Infection & Immunology Flashcards
1
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Learning objectives
A
Answer
2
Q
Define abscess
A
• A painful collection of pus, usually caused by bacterial infection.
3
Q
Explain the aetiology/risk factors of abscesses
A
• They can develop anywhere in the body
• There are TWO main types of abscess:
o Skin abscess
o Internal abscess
• Bacterial infection leads to activation of an immune response and recruitment of neutrophils to the site of infection
• As the white cells attack the bacteria, surrounding tissue is damaged creating a cavity which fills with pus to form an abscess
• Pus = mixture of dead tissue + white cells + bacteria
4
Q
Summarise the epidemiology of abscesses
A
- Skin abscesses are relatively common
- IV drug use is a major risk factor for skin abscesses
- Internal abscesses are less common
5
Q
Recognise the presenting symptoms and signs of abscesses
A
• Swollen, pus-filled lump under the surface of the skin with associated fever and chills
• Internal abscesses are not visible but are characterised by:
o Pain in the affected area (or referred pain)
o Swinging fevers
o Malaise
6
Q
Identify appropriate investigations for abscesses
A
• Ultrasound - can be useful in visualising an abscess
7
Q
Generate a management plan for abscesses
A
• Some small skin abscesses may disappear by themselves
• Incision and Drainage
o Before doing this, check to see whether a foreign object is causing the abscess (e.g. needle fragments in IV drug users)
o The abscess is cut open and drained of pus
• Antibiotics
o Can be used alongside incision and drainage
8
Q
Identify possible complications of abscesses
A
• Recurrence
9
Q
Summarise the prognosis for patients with abscesses
A
• GOOD with treatment
10
Q
Define anaphylaxis
A
Acute life-threatening multisystem syndrome caused by sudden release of mast cell and basophil-derived mediators into the circulation
11
Q
Explain the aetiology / risk factors of anaphylaxis
A
Immunogenic - IgE-mediated or immune complex/complement-mediated
Non-Immunogenic - mast cell or basophil degranulation WITHOUT the involvement of antibodies (e.g. reactions caused by vancomycin, codeine, ACE inhibitors)
Pathophysiology
o Inflammatory mediators such as histamine are released leading to bronchospasm, increased capillary permeability and reduce vascular tone
o This leads to tissue oedema
Common Allergens
o Drugs (e.g. penicillin)
o Latex
o Peanuts
o Shellfish
o NOTE: anaphylaxis can be caused by the repeat administration of blood products in a patient with selective IgA deficiency (due to the formation of anti-IgA antibodies)
12
Q
Summarise the epidemiology of anaphylaxis
A
COMMON
13
Q
Recognise the presenting symptoms of anaphylaxis
A
Wheeze
Shortness of breath and a sense of choking
Swelling of lips and face
Pruritus
Rash
NOTE: patients may have a history of other hypersensitivity reactions (e.g. asthma, allergic rhinitis)
14
Q
Recognise the signs of anaphylaxis on physical examination
A
Tachypnoea Wheeze Cyanosis Swollen upper airways and eyes Rhinitis Conjunctival infection Urticarial rash Hypotension Tachycardia
15
Q
Identify appropriate investigations for anaphylaxis and interpret the results
A
CLINICAL diagnosis
• Serum tryptase, histamine levels or urinary metabolites of histamine may help support the clinical diagnosis
Following an attack
o Allergen skin testing - identifies allergen
o IgE immunoassays - identifies food-specific IgE in the serum
16
Q
Generate a management plan for anaphylaxis
A
ABCDE High flow oxygen IM Adrenaline Chlorpheniramine (antihistamine) Hydrocortisone If continued respiratory deterioration, may require bronchodilator therapy Monitor pulse oximetry, ECG and BP
17
Q
Identify the possible complications of anaphylaxis and its management
A
SHOCK
Organ damage can result from shock
18
Q
Summarise the prognosis for patients with anaphylaxis
A
Good with prompt treatment
19
Q
Define Behcet’s disease
A
• An inflammatory multisystem disease that often presents with orogenital ulceration and uveitis
20
Q
Explain the aetiology/risk factors of Behcet’s disease
A
- UNKNOWN cause
* Associated with HLA-B51
21
Q
Summarise the epidemiology of Behcet’s disease
A
• More common in Turkey, Greece and Central Asia
22
Q
Recognise the presenting symptoms and signs of Behcet’s disease
A
- Recurrent ORAL and GENITAL ulceration
- Uveitis
- Skin lesions (e.g. erythema nodosum)
- Arthritis
- Thrombophlebitis
- Vasculitis
- Myo/pericarditis
- CNS symptoms
- Colitis
23
Q
Identify appropriate investigations for Behcet’s disease
A
- Diagnosis is very CLINICAL
- Pathergy Test - a needle prick becomes inflamed and a sterile pustule develops within 48 hours
- You may measure complement levels and check for a positive family history
24
Q
Define candidiasis
A
• Infection caused by Candida.
