, Klebsiella pneumonia, presenting with swinging fever, persistent pneumonia, copious / foul-smelling sputum - Septic shock - ARDS - Acute renal failure M.Pneumonia - Erythema multiforme - Myocarditis - Haemolytic anaemia - Meningoencephalitis - Transverse myelitis - Guillian-Barre Syndrome
182
Summarise the prognosis for patients with pneumonia.
Most resolve with treatment (1-3 weeks). High mortality of severe pneumonia - Community-acquired - 5-10% - Hospital-acquired - 30% - 50% of those in ITU Markers of Severe Pneumonia (CURB-65 Score) C = Confusion U = Urea >7mmol/L R = RR >30/min B = BP - Systolic <90mmHg, Diastolic <60mmHg Age >65 years. Other markers are: - Hypoxia <8kPa - ECC <4 or >20 x 10^9 /mm^3 - Age >50 years
183
Define septic arthritis.
The infection of 1 or more joints caused by pathogenic inoculation of microbes. Occurs either by direct inoculation or haematogenous spread.
184
Explain the aetiology / risk factors of septic arthritis.
Regard a hot, swollen, acutely painful joint with restriction of movement as septic arthritis until proven otherwise, even in the absence of fever and irrespective of microbiology and blood test results. Risk factors: - Underlying joint disease - Prosthetic joint - Age - Immunosuppression - Contiguous spread - Exposure to ticks - Previous intra-articular corticosteroid injection - Recent joint surgery - Low socioeconomic status
185
Summarise the epidemiology of septic arthritis.
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.
186
Recognise the presenting symptoms of septic arthritis.
- Hot - Swollen - Painful - Restricted - Acute presentation - Fever - Large joint - Prosthetic joint - Single joint affected - Symptoms are out of proportion to elsewhere disease activitiy - Sexual activity - gonoccocal septic arthritis may present with polyarthralgia localising over one joint, fever, chills and skin lesions - Erythema migrans - Risk factors present
187
Recognise the signs of septic arthritis on physical examination.
- Hot - Swollen - Painful - Restricted - Acute presentation - Fever - Large joint - Prosthetic joint - Single joint affected - Symptoms are out of proportion to elsewhere disease activitiy - Sexual activity - gonoccocal septic arthritis may present with polyarthralgia localising over one joint, fever, chills and skin lesions - Erythema migrans - Risk factors present
188
Identify appropriate investigations for septic arthritis and interpret the results.
1st Line: - Synovial fluid microscopy, Gram stain and polarising microscopy - ?micro-organisms, urate or pyrophosphate crystals - Synovial fluid culture and sensitivities - Synovial fluid WCC - Blood culture and sensitivities - WCC - elevated - ESR - elevated - CRP - elevated - U&E - assess for sepsis and end-organ damage - LFTs - assess for sepsis and end-organ damage - Plain X-Ray - reveals degenerative changes or chondrocalcinosis (not diagnostic for septic arthritis) - USS - presence of effusion to guide aspiration Consider: - Procalcitonin (PCT) - raised >0.5ng/mL more specific marker for bacterial infection than CRP, ESR or WCC - MRI - ?associated osteomyelitis - PCR - Swabs for microscopy, culture and sensitivity - Urine dipstick - organisms on microscopy, WCC, blood - ELISA - Synovial biopsy - ? myobacterium tuberculosis, fungi - Calprotectin - high
189
Define tonsillitis.
An acute infection of the parenchyma of the palatine tonsils. DOES NOT INCLUDE TONSILLITIS AS PART OF INFECTIOUS MONONUCLEOSIS.
190
Explain the aetiology / risk factors of tonsillitis.
Difficult to distinguish clinically from viral pharyngitis. The most common bacterium causing tonsillitis is Streptococcus pyogenes (group A streptococcus), the bacterium that causes strep throat. Other strains of strep and other bacteria also may cause tonsillitis. Risk factors: - Age between 5-15 years - Contact with infected people in enclosed spaces - e.g. child care centres, schools, prison
191
Summarise the epidemiology of tonsillitis.
The incidence of tonsillitis is not completely known, research indicates that 15-30% of sore throats in children and 5-10% sore throats in adults are bacterial tonsillitis.
192
Recognise the presenting symptoms of tonsillitis.
- Presence of risk factors - Pain on swallowing - Sudden onset of sore throat - Headache - Abdominal pain - Nausea & vomiting
193
Recognise the signs of tonsillitis on physical examination.
- Fever - >38 degrees - Tonsillar exudate (purulent), especially in Group A B-haemolytic streptococci - Abdominal pain - may lead to false diagnosis of gastroenteritis - Presence of cough or runny nose - Tonsillar erythema - Tonsillar enlargement - Enlarged anterior cervical lymph nodes especially in Group A B-haemolytic streptococci
194
Identify appropriate investigations for tonsillitis and interpret the results.
CENTOR CRITERIA Centor criteria (fever >38.5°C, swollen, tender anterior cervical lymph nodes, tonsillar exudate and absence of cough) are an algorithm to assess the probability of group A β haemolytic Streptococcus (GABHS) as the origin of sore throat, developed for adults. 1st line: - Throat culture (48hr delay) - Rapid streptococcal antigen test - identifies Group A Beta-haemolytic streptococci (GABHS) 2nd line: - Serological testing for streptococci - x4 increase in Anti-streptolysin O (ASO), anti-deoxyribonuclease B or other antibody titres (hyaluronidase, streptokinase, nicotinic acid dehydrogenase) - WBC count and differential - raised neutrophil (bacterial infection) / lymphocytes count (infectious mononucleosis) - Heterophile antibodies - Vaginal and cervical, or penile and rectal cultures - positive culture (Thayer-Martin medium) for Neisseria gonorrhoea - HIV viral load assay - in high-risk patients with persistent infection and severe constitutional symptoms (malaise, tiredness, weight loss, generalised lymphadenopathy) - Lateral cervical view X-ray, exposed for soft tissue - enlarged retropharyngeal and posterior oropharyngeal soft tissue
195
Define tuberculosis.
Granulomatous disease caused by Mycobacterium tuberculosis. Primary - Initial infection may be pulmonary (acquired by inhalation from cough of the infected patient) or occasionally, gastrointestinal Miliary TB - Results when there is hematogenous dissemination Post-Primary - Caused by re-infection or reactivation
196
Explain the aetiology / risk factors of tuberculosis.
M.tuberculosis is an intracellular organism - AKA acid-fast bacilli Survives after being phagocytosed by macrophages.
197
Summarise the epidemiology of tuberculosis.
Annual mortality of 3 million. 95% in developing countries UK incidence annually 6000 Asian immigrants >30 times native UK white population incidence
198
Recognise the presenting symptoms of tuberculosis.