25
Explain the aetiology/risk factors of candidiasis
```
• Caused by 15 different Candida species
• Candida albicans is the MOST COMMON cause of candidiasis in humans
• Main types of candidiasis:
o Oral candidiasis
o Oesophageal candidiasis
o Candidal vulvovaginitis
o Candidal skin infections
o Invasive candidal infections
• Risk Factors
o Broad-spectrum antibiotics
o Immunocompromise (e.g. HIV, corticosteroids)
o Central venous lines
o Cushing's disease
o Diabetes mellitus
o GI tract surgery
```
26
Summarise the epidemiology of candidiasis
* 60% of the healthy adult population are carriers
* Candidiasis occurs in over 80% of people with HIV
* Candida is one of the most common causes of invasive fungal infections in the Western world
27
Recognise the presenting symptoms and signs of candidiasis
• Oral Candidiasis
o Oral Thrush (pseudomembranous oral candidiasis) - curd-like white patches in the mouth, which can be removed easily revealing an underlying red base. Most common in neonates
o There are lots of subtypes of oral candidiasis with slightly different features but the main features are: redness of the tongue and mouth, white plaques
• Oesophageal Candidiasis
o Dysphagia
o Pain on swallowing food or fluids
o It is an AIDS-defining illness
• Candidal Skin Infections
o Soreness and itching
o Skin appearance can be variable
o Red, moist skin area with ragged, peeling edge and possibly papules and pustules
28
Identify appropriate investigations for candidiasis
* Oral Candidiasis - swabs and cultures are not particularly useful because a lot of normal people have candida in their mouth
* Swabs may be relevant to check for drug-resistance
* Therapeutic trials of antifungal (e.g. fluconazole) can help with diagnosis
* Oesophageal Candidiasis: definitive diagnosis is by endoscopy
* Invasive Candidiasis: blood cultures required if candidaemia is possible
29
Define cellulitis
• Acute non-purulent spreading infection of the subcutaneous tissue, causing overlying skin inflammation
Erysipelas is a superficial infection, affecting the upper layers of the skin, while cellulitis affects the deeper tissues. They can overlap, so it is not always possible to make a definite diagnosis between the two.
30
Explain the aetiology/risk factors of cellulitis
```
• Often results from:
o Penetrating injury
o Local lesions (e.g. insect bits)
o Fissuring (e.g. anal fissures)
• These allow pathogenic bacteria to enter the skin
• Most common organisms
o Streptococcus pyogenes
o Staphylococcus aureus
o NOTE: beware of MRSA
• Cellulitis of the orbit (orbital cellulitis) is usually caused by Haemophilus influenzae
• Risk Factors
o Skin break
o Poor hygiene
o Poor vascularisation of tissue (e.g. due to diabetes mellitus)
```
31
Summarise the epidemiology of cellulitis
• VERY COMMON
32
Recognise the presenting symptoms of cellulitis
* History of cut, scratch or injury
* Periorbital Cellulitis - painful swollen red skin around the eye
• Orbital Cellulitis - painful or limited eye movements, visual impairment
33
Recognise the signs of cellulitis on physical examination
```
• Lesion
o Erythema
o Oedema
o Warm tender indistinct margins
o Pyrexia - may suggest systemic spread
• NOTE: exclude the presence of an abscess (aspirate if pus suspected)
• Periorbital
o Swollen eye lids
o Conjunctival infection
• Orbital Cellulitis
o Proptosis
o Impaired visual acuity and eye movements
o Test for RAPD , visual acuity and colour vision
```
34
Identify appropriate investigations for cellulitis
* Bloods - WCC, blood culture
* Discharge - sample and send for MC&S
* Aspiration (if pus is suspected)
* CT/MRI - if orbital cellulitis is suspected (helps assess posterior spread of infection)
35
Generate a management plan for cellulitis
• Medical
o Oral penicillins (e.g. flucloxacillin) or tetracyclines are effective
o If hospital-acquired - treat empirically based on local guidelines and change depending on the sensitivity of cultured organisms
• Surgical
o Orbital decompression may be needed in orbital cellulitis (EMERGENCY)
• Abscess
o Aspirate
o Incision and drainage
o Excised completely
36
Identify possible complications of cellulitis
* Sloughing of overlying skin
* Orbital cellulitis - may cause permanent loss of vision, spread to the brain, abscess formation, meningitis, cavernous sinus thrombosis
The severity can range from mild to severe. This will depend on how large the red area is, which part of the body is affected (erysipelas of the face is more serious) and if there are any other health problems such as an impaired immune system or poorly controlled diabetes. Cellulitis and erysipelas can also lead to complications:
Septicaemia, also known as blood poisoning or sepsis (bacteria spreading through the blood, making the person very ill)
Abscess (a collection of pus in the affected area)
Infection spreading to deeper tissues, like the muscle or bone
Long-term swelling of the affected site due to lymphatic vessel damage
Increased likelihood of further cellulitis or erysipelas at the same site
Kidney damage following streptococcal infection
Meningitis following facial erysipelas
37
Summarise the prognosis for patients with cellulitis
• Good prognosis
38
Define Conjuctivitis
Conjunctivitis is a common condition that causes redness and inflammation of the thin layer of tissue that covers the front of the eye (the conjunctiva).
39
Explain the aetiology / risk factors of conjunctivitis
```
Causes
Viruses
Bacteria
Allergies
A chemical splash in the eye
A foreign object in the eye
In newborns, a blocked tear duct
```
Risk factors:
Exposure to something for which you have an allergy (allergic conjunctivitis)
Exposure to someone infected with the viral or bacterial form of conjunctivitis
Using contact lenses, especially extended-wear lenses
40
Summarise the epidemiology of conjunctivitis
Affects 2% annually. Viral is most common
41
Recognise the presenting symptoms of conjunctivitis
Infective conjunctivitis
If you have infective conjunctivitis, you may also have:
a burning sensation in your eyes
a feeling of grit in your eyes
a sticky coating on the eyelashes – usually when you first wake up in the morning
an enlarged lymph node (gland) in front of the ear
Allergic conjunctivitis
You may have itchy eyes if you have allergic conjunctivitis.
The pattern of symptoms for allergic conjunctivitis depends on the substance you're allergic to.
Allergies to pollen (hay fever) occur during certain parts of the year. You can have an allergy to:
tree pollen, released during spring
grass pollen, released during the end of spring and beginning of summer
weed pollen, released any time from early spring to late autumn
42
Recognise the signs of conjunctivitis on physical examination
When symptoms are mild, a diagnosis of viral conjunctivitis can often be made without seeing a doctor, and the condition can be treated at home.
43
Identify appropriate investigations for conjunctivitis and interpret the results
Based on symptoms, microbial culture
44
Define encephalitis
• Inflammation of the brain parenchyma
45
Explain the aetiology / risk factors of encephalitis
```
Most commonly due to VIRAL INFECTION
Viral Causes
o Herpes Simplex Virus - MOST COMMON in the UK
o VZV
o Mumps
o Adenovirus
o Coxsackie
o EBV
o HIV
o Japanese encephalitis
Non-Viral (RARE)
o Syphilis
o Staphylococcus aureus
In immunocompromised patients
o CMV
o Toxoplasmosis
o Listeria
Autoimmune or Paraneoplastic
o Associated with certain antibodies (e.g. anti-NMDA, anti-VGKC)
```
46
Summarise the epidemiology of encephalitis
• UK incidence: 7.4/100,000
47
Recognise the presenting symptoms of encephalitis
* In most cases, encephalitis is self-limiting and mild
* Subacute onset (hours to days)
* Headache
* Fever
* Vomiting
* Neck stiffness
* Photophobia
* Behavioural changes
* Drowsiness
* Confusion
* History of seizures
* Focal neurological symptoms (e.g. dysphagia, hemiplegia)
* Obtain a detailed TRAVEL HISTORY
48
Recognise the signs of encephalitis on physical examination
* Reduce consciousness
* Deteriorating GCS
* Seizures
* Pyrexia
Signs of Meningism:
o Neck stiffness
o Photophobia
o Kernig's test positive
Signs of raised ICP:
o Cushing's Response: hypertension + bradycardia + irregular breathing
o Papilloedema
Focal neurological signs
MMSE may reveal cognitive/psychiatric disturbance
49
Identify appropriate investigations for encephalitis and interpret the results
```
Bloods
o FBC - high lymphocytes (indicates viral cause)
o U&Es - SIADH may occur as a result of encephalitis
o Glucose
o Viral serology
o ABG
MRI/CT
o Exclude mass lesion
o HSV causes oedema of the temporal lobe on MRI
Lumbar Puncture
o High lymphocytes
o High monocytes
o High protein
o Glucose is usually normal
o Viral PCR
EEG - may show epileptiform activity
Brain biopsy (rarely needed)
```
50
Define epididymitis and orchitis
• Inflammation of the epididymis or testes
o 60% of epididymitis is associated with orchitis
o Most cases of orchitis are associated with epididymitis
51
Explain the aetiology/risk factors of epididymitis and orchitis
```
• Most cases are INFECTIVE in origin
• Bacterial
o If < 35 yrs: Chlamydia and Gonococcus
o If > 35 yrs: mainly coliforms (e.g. Enterobacter, Klebsiella)
o RARE: TB, syphilis
• Viral
o Mumps
• Fungal
o Candida if immunocompromised
• 1/3 are IDIOPATHIC
• Risk Factors
o Diabetes
o Rare: vasculitis (e.g. Henoch-Schonlein purpura)
```
52
Summarise the epidemiology of epididmytis and orchitis
* COMMON
* Affects all age groups
* Most commonly: 20-30 yrs
53
Recognise the presenting symptoms of epididymitis and orchitis
* Painful, swollen and tender testis or epididymis
* NOTE: less acute onset than testicular torsion