Primary TB - Asymptomatic - Fever - Malaise - Cough - Wheeze - Erythema nodosum - Phlyctenular conjunctivitis (allergic manifestations) Miliary TB - Fever - Weight loss - Meningitis - Yellow caseous tubercles spread to other organs - e.g. bone and kidney may remain dormant for years Post-Primary TB - Fever - Night sweats - Malaise - Weight loss - Breathlessness - Cough - Sputum - Haemoptysis - Pleuritic pain - Signs of pleural effusion - Collapse - Consolidation - Fibrosis Non-Pulmonary TB - Particularly in immunocompromised Lymph Nodes - Suppuration of cervical lymph nodes leading to abscesses or sinuses, which discharge pus and spread to skin = scrofuloderma CNS - Meningitis - Tuberculoma Skin - Lupus vulgaris - jellylike reddish-brown glistening plaques Heart - Percardial effusion - Constrictive pericarditis Gastrointestinal - Subacute obstruction - Change in bowel habit - Weight loss - Peritonitis - Ascites Adrenal - Insufficiency Bone/Joints - Osteomyelitis - Arthritis - Paravertebral Abscesses - Vertebral collapse - Pott's disease - Spinal cord compression from abscesses
199
Recognise the signs of tuberculosis on physical examination.
Primary TB - Asymptomatic - Fever - Malaise - Cough - Wheeze - Erythema nodosum - Phlyctenular conjunctivitis (allergic manifestations) Miliary TB - Fever - Weight loss - Meningitis - Yellow caseous tubercles spread to other organs - e.g. bone and kidney may remain dormant for years Post-Primary TB - Fever - Night sweats - Malaise - Weight loss - Breathlessness - Cough - Sputum - Haemoptysis - Pleuritic pain - Signs of pleural effusion - Collapse - Consolidation - Fibrosis Non-Pulmonary TB - Particularly in immunocompromised Lymph Nodes - Suppuration of cervical lymph nodes leading to abscesses or sinuses, which discharge pus and spread to skin = scrofuloderma CNS - Meningitis - Tuberculoma Skin - Lupus vulgaris - jellylike reddish-brown glistening plaques Heart - Percardial effusion - Constrictive pericarditis Gastrointestinal - Subacute obstruction - Change in bowel habit - Weight loss - Peritonitis - Ascites Adrenal - Insufficiency Bone/Joints - Osteomyelitis - Arthritis - Paravertebral Abscesses - Vertebral collapse - Pott's disease - Spinal cord compression from abscesses
200
Identify appropriate investigations for tuberculosis and interpret the results.
1. Sputum / Pleural Fluid /Bronchial Washings - microscopy, culture (6 weeks), low sensitivity 2. Tuberculin Tests - positive in previous exposure, strongly positive = infection (and not BCG) 3. Mantoux Test - intradermal injection of PPD, induration and erythema after 72h 4. Heaf Test - place drop of PPD on forearm, fire spring-loaded needled gun, read after 3-7 days, graded according to papule size and vesiculation 5. Interferon-Gamma Tests - latent TB, esposure of host T-cells to TB antigens causes release of interferon (negative with BCG vaccination) 6. CXR - Primary infection - peripheral consolidation, hilar lymphadenopathy - Miliary - fine shadowing - Post-primary - upper lobe shadowing, streaky fibrosis, cavitation, calcification, pleural effusion, hilar lymphadenopathy 7. HIV Testing - to co-incident disease (2% may be HIV positive) 8. CT, Lymph Nodes, Pleural Biopsy, Sampling of Other Affected Systems
201
Define urticaria (acute and chronic).
A skin condition consisting of erythematous, blanching, oedematous, non-painful, pruritic lesions that develop rapidly, usually over minutes. Typically lasts less than 24hours and leaves no residual skin markings upon resolutions. Acute episodes - period of less than 6 weeks, caused by specific stimulus and are self-limiting. Chronic episodes - period of over 6 weeks, not attributable to a specific stimulus.
202
Explain the aetiology / risk factors of urticaria (acute and chronic).
Acute: - Lasts less than 6 weeks - Hypersensitivity reaction to a specific trigger - Viral infections Chronic : - Daily or near-daily episodes of hives occuring for 6 weeks or more - Complex aetiology Risk Factors: - Positive family history - Female sex - Exposure to drug or food trigger - Recent viral infection - Recent insect bite or sting
203
Summarise the epidemiology of urticaria (acute and chronic).
A recent studies reported that the lifetime prevalence of all types of urticaria was 8.8% to 10.8%, with a female predominance and a mean age of 35 to 39 years. Angio-oedema - swelling involving the deeper layers of the subdermis and occurs in association with urticaria in 40% of cases. Involves face and neck, potentially compromise airway.
204
Recognise the presenting symptoms of urticaria (acute and chronic).
- Pruritus - unpleasant sensation of the skin that provokes the urge to scratch - Resolution in 24 hours - Swelling of face, tongue or lips - Erythematous oedematous lesions - Blanching lesions - Stridor
205
Recognise the signs of urticaria (acute and chronic) on physical examination.
- Pruritus - unpleasant sensation of the skin that provokes the urge to scratch - Resolution in 24 hours - Swelling of face, tongue or lips - Erythematous oedematous lesions - Blanching lesions - Stridor
206
Identify the appropriate investigations of urticaria (acute and chronic).
- FBC - normal, eosinophilia, neutrophilia - ESR - elevated or normal - CRP - elevated or normal - C4 - decreased in hereditary and acquired angio-oedema - TSH - elevated or normal - ANA - anti-nuclear antibodies - positive in rheumatological disease - Skin prick testing - may be positive - Allergen avoidance diet - Serum tryptase - Skin biopsy - C1 esterase inhibitor level and function, C1q levels - Specific IgE to suspected allergen
207
Define varicella zoster.
Primary infection is called vaircella (chicken pox). Reactivation of the dormant virus in the dorsal root ganglia, causes zoster (shingles).
208
Explain the aetiology / risk factors of varicella zoster.
- Herpes ds-DNA virus - Highly contagious - Transmission by aerosol inhalation or direct contact with vesicular secretions Viral inhalation and infection of the URT. Replication in regional lymph nodes, liver and spleen. Week 2-3 - spreads to skin, producing rash and then leading to clinical resolution. Remains latent in dorsal root ganglia. Reactivation causes virus to travel down sensory axon to produce dermatomal shingles rash.
209
Summarise the epidemiology of varicella zoster.
Chickenpox peak incidence occurs at 4-10 years. Shingles peak incidence at >50 years. 90% of adults are VZV IgG positive (previously infected).
210
Recognise the presenting symptoms of varicella zoster.
- Incubation period 14-21 says Chicken Pox: - Prodromal malaise - Mild pyrexia - Sudden appearance of an intensely itchy spreading rash - Affecting the face and trunk more than the extremities, the oropharynx, conjunctivae, genitourinary tract - Vesicles weep and crust over, forming new vesicles - Contagious from 48h before the rash and until all the vesicles have crusted over - within 7-10 days Shingles: - May occur after a period of stress - Tingling / hyperaesthesia in a dermatomal distribution - Painful skin lesions - Recovering in 10-14 days
211
Recognise the signs of varicella zoster on physical examination.
Chicken Pox: - Macular papular rash - Evolves into crops of vesicles - Areas of weeping and crusting - Skin excoriation - from scratching - Mild pyrexia Shingles: - Vesicular macular papular rash - Dermatomal distribution - Skin excoriation
212
Identify appropriate investigations for varicella zoster and interpret the results.
Both chickenpox and shingles usually clinical diagnosis. Vesicle Fluid - Electron microscopy - Direct immunofluorescence - Cell culture - Viral PCR - all rarely necessary Chicken Pox - Consider HIV testing - Especially in adults with prior history of varicella infection
213
Generate a management plan for varicella zoster.