* Penile discharge
* IMPORTANT: ask about sexual history
54
Recognise the signs of epididymitis and orchitis on physical examination
* Swollen and tender epididymis or testis
* Scrotum may be erythematous and oedematous
* Pyrexia
* Walking will be painful
* Eliciting a cremasteric reflex may be painful
55
Identify appropriate investigations for epididymitis and orchitis
```
• Urine
o Dipstick
o Early morning urine collections for MC&S
• Bloods
o FBC - high WCC
o High CRP
o U&Es
• Imaging
o Increased blood flow on duplex examination
```
56
Generate a management plan for epididymitis and orchitis
```
• Medical
o Antibiotics
• Surgical
o Exploration of testicles if testicular torsion cannot be excluded clinically
o Required if an abscess develops
```
57
Identify possible complications of epididymitis and orchitis
* Pain
* Abscess
* Fournier's gangrene (if the infection is left untreated and spreads)
* Mumps orchitis could cause testicular atrophy and fertility issues
58
Summarise the prognosis for patients with epididymitis and orchitis
* GOOD if treated
| * May take up to 2 months for the swelling to resolve
59
Define gastroenteritis
• Acute inflammation of the lining of the GI tract, manifested by nausea, vomiting, diarrhoea and abdominal discomfort.
60
Explain the aetiology/risk factors of gastroenteritis
```
• Caused by viruses, bacteria, protozoa or toxins contained in contaminated food or water (faecal-oral route)
• Viral:
o Rotavirus
o Adenovirus
o Astrovirus
o Calcivirus
o Norwalk virus
o Small round structures viruses
• Bacterial:
o Campylobacter jejuni
o Escherichia coli (particularly O157)
o Salmonella
o Shigella
o Vibrio cholerae
o Listeria
o Yersinia enterocolitica
• Protozoal:
o Entamoeba histolytica
o Cryptosporidium parvum
o Giardia lamblia
• Toxins from:
o Staphylococcus aureus
o Clostridium botulinum
o Clostridium perfringens
o Bacillus cereus
o Mushrooms
o Heavy metals
o Seafood
• Commonly contaminated foods:
o Improperly cooked meat
o Old rice
o Eggs and poultry
o Milk and cheeses
o Canned food
```
61
Summarise the epidemiology of gastroenteritis
* COMMON
| * Serious cause of morbidity and mortality in the developing world
62
Recognise the presenting symptoms of gastroenteritis
• Sudden onset nausea, vomiting, anorexia
• DIARRHOEA (bloody or watery)
• Abdominal pain or discomfort
• Fever and malaise
• IMPORTANT: enquire about recent travel, antibiotic use and recent food intake (how the food was cooked, sourced and whether anyone else is ill)
• Time of Onset:
o Toxins = early (1-24 hours)
o Bacterial/viral/protozoal = 12+ hours
• Pay attention to the other effects of toxins:
o Botulinum causes paralysis
o Mushrooms can cause fits, renal or liver failure
63
Recognise the signs of gastroenteritis on physical
* Diffuse abdominal tenderness
* Abdominal distension
* Bowel sounds are often INCREASED
* In SEVERE gastroenteritis: pyrexia, dehydration, hypotension and peripheral shutdown
IMPORTANT: ANY DIARRHOEAL CONDITION CAN LEAD TO DEHYDRATION so assess and address the patient's hydration status immediately
64
Identify appropriate investigations for gastroenteritis
* Bloods: FBC, blood culture (identify bacteraemia), U&Es (dehydration)
* Stool: faecal microscopy and analysis for toxins (particularly for the toxin causing pseudomembranous colitis (C. difficile toxin)
* AXR or ultrasound: exclude other causes of abdominal pain (e.g. bowel perforation)
* Sigmoidoscopy: usually unnecessary unless inflammatory bowel disease needs to be excluded
65
Generate a management plan for gastroenteritis
* Bed rest
* Fluid and electrolyte replacement with oral rehydration solution (contains glucose and salt)
* IV rehydration may be necessary in those with severe vomiting
* Most infections are self-limiting (so will go away with time)
* Antibiotic treatment is only used if severe or if infective agent has been identified
* NOTE: if botulism is present (due to Clostridium botulinum) treat with botulinum antitoxin (IM) and manage in ITU
* NOTE: this is often a notifiable disease and is an important public health issue
66
Identify the possible complications of gastroenteritis
* Dehydration
* Electrolyte imbalance
* Prerenal failure (due to dehydration)
* Secondary lactose intolerance (particularly in infants)
* Sepsis and shock
* Haemolytic uraemic syndrome (associated with toxins from E. coli O157)
* Guillain-Barre Syndrome may occur weeks after recovery from Campylobacter gastroenteritis
* NOTE: botulism can lead to respiratory muscle weakness or paralysis
67
Summarise the prognosis for patients with gastroenteritis
• Good prognosis because most cases are self-limiting
68
Define infectious colitis
• Inflammation of the colon due to bacteria, parasites or viruses
69
Explain the aetiology/risk factors of infectious colitis
```
• Infection leads to inflammation of the colon
• Risk Factors
o Lack of sanitation
o Drinking contaminated water
o Antibiotic use
```
70
Summarise the epidemiology of infectious colitis
• Quite COMMON
71
Recognise the presenting symptoms & signs of infectious colitis
* Diarrhoea
* Blood and mucus in the stools
* Lower abdominal pain
* Malaise
* Low-grade fever
72
Identify appropriate investigations for infectious colitis
* Diagnosis is largely CLINICAL
| * Stool culture may be used to identify the causative organism
73
Define herpes simplex
• Disease resulting from HSV1 or HSV2 infection
74
Explain the aetiology/risk factors of herpes simplex
• Transmitted via close contact (e.g. kissing, sexual intercourse) with an individual that is shedding the virus
• Pathophysiology
o After primary infection, the virus will become dormant (within nerve ganglia)
o Reactivation may occur in response to physical and emotional stresses or immunosuppression
o The virus causes cytolysis of infected epithelial cells leading to vesicle formation
75
Summarise the epidemiology of herpes simplex
* 90% of adults are seropositive for HSV1 by 30 yrs
* 35% of adults > 60 yrs are seropositive for HSV2
* More than 1/3 of the world population have recurrent HSV infections
76
Recognise the presenting symptoms of herpes simplex
• HSV1 - primary infection is often asymptomatic
• Possible symptoms of primary HSV1 infection:
o Pharyngitis
o Gingivostomatitis (eating might be painful)
o Herpetic whitlow (abscess at the end of the finger caused by infection with HSV - it is very painful)
• Symptoms of reactivation of HSV1:
o Prodrome of perioral tingling and burning
o Vesicles appear - they will ulcerate and crust over
o Complete healing within 8-10 days
• Symptoms of HSV2:
o Painful blisters and rash in the genital, perigenital and anal area
o Dysuria
o Fever
o Malaise
• Symptoms of HSV encephalitis:
o Usually caused by HSV1 so causes HSV1 type symptoms
• Symptoms of HSV keratoconjunctivitis
o Watering eyes
o Photophobia
77
Recognise the signs of herpes simplex on physical examination
• HSV1 Primary Infection
o Tender cervical lymphadenopathy
o Erythematous, oedematous pharynx
o Oral ulcers filled with yellow slough (gingivostomatitis)
```
o Herpetic whitlow
• Herpes Labialis (reactivation affecting the mouth)
o Perioral vesicles/ulcers/crusting
• HSV2
o Maculopapular rash
o Vesicles
o Ulcers
o All of these are found on the external genitalia, anal margin and upper thighs
o Others: inguinal lymphadenopathy, pyrexia
• HSV2 Encephalitis
o Signs of encephalitis
• HSV Keratoconjunctivitis
```
o Dendritic ulcer on the iris (better visualised with fluorescein)
78
Identify appropriate investigations for herpes simplex
* Diagnosis is usually CLINICAL
| * Vesicle fluid can be sampled and sent for electron microscopy, PCR
79
Define HIV
• Infection with the human immunodeficiency virus (HIV)
80
Explain the aetiology/risk factors of HIV
• HIV is transmitted by:
o Sexual intercourse
• Heterosexual intercourse is the MOST COMMON mode of transmission
• Homosexuals are at greater risk in the West
o Blood (and other bodily fluids)
• Mother to child (intrauterine, childbirth, breastfeeding)
• Needles
• Blood transfusions
• Organ transplantation
• Pathophysiology
o HIV enters CD4+ lymphocytes by binding to their gp120 receptors
o Reverse transcriptase allows the incorporation of HIV genetic material into the host genome
o This leads to dissemination of HIV, cell death and eventual T-cell depletion
81
Summarise the epidemiology of HIV
• Increasing in incidence in Africa and Asia
82
Recognise the signs and presenting symptoms of HIV
• There are THREE phases of HIV:
o Seroconversion
• Self-limiting
• Fever
• Night sweats
• Generalised lymphadenopathy
• Sore throat
• Others: oral ulcers, rash, myalgia, headache, encephalitis, diarrhoea