Chicken Pox: - Children - treat symptoms with calamine lotion, analgesia, antihistamines - Adults - consider aciclovir, valaciclovir, famciclovir if within 24h of rash onset especially if elderly, smoker, immunocompromised or pregnant Shingles: - Aciclovir, valaciclovir, famciclovir if within 72h of rash onset if elderly, immunocompromised or ophthalmic involvement - Low-dose amitriptyline if in moderate / severe discomfort - Simple analgesia (paracetamol) Prevention: - VZIG may be indicated in immunosuppressed and pregnant women exposed to varicella zoster - Chickenpox vaccine licensed in the UK, but no guidelines avaliable for appropriate use
214
Identify the possible complications of varicella zoster and its management.
Chicken Pox: - Secondary infection - Scarring - Pneumonia - Encephalitis - Cerebellar syndrome - Congenital varicella syndrome Shingles: - Postherpetic neuralgia - Zoster opthalmicus - rash involves ophthalmic division of Trigeminal Nerve (CN V) - Ramsay Hunt's Syndrome - reactivation in geniculate ganglion causing zoster of the ear and facial nerve palsy (vesicles behind pinna of ear or in canal) - Sacral zoster may lead to urinary retention - Motor zoster - muscle weakness of myotome at the similar level as involved dematome
215
Summarise the prognosis for patients with varicella zoster.
Depends on complications. Worse in pregnancy, elderly and immunocompromised.
216
Define viral hepatitis - A&E.
Hepatitis caused by infection with the RNA viruses, hepatitis A (HAV) and hepatitis E virus (HEV), that follow an acute course without progression to chronic carriage.
217
Explain the aetiology / risk factors of viral hepatitis - A&E.
``` HAV = picornavirus HEV = calcivirus ``` - Small - Non-enveloped - Single-stranded - Linear - RNA viruses - Transmission by faecal-oral route - Replicate in hepatocytes - Secreted into bile - Immune responses causes liver inflammation and hepatocyte necrosis = CD8+ T-cells, NK cells - Inflammatory cell infiltration of poral tracts = neutrophils, macrophages, eosinophils, lymphocytes - Zone 3 necrosis - Bile duct proliferation
218
Summarise the epidemiology of viral hepatitis - A&E.
HAV - Endemic in developing world, infection occurs sub-clinically - Better sanitation in developed world - age of exposure increases = more likely to be symptomatic 5000 cases (5% seroprevalence). HEV - Endemic in Asia, Africa and Central America
219
Recognise the presenting symptoms of viral hepatitis - A&E.
Incubation period of 3-6 weeks. Prodromal Period - Malaise - Anorexia - distate for cigarettes in smokers - Fever - Nausea - Vomiting Hepatitis - Dark urine - Pale stools - Jaundice lasting 3 weeks - Itching & prolonged jaundice in HAV - due to cholestatic hepatitis
220
Recognise the signs of viral hepatitis - A&E on physical examination.
- Pyrexia - Jaundice - Tender hepatomegaly - Palpable spleen in 20% - Absence of stigmata of chronic liver disease - Few spider naevi transiently
221
Identify appropriate investigations for viral hepatitis - A&E and interpret the results.
1. Bloods 2. Viral Serology 3. Urinalysis Bloods - LFT - High AST and ALT, High bilirubin, High AlkPhos - High ESR - Low albumin - High platelets Viral Serology - Hep A - anti-HAV IgM (during acute illness, disappears after 3-5 months), anti-HAV IgG (recovery phase, lifelong persistence) - Hep E - anti-HEV IgM (high 1-4 weeks after onset), anti-HEV IgG - Hep B & C - rule out Urinalysis - +ve for bilirubin - High urobilinogen
222
Generate a management plan for viral hepatitis - A&E.
- No specific management - Bed rest and symptomatic treatment - e.g. antipyretic, antiemetics - Colestyramine for severe pruritis Prevention: - Public health - e.g. safe water, sanitation, food hygiene, notifiable disease, personal hygiene, sensible dietary precautions when travelling - Immunization (HAV) - passive IM human immunoglobulin effective for short period, active attenuated HAV vaccine for travellers, high-risk individuals
223
Identfiy the possible complications of viral hepatitis - A&E and its management.
- Fulminant hepatic failure - 0.1% HAV cases, 1-2% HEV cases, 20% if pregnant - Cholestatic hepatitis with prolonged jaundice and pruritis after HAV infection - Post-hepatitis syndrome - continued malaise for weeks-months
224
Summarise the prognosis for patients with viral hepatitis - A&E.
3-6 weeks recovery Relapse during recovery occasionally No chronic sequelae Fulminant hepatic failure has 80% mortality
225
Define viral hepatitis - B& D.
Hepatitis caused by infection with hepatitis B virus (HBV), which may follow an acute or chronic (defined as viraemia and hepatic inflammation continuing >6 months) course. Hepatitis D virus (HDV), a defective virus, may only co-infect with HBV or superinfect persons who are already carriers of HBV.
226
Explain the aetiology / risk factors of viral hepatitis - B& D.
HBV - Enveloped - Partially double-stranded DNA virus - Sexual contact, blood and vertical transmission - Viral proteins produced - e.g. HBcAg, HBsAg, HBeAG = core, surface and e antigens HDV - Single-stranded RNA virus - Coated with HBsAG = surface antigen Antibody and cell-mediated immune responses to viral replication lead to liver inflammation and heptocyte necrosis. Mild-severe inflammation. Changes of cirrhosis. Risk Factors: - IV drug abuse - Unscreened blood and blood products - Infants of HBeAg-positive mothers - Sexual contact with HBV carrier - Younger individuals more likely to develop chronic carriage - Genetic factors - higher rates of viral clearance
227
Summarise the epidemiology of viral hepatitis - B& D.
Common 350 million worldwide infected with HBV 1-2million deaths annually Common in SE Asia, Africa, Mediterranean countries HDV found worldwide HBV uncommon in UK
228
Recognise the presenting symptoms of viral hepatitis - B& D.
- Incubation period of 3-6 months - 1-2 week prodrome - malaise, headache, anorexia, N&V, diarrhoea, RUQ pain - Serum-sickness-type illness - e.g. fever, arthralgia, polyarthritis, urticaria, maculopapular rash - Jaundice - Dark urine - Pale stools Recovery usually within 4-8 weeks - 1% may develop fulminant liver failure Chronic carriage diagnosed after routine LFT testing or if cirrhosis or decompensation develops.
229
Recognise the signs of viral hepatitis - B& D on physical examination.
Acute - Jaundice - Pyrexia - Tender hepatomegaly - Splenomegaly - Cervical lymphadenopathy (10-20%) - Urticaria - Maculopapular rash Chronic - No findings - Signs of chronic liver disease or decompensation
230
Identify appropriate investigations for viral hepatitis - B& D.
1. Viral Serology 2. PCR 3. LFT 4. Clotting 5. Liver biopsy Viral Serology - Acute - HBsAg positive, IgM anti-HBcAg - Chronic - HBsAg positive, igG anti-HBcAg, HBeAg positive or negative - HBV cleared or immunity - anti-HBsAg positive, IgG anti-HBcAg - HDV infection - detected by IgM or IgG against HDV PCR - Detection of HBV DNA - most sensitive measure LFT - High AST, ALT - High bilirubin - High AlkPhos Clotting - High PT in severe disease Liver Biopsy - Percutaneous - Transjugular if clotting is deranged or ascites present
231
Generate a management plan for viral hepatitis - B& D.