o Early/Asymptomatic
• Apparently well
• Some may have persistent lymphadenopathy
• Progressive minor symptoms (e.g. rash, oral thrush, weight loss)
o AIDS
• Syndrome of secondary diseases resulting from immunodeficiency
• Direct Effects of HIV Infection
o Neurological: polyneuropathy, dementia
o Lung: lymphocytic interstitial pneumonitis
o Heart: cardiomyopathy, myocarditis
o Haematological: anaemia, thrombocytopaenia
o GI: anorexia, wasting
o Eyes: cotton wool spots
• Secondary effects resulting from immunodeficiency
o Bacterial Infection: TB, skin infections, pneumococcal infections
o Viral: CMV, HSV, VZV, HPV, EBV
o Fungal: pneumocystic jirovecii pneumonia, Cryptococcus, candidiasis, invasive aspergillosis
o Protozoal: toxoplasmosis, cryptosporidia
o Tumours: Kaposi sarcoma, SCC, non-Hogkin's lymphoma, Hodgkin's lymphoma
83
Identify appropriate investigations for HIV
• HIV testing - HIV antibodies, PCR for viral RNA, CD4 count, viral load
• Others
o Pneumocystic pneumonia - CXR
o Cryptococcal meningitis - brain CT or MRI, LP
o CMV (colitis) - colonoscopy and biopsy
o Toxoplasmosis - brain CT or MRI
o Cryptosporidia - stool microscopy
84
Define infectious mononucleosis
• Clinical syndrome caused by primary EBV infection
| o AKA glandular fever
85
Explain the aetiology/risk factors of infectious mononucleosis
* EBV is a gamma-Herpes virus (dsDNA)
* It is found in the pharyngeal secretions of infected individuals and is transmitted by close contact (e.g. kissing, sharing eating utensils)
* EBV infection of the epithelial cells of the oropharynx leads to B cell infection
* The infected B cells disseminate EBV across the body leading to a humoral and cellular immune response
* Atypical lymphocytes in the peripheral blood are a classic feature of infectious mononucleosis
* EBV remains latent in lymphocytes
* Reactivation may occur following stress or immunosuppression
86
Summarise the epidemiology of infectious mononucleosis
• COMMON
• TWO age peaks:
o 1-6 yrs
o 14-20 yrs
87
Recognise the presenting symptoms of infectious mononucleosis
```
• Incubation period: 4-8 weeks
• Abrupt onset of symptoms:
o Sore throat
o Fever
o Fatigue
o Headache
o Malaise
o Anorexia
o Sweating
o Abdominal pain
```
88
Recognise the signs of infectious mononucleosis on physical examination
* PYREXIA
* Oedema and erythema of the pharynx
* White/creamy exudate on the tonsils
* Palatal petechiae
* Cervical/generalised lymphadenopathy
* Splenomegaly
* Hepatomegaly
* Jaundice (5-10%)
* Widespread maculopapular rash (in patients who have received ampicillin)
89
Identify appropriate investigations for infectious mononucleosis
• Bloods
o FBC - leucocytosis
o LFTs - high AST/ALT
• Blood Film - lymphocytosis with atypical lymphocytes
• Heterophil Antibody Test (aka Monospot Test, Paul Bunnell Test)
o Based on EBV antigens being similar to antigens on RBCs of many animals but NOT humans
o Mixing blood of an EBV-positive human with animal blood will make the animal's red cells aggregate and precipitate out of solution
o May give false-negatives in the early stages of infection before antibodies are generated
• Throat swabs - exclude streptococcal tonsillitis
• IgM or IgG to EBV viral capsid antigen
• IgG against Epstein-Barr nuclear antigen (EBNA)
90
Generate a management plan for infectious mononucleosis
* Bed rest
* Paracetamol and NSAIDs - helps with fever, malaise
* Corticosteroids in SEVERE cases
* IMPORTANT: do NOT give AMPICILLIN or AMOXICILLIN if infectious mononucleosis is suspected - nearly 100% of patients with glandular fever develop a maculopapular rash
* Advice - avoid contact sports for 2 weeks (because of risk of rupturing your spleen)
91
Identify possible complications of infectious mononucleosis
* Lethargy for several months
* Respiratory - airway obstruction from oedematous pharynx, secondary bacterial throat infection, pneumonitis
* Haematological - haemolytic or aplastic anaemia, thrombocytopenia
* GI/Renal - splenic rupture, fulminant hepatitis, pancreatitis, mesenteric adenitis, renal failure
* CNS - Guillain-Barre syndrome, encephalitis, viral meningitis
* EBV-associated malignancy - Burkitt's lymphoma (in sub-Saharan Africa), nasopharyngeal cancer, Hodgkin's lymphoma
92
Summarise the prognosis for patients with infectious mononucleosis
* Most make uncomplicated recovery (within 3 weeks)
| * Immunodeficiency and death are VERY RARE
93
Define infective endocarditis
• Infection of intracardiac endocardial structures (mainly heart valves)
94
Explain the aetiology / risk factors of infective endocarditis
• Most common organisms causing infective endocarditis:
o Streptococci (40%) - mainly a-haemolytic S. viridans and S. bovis
o Staphylococci (35%) - S. aureus and S. epidermidis
o Enterococci (20%) - usually E. faecalis
o Other organisms:
• Haemophilus
• Actinobacillus
• Cardiobacterium
• Coxiella burnetii
• Histoplasma (fungal)
• Pathophysiology
o Vegetations form when organisms deposit on the heart valves during a period of bacteraemia
o The vegetations are made up of platelets, fibrin and infective organisms
o They destroy valve leaflets, invade the myocardium or aortic wall leading to abscess cavities
o Activation of the immune system can lead to the formation of immune complexes --> vasculitis, glomerulonephritis, arthritis
• Risk Factors
o Abnormal valves (e.g. congenital, calcification, rheumatic heart disease)
o Prosthetic heart valves
o Turbulent blood flow (e.g. patent ductus arteriosus)
o Recent dental work/poor dental hygiene (source of S. viridans)
95
Summarise the epidemiology of infective endocarditis
• UK Incidence: 16-22/1 million per year
96
Recognise the presenting symptoms of infective endocarditis
```
• Fever with sweats/chills/rigors
o NOTE: this might be relapsing and remitting
• Malaise
• Arthralgia
• Myalgia
• Confusion
• Skin lesions
• Ask about recent dental surgery or IV drug use
```
97
Recognise the signs of infective endocarditis on physical examination
```
• Pyrexia
• Tachycardia
• Signs of anaemia
• Clubbing
• New regurgitant murmur or muffled heart sounds
• Frequency of heart murmurs:
o Mitral > Aortic > Tricuspid > Pulmonary
• Splenomegaly
• Vasculitic Lesions
o Roth spots on retina
```
o Petechiae on pharyngeal and conjunctival mucosa
o Janeway lesions (painless macules on the palms which blanch on pressure)
o Osler's nodes (tender nodules on finger/toe pads)
o Splinter haemorrhages
98
Identify appropriate investigations for infective endocarditis and interpret the results
• Bloods
o FBC - high neutrophils, normocytic anaemia
o High ESR/CRP
o U&Es
o NOTE: a lot of patients with infective endocarditis tend to be rheumatoid factor positive
• Urinalysis
o Microscopic haematuria
o Proteinuria
• Blood Culture
o Do microscopy and sensitivities as well
• Echocardiography
o Transthoracic or transoesophageal (produces better image)
• Duke's Classification - a method of diagnosing infective endocarditis based on the findings of the investigations and the symptoms/signs
99
Generate a management plan for infective endocarditis
```
• Antibiotics for 4-6 weeks
• On clinical suspicion = EMPIRICAL TREATMENT
o Benzylpenicillin
o Gentamicin
• Streptococci - continue the same as above
• Staphylococci
o Flucloxacillin/vancomycin
o Gentamicin
• Enterococci
o Ampicillin
o Gentamicin
• Culture Negative
o Vancomycin
o Gentamicin
• SURGERY - urgent valve replacement may be needed if there is a poor response to antibiotics
```
100
Identify the possible complications of infective endocarditis and its management
* Valve incompetence
* Intracardiac fistulae or abscesses
* Aneurysm
* Heart failure
* Renal failure
* Glomerulonephritis
* Arterial emboli from the vegetations shooting to the brain, kidneys, lungs and spleen
101
Summarise the prognosis for patients with infective endocarditis
* FATAL if untreated
| * 15-30% mortality even WITH treatment
102
Define malaria
```
• Infection with protozoan Plasmodium
• FIVE types of Plasmodium:
o Plasmodium falciparum - MOST SERIOUS
o Plasmodium vivax
o Plasmodium ovale
o Plasmodium malariae
o Plasmodium knowlesi
```
103
Explain the aetiology/risk factors of malaria
* Transmitted by the bite of the female Anopheles mosquito
* The protozoa grow in red blood cells
* Life Cycle
o Injection of sporozoites into the blood stream by mosquito
o Invasion and replication in hepatocytes
o Parasites reinvade the blood and enter red blood cells
o They replicate within red blood cells and develop ring forms
o Red blood cells rupture and release merozoites, which reinfect other red blood cells