Prevention: - Passive immunization - HepB immunoglobulin (HBIG) - if acute exposure, neonates born to HBeAg-positive mothers - Active immunization - recombinant HBsAg vaccine - individuals at risk, neonates born to HBV-positive mothers, also protects against HDV Acute HBV Hepatitis: - Symptomatic treatment - e.g. bed rest, antiemetics, antipyretics, cholestyramine for pruritis - Notification of communicable disease Chronic HBV Heptaitis: - Indications for treatments with anti-virals = HBeAg-positive, HBeAg negative chornic hepatitis (dependents on ALT, HBV DNA), compensated cirrhosis and HBV DNA >2,000 IU/mL, decompensated cirrhosis and detectable HBV DNA by PCR - Interferon alpha - high half life - Nucleoside/nucleotide analogues - watch out for drug resistance - e.g. adefovir, entecavir, telbivudine, tenofovir, lamivudine Interferon Alpha - Cytokine - Augments natural antiviral mechanisms - SE: flu-like symptoms, fevers, chills,myalgia, headaches, bone marrow suppression, bone marrow depression
232
Identify possibel complications of viral hepatitis - B& D and it's management.
- Fulminant hepatic failure - 1% - Chronic HBV infection (10% adults, higher in neonates) - Cirrhosis - Hepatocellular carcinoma - Extrahepatic immune complex disorders- e.g. glomerulonephritis, polyarteritis nodosa - Superinfection with DHV --> acute liver failure
233
Summarise the prognosis for patients with viral hepatitis - B& D
10% of infections become chronic 20-30% of those will develop cirrhosis Factors of good response to inferferon: - High serum transaminases - Low HBV DNA - Active histological changes - Absence of complicating disease
234
Define viral hepatitis C.
Hepatitis caused by infection with Hepatitis C (HCV), often following a chronic course. (80% cases).
235
Explain the aetiology / risk factors of viral hepatitis C. Additionally summarise the epidemiology of viral hepatitis C.
HCV - Small - Eneveloped - Single-stranded RNA virus - Flavivirus family Poor fidelity of replication High mutation rates Different HCV genotypes - quasi-species Transmission: - Parenteral route - Recipients of blood and blood products prior to blood screening - IV drug users - Non-sterile acupuncture - Tattooing - Haemodialysis - Health care workers - Sexual and vertical transmission uncommon - 1-5%, increased risk in those co-infected with HIV Pathology - Hepatotropic - Not directly hepatotoxic - Humoural and cell-mediated response leads to hepatic inflammation and necrosis - Liver biopsy - chronic hepatitis - Lymphoid follicles in portal tracts - Fatty changes - Features of cirrhosis Common 0.5-2% in developed countries. Higher in certain areas due to poor sterilisation practices. Different HCV genotypes have different geographical prevalence.
236
Recognise the presenting symptoms of viral hepatitis C.
99% of acute infections = asymptomatic <10% jaundiced with flu-like illness Diagnosed after incidental abnormal LFT or in older individuals with complications of cirrhosis
237
Recognise the signs of viral hepatitis C on physical examination.
No signs of chronic liver disease in long-standing infection Les common: - Skin rash - due to mixed cryoglobulinaemia causing a small-vessel vasculitis - Renal dysfunction - due to glomerulonephritis
238
Identify appropriate investigations for viral hepatitis C and interpretthe results.
1. Bloods 2. Liver Biopsy Bloods - HCV serology - anti-HCV antibodies (IgM acute, IgG past or chronic) - Reverse transcriptase PCR - detection of HCV RNA, confirm antibody testing - LFT - acute = high AST, ALT, chronic = 2-8x elevation of AST and ALT Liver biopsy - Assess degree of inflammation and liver damage as transaminase levels bear little correlation to histological changes - Diagnose cirrhosis - monitoring for hepatocellular carcinoma
239
Generate a management plan for viral hepatitis C.
Prevention - Screening of blood, blood products and organ donors - Needly exchange schemes for IV drug abusers - Instrument sterilization - No vaccine avaliable at present Medical Acute - No specific management and mainly supportive - e.g. anti-pyretics, anti-emetics, cholestyramine - Specific antiviral treatment delayed for 3-6 months Chronic - Combined treatment with pegylated interferon-alpha and ribavirin - Interferon-alpha = cytokine which auments natural antiviral mechanisms - Ribavirin = guanosine nucleotide analogue - HCV 1 or 4 = 24-48 weeks - HCV 2 or 3 = 12-24 weeks Monitoring of HCV load recommended after 12 weeks of treatment to determine efficacy of treatment. Regular ultrasound of liver may be necessary if the patient has cirrhosis.
240
Identify the possible complications of viral hepatitis C and its management.
- Fulminant hepatic failure in acute phase (0.5%) - Chronic HCV carriage - Cirrhosis - Hepatocellular carcinoma - Porphyria cuteanea tarda - Cryoglobulinaemia - Glomerulonephritis
241
Summarise the prognosis for patients with viral hepatitis C.
80% of exposed progress to HCV chronic. | 20-30% of these develop cirrhosis over 10-20 years.
242
Define Sjogren's Syndrome.
A systemic auto-immune disorder, characterised by keratoconjunctivitis sicca and xerostomia as a consequences of lymphocytic infiltration into the lacrimal salivary glands.
243
Explain the aetiology / risk factors of Sjogren's Syndrome.
Primary - occurs alone Secondary - occurs along with another auto-immune disease - e.g. lupus, RA, systemic sclerosis Risk factors: - Female - SLE - RA - Systemic sclerosis (scleroderma) - HLA Class I markers - Age peaks in 20-30s and after menopause - Genetic inheritance
244
Summarise the epidemiology fo Sjogren's Syndrome.
Sjogren syndrome is far from a rare disorder with an incidence approaching approximately one-half of that of rheumatoid arthritis (RA) or affecting 0.5% to 1.0% of the population. Between 400,000 and 3.1 million adults have Sjögren's syndrome.
245
Recognise the presenting symptoms of Sjogren's Syndrome.
- Dry eyes - keratoconjunctivitis sicca - Dry mount - xerostomia - Dryness of skin, nose, throat, vagina - Arthralgias - Myalgias - Peripheral neuropathies - Lymphoma - Fatigue - Vasculitis - Dental caries - Increased oral fungal and bacterial infections - Arthritis - Kidney disease - Corneal ulceration - No salvia pool - Enlarged salivary glands - Facial pain - Burning mouth syndrome - History of VTE - History of AA or dissection
246
Recognise the signs of Sjogren's Syndrome on physical examination.
- Dry eyes - keratoconjunctivitis sicca - Dry mount - xerostomia - Dryness of skin, nose, throat, vagina - Arthralgias - Myalgias - Peripheral neuropathies - Lymphoma - Fatigue - Vasculitis - Dental caries - Increased oral fungal and bacterial infections - Arthritis - Kidney disease - Corneal ulceration - No salvia pool - Enlarged salivary glands - Facial pain - Burning mouth syndrome - History of VTE - History of AA or dissection
247
Identify appropriate investigations for Sjogren's Syndrome and interpret the results.
1st Line: - Schirmer's test - positive (filter paper placed in lower conjunctival sac, less than 5mm of paper is wetted after 5 mins) - Anti-60 kD (SS-A) Ro and anti-La (SS-B) - positive Consider: - Sialometry - decreased - Minor salivary gland biopsy - focus score 1 or greater - Lissamine green test - score of 3 or more - Fluorescein corneal staining test - score of 3 or more - Parotid sialography - gross distortion of the normal pattern of parotid ductules coupled with significant retention of contrast material - Salivary gland Technetium-99m pertechnetate scintigraphy - decreased uptake and secretion - Skin biopsy - focal and segmental transmural necrotising inflammation in a medium-sized vessel (i.e., a small or medium-sized artery) - Angiography - beading, aneurysm, or smooth, tapering vessel stenosi - Urinalysis - may show abnormal levels of phosphate, calcium, potassium, glucose due to renal tubular acidosis - Serum electrolytes - may show hypokalaemia with a normal anion gap; hyperchloraemic metabolic acidosis - MRI salivary glands - inflammation of salivary glands - US salivary glands - high salivary gland ultrasonography score
248
Define SLE.
A chronic multi-system disorder that most commonly affects women during their reproductive years.
249
Explain the aetiology / risk factors of SLE.
- Anti-nuclear antibodies + constitutional symptoms - Involves skin and joints - Serositis, nephritis, haematological cytopenias and neurological manifestations Risk factors: - Female sex - Age 15-45 years - African / Asian descent in Europe and US - Drugs - Sun exposure - Family history of SLE - Tobacco smoking
250
Summarise the epidemiology of SLE.
The reported prevalence of systemic lupus erythematosus (SLE) in the United States is 20 to 150 cases per 100,000 [1-3]. In women, prevalence rates vary from 164 (white) to 406 (African American) per 100,000 [2].
251
Recognise the presenting symptoms of SLE.
- Malar (butterfly) rash - Photosensitive rash - Discoid rash - Fatigue - Weight loss - Fever - Oral ulcers - Alopecia - Arthralgia / artritis - Fibromyalgia - Raynaud's phenomenon - Chest pain and SOB - Venous or arterial thrombosis - Hypertension - Signs of nephrosis (e.g. oedema) - Lymphadenopathy - Abdominal pain, vomiting or diarrhoea - Nose ulcers - Poorly localised proximal limb inflammatory pain with weakness - Dysrhythmias - e.g. tachycardia - Conduction defects or unexplained cardiomegaly - CNS signs - seizures, CNS abnormalities, cognitive defects, psychosis - Dysphagia
252
Recognise the signs of SLE on physical examination.
- Malar (butterfly) rash - Photosensitive rash - Discoid rash - Fatigue - Weight loss - Fever - Oral ulcers - Alopecia - Arthralgia / artritis - Fibromyalgia - Raynaud's phenomenon - Chest pain and SOB - Venous or arterial thrombosis - Hypertension - Signs of nephrosis (e.g. oedema) - Lymphadenopathy - Abdominal pain, vomiting or diarrhoea - Nose ulcers - Poorly localised proximal limb inflammatory pain with weakness - Dysrhythmias - e.g. tachycardia - Conduction defects or unexplained cardiomegaly - CNS signs - seizures, CNS abnormalities, cognitive defects, psychosis - Dysphagia
253
Identify appropriate investigations for SLE and interpret the results.
1st Line: - FBC and differential - anaemia, leukopenia, thrombocytopenia, pancytopenia - Activated PTT - anti-phospholipid antibody patients have prolonged PTT - U&E - high urea, high creatinine - ESR and CRP - high - Anti-nuclear antibodies, dsDNA, Smith antigen - positive - Urinalysis - haematuria, casts (red cell, granular, tubular or mixed), proteinuria - CXR - pleural effusion, infiltrates, cardiomegaly - ECG - exclude other causes Consider: - Blood and urine cultures - exclude infection - Antiphospholipid antibodies - positive - Coombs test - positive - 24-hour urine collection for protein or spot urine for protein/creatinine ratio - proteinuria - Complement levels - complement consumption - Creatinine phosphokinase - elevated - Plain XR of affected joints - inflammation, non-erosive arthritis - Renal USS - exclusion - Chest CT - lung fibrosis, effusions - PFT - restrictive pattern - Pleural aspiration - exudate - Brain MRI - white matter changes - Echocardiography - pericarditis, pericardial effusion, pulmonary hypertension - Skin biopsy - immune deposits at the dermal-epidermal junction on immunofluorescence or non-specific inflammation - Renal biopsy - immune deposits, mesangial hypercellularity, focal, segmental or global glomerulonephritis - TSH - exclusion
254
Define systemic sclerosis.
A multi-system, autoimmune disease, characterised by functional and structural abnormalities of small blood vessels, fibrosis of skin and internal organs, production of autoantibodies.
255
Explain the aetiology / risk factors of systemic sclerosis.
Unknown. 2 TYPES: - Limited cutaneous SSc - Diffuse cutaneous SSc Limit - less severe internal organ involvement, better prognosis Risk factors: - Family history - Immune dysregulation - e.g. positive ANA - Exposure to environmental substances and toxins - e.g. silica dust, solvents
256
Summarise the epidemiology of systemic sclerosis.
Scholarly articles for epidemiology of systemic sclerosis Epidemiology of systemic sclerosis - ‎Nikpour - Cited by 114 Epidemiology of systemic sclerosis: incidence, … - ‎Barnes - Cited by 310 Epidemiology of systemic sclerosis (scleroderma) - ‎MEDSGER JR - Cited by 343 A 2019 epidemiology study reported that based on 39 publications, the prevalence of systemic sclerosis in Europe and North America was 7.2-33.9 cases per 100,000 individuals, with an annual incidence rate of 0.6-2.3 cases per 100,000 individuals. Systemic sclerosis is rare in the resident population of Japan and China.
257
Recognise the presenting symptoms of systemic sclerosis.
- Raynaud;'s phenomenon - Digital pits or ulcers - Swelling of the hands and feet - Skin thickening - Loss of function of hands - Sclerodactyly - Heartburn reflux and dysphagia - Bloating - Faecal incontinence - Athralgias and myalgias - Abnormal nail-fold capillaroscopy - Telangiectasia - Subcutaneous calcinosis - Dyspnoea - Dry crackles at lung bases - Tendon friction rub - Abrupt onset moderate / marked hypertension - Fatigue - Dry cough - Decreased exercise tolerance - Weight loss - Inflammatory arthritis - Proximal muscular weakness (inflammatory myositis) - Synovitis - Increased accentuation of the pulmonic component of S2 heart sound - Signs of anaemia
258
Recognise the signs of systemic sclerosis on physical examination.
- Raynaud;'s phenomenon - Digital pits or ulcers - Swelling of the hands and feet - Skin thickening - Loss of function of hands - Sclerodactyly - Heartburn reflux and dysphagia - Bloating - Faecal incontinence - Athralgias and myalgias - Abnormal nail-fold capillaroscopy - Telangiectasia - Subcutaneous calcinosis - Dyspnoea - Dry crackles at lung bases - Tendon friction rub - Abrupt onset moderate / marked hypertension - Fatigue - Dry cough - Decreased exercise tolerance - Weight loss - Inflammatory arthritis - Proximal muscular weakness (inflammatory myositis) - Synovitis - Increased accentuation of the pulmonic component of S2 heart sound - Signs of anaemia
259
Identify appropriate investigations for systemic sclerosis and interpret the results.
1st Line: - Serum auto-antibodies - positive ANA - FBC - microcytic anaemia (GI bleed), microangiopathic haemolytic anaemia (MAHA) in scleroderma renal crisis - Urea and serum creatinine - high in scleroderma renal crisis - ESR and CRP - high - Urine microscopy - proteinuria, cells or casts in scleroderma renal crisis - Complete PFTs - spirometry, lung volumes and diffusing capacity measurement - interstitial lung disease = low FVC, low DLCO plus restrictive pattern , pulmonary hypertension, disproportionate drop in DLCO compared with FVC - ECG - cardiac involvement - Echocardiogram - pulmonary hypertension, rise in RVSP, pericardial effusion, RV or LV diastolic dysfunction present - CXR- interstitial lung disease (bi-basilar interstitial infiltrates), cardiomegaly, RHF - Barium swallow - diminished oesophageal peristalsis and gastroparesis, diminished muscle tone in lower oesophagus, reflux of barium, strictures Consider: - CT chest - interstitial lung disease (ground glass opacities, thickened interstitium, interstitial fibrosis), traction bronchiectasis, honey-combing - OGD + biopsy - oesophageal inflammation, ulceration, strictures, gastric antral vascular ectasia, Barrett's metaplasia, adenocarcinoma may be present - Serum muscle enzymes - elevated in scleroderma myopathy - Electromyogram /nerve conduction studies - inflammatory myositis - Muscle biopsy - inflammatory myositis
260
Define thyroiditis.
Inflammation of the thyroid gland, which can lead to over or under-production of thyroid hormones.
261
Explain the aetiology / risk factors of thyroiditis.
3 PHASES: - Thyrotoxic phase - inflamed, hyperthyroid - Hypothyroid phase - due to excessive previous release - Euthyroid phase - resumes normal hormone levels TYPES: - Hashimoto's Thyroiditis - anti-thyroid peroxidase antibodies, hypothyroid - Silent thyroiditis or painless thyroiditis - autoimmune, female - Post-partum thyroiditis - - Radiation induced thyroiditis - Subacute granulomatous thyroiditis (de Quervain's) - caused by viral infection, painful, 20-50yrs, high temperature, pain in neck, jaw or ear - Acute thyroiditis or suppurative thyroiditis - Drug-induced thyroiditis - e.g. amiodarone, interferons, lithium, cytokines Risk factors: - >60 years - Family history - Autoimmune disease - e.g. T1DM, coeliac - Treated previously with radioactive iodine or anti-thyroid medications
262
Summarise the epidemiology of thyroiditis.
Studies in the United States and Western Europe report a prevalence of 1.2% in individuals aged 11-18 years. Approximately 25% of adults with type 1 diabetes have thyroiditis, about one half of whom have hypothyroidism. Approximately 10% of children with type 1 diabetes have antithyroid antibodies.
263
Recognise the presenting symptoms of thyroiditis.
Hyperthyroidism: - Exopthalamos - Opthalmoplegia - Goitre - with bruit in Graves' - Tachycardia - Angina - AF - Systolic hypertension - Oligomenorrhoea - Diarrhoea - Sweaty, tremulous, warm hands - Proximal myopathy - Pretibial myxoedema (Graves') - Ankle swelling (heart failure) - Weight loss - Increased appetite - Heart intolerance - Anxiety - Irritability - Fast, fine tremor Hypothyroidism: - Periorbital oedema - Husky voice - Bradycardia - Carpal tunnel syndrome - Menorrhagia - Constipation - Low metabolic rate, weight gain - Sensitivity to cold - Lethargy - Mental impairment - Depression
264
Recognise the signs of thyroiditis on physical examination.
Hyperthyroidism: - Exopthalamos - Opthalmoplegia - Goitre - with bruit in Graves' - Tachycardia - Angina - AF - Systolic hypertension - Oligomenorrhoea - Diarrhoea - Sweaty, tremulous, warm hands - Proximal myopathy - Pretibial myxoedema (Graves') - Ankle swelling (heart failure) - Weight loss - Increased appetite - Heart intolerance - Anxiety - Irritability - Fast, fine tremor Hypothyroidism: - Periorbital oedema - Husky voice - Bradycardia - Carpal tunnel syndrome - Menorrhagia - Constipation - Low metabolic rate, weight gain - Sensitivity to cold - Lethargy - Mental impairment - Depression
265
Identify appropriate investigations for thyroiditis and interpret the results.
- TFTs - Antibodies - TPO (thyroid peroxidase antibodies) or TRAb (thyroid receptor stimulating antibodies) - ESR, CRP - USS - evaluate anatomy of thyroid gland, see if there's any nodules, change in blood flow or echotexture (intensity and density) - Radioactive iodine uptake (RAIU) - low in thyrotoxic phase
266
Generate a management plan for thyroiditis.
- Depends on the type, symptoms and phase of thyroiditis - Thyrotoxic phases may recover, go to euthyroid or hypothyroid - May be temporary of permenant - May not be necessary to treat symptoms in subacute, painless or post-partum - Thyroidal pain - NSAIDs, steroids - Anxiety symptoms - beta-blockers - Stop drugs inducing thyroiditis - Treat infection - Thyroid hormone replacement therapy for 6-12 months, or permenantly for Hashimoto's thyroiditis
267
Identify the possible complications of thyroiditis and its management.
- Goitre - Heart problems - Mental health issues - Myxoedema - Birth defects
268
Summarise the prognosis for patients with thyroiditis.
In the case of Hashimoto's thyroiditis, the resulting hypothyroidism is generally permanent. People who develop subacute thyroiditis usually have symptoms for 1 to 3 months, but complete recovery of thyroid function can take up to 12 to 18 months. These people have about a 5 percent chance of developing a permanent condition of hypothyroidism. The time frame for recovery to a thyroid that functions normally for post-partum, silent or painless thyroiditis is also about 12 to 18 months. People with these conditions have about a 20 percent chance of developing permanent hypothyroidism.
269
Define urinary tract infection.
Characterised by presence of >100,000 of colony-forming units per milllitre of urine. May affect bladder (cystitis), kidney (pyelonephritis) or prostate (prostatitis).
270
Explain the aetiology / risk factors of urinary tract infection.
Transurethral ascent of normal colonic organisms. Escherichia coli Proteus mirabilis Klebsiella Enterococci (hospitals)
271
Summarise the epidemiology of urinary tract infection.
30% of women experience UTI at some point in their lives. 5% of pregnant women, 2% of non-pregnant women, 20% elderly living at home, 50% institutionalized elderly. Rare in children and young men (if present, suspect an underlying cause).
272
Recognise the presenting symptoms of urinary tract infection.
- Silent - asymptomatic bacteruria Cystitis: - Frequency - Urgency - Dysuria - pain on micturition - Haematuria - Suprapubic pain - Smelly urine Pyelonephritis (acute): - Feber - Malaise - Rigors - Loin / flank pain Prostatitis: - Fever - Low back / perineal pain - Irritative and obstructive symptoms - e.g. hesitancy, urgency, intermittency, poor stream, dribbling Elderly: - Malaise - Nocturia - Incontinence - Confusion Up to 30% of women with UTI symptoms may not have bacteruria.
273
Recognise the signs of urinary tract infection on physical examination.
May be asymptomatic. Cystitis: - Fever - Abdominal / suprapubic / loin tenderness - Bladder distension Pyelonephritis - Fever - Loin / flank tenderness Prostatitis: - Tender - Swollen prostate
274
Identify appropriate investigations for urinary tract infection and interpret the results.
MSU - Dipstick test - blood, protein, leucocytes, nitrites - Microscopy, culture and sensitivity - >10^5 colonies/mL indicates significant bacteriuria, but with UTI symptoms threshold becomes lower = women (>10^2/mL), men (>10^5/mL) - If there is sterile pyuria (pus cells with no organisms), consider if this may be partially treated UTI, tuberculosis stones, tumour, interstitial nephritis, renal papillary necrosis Imaging - Renal USS or IV urogram if women with frequent UTI and children/men
275
Generate a management plan for urinary tract infection.
Cystitis: - Local microbiological polices - Commonly used: oral co-trimoxazole, trimethoprim, nitrofurantoin, amoxicilliin, ciprofloxacin (males) Pyelonephritis: - IV gentamicin, cefuroxime, ciprofloxacin Catheterized patients: - Obtain culture - Change catheter - Do not treat unless patient is symptomatic Prophylaxis: - High fluid intake - Regular micturation to keep bladder empty - Cranberry-based products reduced frequency of recurrence - Low-dose long-term (6-12 months) antibiotics if frequently having UTIs Surgical: - Rarely necessary - May be necessary for relief of any obstruction and removal of any renal calculi
276
Identify the possible complications of urinary tract infection and its management.
- Renal papillary necrosis - in those with underlying renal disease - e.g. DM, stones - Renal / perinephric abscess - seen on renal USS - Pyonephritis - pus in palvicalyceal system - Gram-negative septicaemia
277
Summarise the prognosis for patients with urinary tract infection.
Mostly resolve with treatment. Among pregnant women, 20% develop acute pyelonephritis if not treated, however there is a high relapse rate.
278
# Define vasculitides. - Eosinophilic granulomatosis with polyangiitis (Churg-Strauss Syndrome) - Granulomatosis with polyanigiitis - Microscopic polyangitis - Polyarteritis nodosa - Takayasu arteritis - Giant cell arteritis (GCA)
Vasculitis - the inflammation and necrosis of blood vessels. Classification according to vessel size: - LARGE = Giant cell arteritis, Takayasu's aortitis - MEDIUM = Polyarteritis nodosa, Kawasaki's disease - SMALL = Churg-Strauss Syndrome, microscopic polyangiitis, Henoch-Schonlein purpura, Wegener's granulomatosis, mixed essential cryoglobinaemia, relapsing polychondritis Summary: Large = GCA, TA Medium - PN, KD Small = CSS, MP, HSP, WG, MEC, RP EOSINOPHILIC GRANULOMATOSIS WITH POLYANGIITIS (CSS) - Triad of tissue eosinophilia, granulomatous inflammation + vasculitis GRANULOMATOSIS WITH POLYANGIITIS (WG) - Triad of upper and lower respiratory tract involvement and pauci-immune glomerulonephritis MICROSCOPIC POLYANGIITIS - Ill-defined - Characterised by systemic, pauci-immune, necrotizing, small vessel vasculitis without evidence of necrotizing granulomatous inflammation POLYARTERITIS NODOSA - Necrotising inflammation of medium-sized or small arteries - Without glomerulonephritis or vasculitis in arterioles, capillaries or venules TAKAYASU'S ARTERITIS - Affects aorta and main branches - Can cause stenosis, occlusion and aneurysm formation GIANT CELL ARTERITIS / TEMPORAL ARTERITIS - Granulomatous inflammation of large arteries - Branches of external carotid artery - temporal artery most common
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Explain the aetiology / risk factors of vasculitides. - Eosinophilic granulomatosis with polyangiitis (Churg-Strauss Syndrome) - Granulomatosis with polyanigiitis - Microscopic polyangitis - Polyarteritis nodosa - Takayasu arteritis . - Giant cell arteritis (GCA)
Unknown aetiology. ?Autoimmune origin. Immune complex deposition in vessel walls triggers classical complement activation and inflammation. EOSINOPHILIC GRANULOMATOSIS WITH POLYANGIITIS (CSS) - May have perinuclear anti-neutrophil cytoplasmic antibodies (p-ANCA) directed against myeloperoxidase (MPO) - Risk factors - history of asthma, allergic rhinitis, sinusitis GRANULOMATOSIS WITH POLYANGIITIS (WG) - Anti-neutrophil cytoplasmic antibody (ANCA) - Common involvement of cutaneous, ocular, MSK and peripheral nervous system tissue - Small and medium vessels - Risk factors - genetic (HLA-DP, alpha-1-antitrypsin, proteinase 3, ANCA), infection with Staph aureus, environmental triggers (silica) MICROSCOPIC POLYANGIITIS - p-ANCA triggering neutrophil degranulation and endothelial injury - anti-MPO antibodies can cause necrotizing and crescentic glomerulonephritis POLYARTERITIS NODOSA - Only medium sized vessels - Risk factors - HBV, 40-60 yrs, hairy cell leukaemia, blood transfusion pre-HBV screening, HCV, male TAKAYASU'S ARTERITIS - Symptoms due to claudication and stroke - Diminished or absent pulses and hypertension is common - Risk factors - genetic predisposition, female, <40, Asian GIANT CELL ARTERITIS / TEMPORAL ARTERITIS - Unknown - Increasing age, genetic and ethnic background, infection - Associated with HLA-DR4 and HLA-DRB1
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Summarise the epidemiology of vasculitides. - Eosinophilic granulomatosis with polyangiitis (Churg-Strauss Syndrome) - Granulomatosis with polyanigiitis - Microscopic polyangitis - Poarteritis nodosa - Takayasu arteritis - Giant cell arteritis (GCA)
EOSINOPHILIC GRANULOMATOSIS WITH POLYANGIITIS (CSS) - 10.7-14 per million adults. No gender difference. GRANULOMATOSIS WITH POLYANGIITIS (WG) - Descriptive epidemiological studies carried out primarily in European countries estimate a prevalence of WG ranging from 24 to 157 per million and annual incidence rates from 3 to 14 per million MICROSCOPIC POLYANGIITIS Annual incidence of 3.6 cases per million persons. The prevalence is one to three cases per 100,000 population. POLYARTERITIS NODOSA Rare disease, with an incidence of about 3-4.5 cases per 100,000 population annually TAKAYASU'S ARTERITIS - Women - <40 yrs GIANT CELL ARTERITIS - 18 in 100,000 - M:F = 2-4:1 - 65-70 yrs
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Recognise the presenting symptoms of vasculitides. - Eosinophilic granulomatosis with polyangiitis (Churg-Strauss Syndrome) - Granulomatosis with polyanigiitis - Microscopic polyangitis - Poarteritis nodosa - Takayasu arteritis - Giant cell arteritis (GCA)
Features of All Disease: - General - fever, night sweats, malaise, weight loss - Skin - rash (vasculitic, purpuric, maculopapular, livedo reticularis) - Joint - arthralgia, arthritis - GI - abdominal pain, haemorrhage from mucosal ulceration, diarrhoea - Kidney - glomerulonephritis, renal failure - Lung - dyspnoea, cough, chest pain, haemoptysis, lung haemorrhage - CVS - pericarditis, coronary arteritis, myocarditis, heart failure, arrhythmias - CNS - mononeuritis multiplex, infarctions, meningeal involvement - Eyes - retinal haemorrhage, cotton wool spots EOSINOPHILIC GRANULOMATOSIS WITH POLYANGIITIS (CSS) - Asthma - Allergic rhinitis - Sinusitis - Eosinophilia GRANULOMATOSIS WITH POLYANGIITIS (WG) - Granulomatous vasculitis of upper and lower respiratory tract - Nasal discharge - Ulceration - Deformity - Haemoptysis - Sinusitis - Corneal thinning - Glomerulonephritis MICROSCOPIC POLYANGIITIS - Non-specific with multiple organs affected - Glomerulonephritis with no glomerular Ig deposits POLYARTERITIS NODOSA - Microaneurysms - Thrombosis - Infarctions (causing GI perforation) - Hypertension - Testicular pain TAKAYASU'S ARTERITIS - Constitutional upset - Head or neck pain - Tenderness over affected arteries - aorta and major branches - Dizziness - Fainting - Low peripheral pulses - Hypertension GIANT CELL ARTERITIS - Subacute onset, usually over a few weeks - Scalp and temporal tenderness - pain on combing hair - Jaw and tongue claudication - Blurred vision - Sudden blindness in one eye - amaurosis fugax - Malaise, low-grade fever, lethargy, weight loss, depression - Early morning pain and stiffness of the muscles of the shoulder and pelvic girdle - 40-60% of cases associated with PMR
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Recognise the signs of vasculitides on physical examination. - Eosinophilic granulomatosis with polyangiitis (Churg-Strauss Syndrome) - Granulomatosis with polyanigiitis - Microscopic polyangitis - Poarteritis nodosa - Takayasu arteritis - Giant cell arteritis (GCA)
Features of All Disease: - General - fever, night sweats, malaise, weight loss - Skin - rash (vasculitic, purpuric, maculopapular, livedo reticularis) - Joint - arthralgia, arthritis - GI - abdominal pain, haemorrhage from mucosal ulceration, diarrhoea - Kidney - glomerulonephritis, renal failure - Lung - dyspnoea, cough, chest pain, haemoptysis, lung haemorrhage - CVS - pericarditis, coronary arteritis, myocarditis, heart failure, arrhythmias - CNS - mononeuritis multiplex, infarctions, meningeal involvement - Eyes - retinal haemorrhage, cotton wool spots EOSINOPHILIC GRANULOMATOSIS WITH POLYANGIITIS (CSS) - Asthma - Allergic rhinitis - Sinusitis - Eosinophilia GRANULOMATOSIS WITH POLYANGIITIS (WG) - Granulomatous vasculitis of upper and lower respiratory tract - Nasal discharge - Ulceration - Deformity - Haemoptysis - Sinusitis - Corneal thinning - Glomerulonephritis MICROSCOPIC POLYANGIITIS - Non-specific with multiple organs affected - Glomerulonephritis with no glomerular Ig deposits POLYARTERITIS NODOSA - Microaneurysms - Thrombosis - Infarctions (causing GI perforation) - Hypertension - Testicular pain TAKAYASU'S ARTERITIS - Constitutional upset - Head or neck pain - Tenderness over affected arteries - aorta and major branches - Dizziness - Fainting - Low peripheral pulses - Hypertension GIANT CELL ARTERITIS - Swelling and erythema overlying the temporal artery - Scalp and temporal tenderness - Thickened non-pulsatile temporal artery - Low visual acuity
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Identify appropriate investigations for vasculitides and interpret the results. - Eosinophilic granulomatosis with polyangiitis (Churg-Strauss Syndrome) - Granulomatosis with polyanigiitis - Microscopic polyangitis - Poarteritis nodosa - Takayasu arteritis - Giant cell arteritis (GCA)
EOSINOPHILIC GRANULOMATOSIS WITH POLYANGIITIS (CSS) - FBC with differential - eosinophilia - ANCA - positive - CRP - high - ESR- high - Urea & creatinine - normal or high - Urinalysis - normal or abnormal (may show glomerulonephritis - haematuria, proteinuria, RBC casts) - PFT - reversible airway obstruction - CXR- interstitial infiltrates or nodules - Echo - left ventricular regional wall motion abnormlaities, intracardiac thrombus, pericardial effusion GRANULOMATOSIS WITH POLYANGIITIS (WG) - Urinalysis and microscopy - haematuria, proteinuria, dysmorphic RBC, RBC casts - CT chest - lung nodules, infiltrates - ANCA - cANCA, pANCA - FBC and differential - anaemia - Creatinine - high - ESR - high MICROSCOPIC POLYANGIITIS - ESR - high - CRP - high - FBC - anaemia - Creatinine - high - pANCA with MPO specificity - positive - Urinalysis - haematuria, proteinuria, RBC casts - If neuropathy, EMG may reveal sensorimotor peripheral neuropathy POLYARTERITIS NODOSA - CRP - high - ESR - high - FBC - normocytic anaemia, high WBC, high platelet - Complement - low - Creatinine - high or normal - Midstream urine - proteinuria (mild) or normal - LFTs - high liver enzymes - HBV - HbsAg positive and/or HbeAg positive - HCV - positive anti-HCV antibodies - Cryoglobulins - none - Blood culture - no growth - CK - normal or mildly elevated - ANCA - negative - ANA - negative - Anti-dsDNA - negative - RF - negative - Anti-CCP - negative - Lupus anticoagulant - negative - IgG antiphospholipid antibodies - negative - B2 glycoprotein - negative - Fibrinogen - normal or high - Conventional digital subtraction angiography - microaneurysms, vessel actasia, focal occlusive lesions in medium sized vessels - Echo - normal TAKAYASU'S ARTERITIS - ESR- >50mm/hr with active disease - CRP - high - CTA - segmental narrowing or occlusion, dilation of affected vessels, aortic aneurysms seen, thickening of vessel walls seen - MRA - segmental narrowing, occlusion or dilation of involved arteries, vessel wall inflammation GIANT CELL ARTERITIS - ESR - >50mm/hr - CRP - high - FBC - normochromic, normocytic anaemia, normal WBC, high platelet, mild leukocytosis - LFTs - AST, ALT, ALP mildly high - Temporal artery USS - wall thickening (halo sign), stenosis or occlusion - Temporal artery biopsy - granulomatous inflammation in 50% of cases, multinucleated giant cells present, inflammatory infiltrate focal and segmental - Aortic arch angiography - stenosis or occlusion of SC, axillary or proximal brachial arteries
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Generate a management plan for Giant Cell Arteritis.
SUSPECTED - No visual neurological symptoms - Prednisolone 4 weeks, taper over 6-12 months - Visual or neurological symptoms - Methylprednisolone pulse therapy 1g IV for 3 days CONFIRMED - Prednisolone - 4 weeks, taper over 6-12 months - Aspirin - 75mg OD oral - Osteoporosis prevention - Calcium Carbonate + Ergocalciferol + Alendronic Acid / Risedronate Sodium - Tocilizumab or Methotrexate
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Identify the possible complications for giant cell arteritis and its management.
- Carotid artery or aortic aneurysms - Thrombosis - Recanalization or embolism to opthalamic artery - Visual disturbances - Amaurosis fugax - cannot see out of one or both eyes due to lack of blood flow to eyes - Sudden monoocular blindness
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Summarise the prognosis for patients with giant cell arteritis.
For most condition lasts for 2 years before complete remission.