o Gametocytes are taken up when another mosquito feeds, and develop into sporozoites in the gut of the mosquito
o They then move to the salivary gland of the mosquito to be transmitted with the next bite
• Some populations have innate immunity to malaria:
o Sickle cell trait
o G6PD deficiency
o Pyruvate kinase deficiency
o Thalassemia
104
Summarise the epidemiology of malaria
* Endemic in the tropics
| * 250 million people worldwide
105
Recognise the presenting symptoms of malaria
```
• Feverish traveller (incubation period can be up to 1 year)
• Symptoms are CYCLICAL:
o High fever
o Flu-like symptoms
o Severe sweating
o Shivering cold/rigors
• NOTE: the interval between cycles of symptoms are slightly different in different types of malaria
• Cerebral Malaria Symptoms:
o Headache
o Disorientation
o Coma
```
106
Recognise the signs of malaria on physical examination
* Pyrexia
* Anaemia (haemolytic)
* Hepatosplenomegaly
107
Identify appropriate investigations for malaria
• Thick/Thin Blood Films
o Thick for quantifying
o Thin for identifying type of malaria
```
• Bloods
o FBC - haemolytic picture
o U&Es
o LFTs
o ABG
• Urinalysis -check for blood or protein
```
108
Define mastitis/breast abscesses
```
Define breast abscess
• Abscess formation in breast tissues.
o TWO main forms:
• Lactational
• Non-Lactational
```
109
Explain the aetiology / risk factors of mastitis/breast abscesses
```
• Caused by INFECTION
• Causative organisms defer based on whether the abscess is:
o Lactational
• Staphylococcus aureus
o Non-Lactational
• Staphylococcus aureus
• Anaerobes
• Risk Factors
o Lactation
o SMOKING
o Mammary duct ectasia
o Periductal mastitis
o Wound infections (e.g. from breast surgery)
```
110
Summarise the epidemiology of mastitis/breast abscesses
* Lactational breast abscess are COMMON and tend to occur soon after starting breast feeding or weaning
* Non-lactational breast abscesses are more common in 30-60 yo smokers
111
Recognise the presenting symptoms of mastitis/breast abscesses
* Breast discomfort
* Painful swelling
* Generally unwell and feverish
* Non-lactational - tend to present with a history of previous infections with less pronounced systemic upset
112
Recognise the signs of mastitis/breast abscesses on physical examination
• Local
o Swollen, warm and tender area of the breast
o Overlying skin may be inflamed
o The nipple may be cracked
o Non-Lactational
• Scars or tissue distortion from previous episodes
• Signs of duct ectasia (e.g. nipple retraction)
• Systemic
o Pyrexia
o Tachycardia
113
Identify appropriate investigations for mastitis/breast abscesses and interpret the results
* Ultrasound
| * MC&S of pus samples
114
Generate a management plan for mastitis/breast abscesses
• Medical
o Antibiotics
• Lactational: flucloxacillin
• Non-Lactational: flucloxacillin + metronidazole
• Surgical
o Lactational: Incision and drainage
o Non-Lactational: open drainage should be avoided. The involved duct system should be excised once the infection has settled
115
Identify the possible complications of mastitis/breast abscesses and its management
* Mammary fistula
| * Overlying skin may (rarely) undergo necrosis
116
Summarise the prognosis for patients with mastitis/breast abscesses
* If untreated, a breast abscess may discharge onto the skin surface
* Non-lactational breast abscesses tend to recur
117
Define meningitis
• Inflammation of the leptomeningeal (pia and arachnoid mater) coverings of the brain, most commonly due to infection
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
• Streptococcus pneumoniae
• Tuberculosis
Elderly
• Streptococcus pneumoniae
• Listeria monocytogenes
```
```
VIRAL
o Enteroviruses
o Mumps
o HSV
o VZV
o HIV
```
```
Fungal
o Cryptococcus (common cause of meningitis in HIV patients)
```
Others
o Aseptic meningitis (not due to microbes)
o Mollaret's meningitis (recurrent benign lymphocytic meningitis)
```
RISK FACTORS
o Close communities (e.g. college halls)
o Basal skull fractures
o Mastoiditis
o Sinusitis
o Inner ear infections
o Alcoholism
o Immunodeficiency
o Splenectomy
o Sickle cell anaemia
o CSF shunts
o Intracranial surgery
```
119
Summarise the epidemiology of meningitis
• UK: 2500 notifications/yr
120
Recognise the presenting symptoms of meningitis
* Severe headache
* Photophobia
* Neck or backache
* Irritability
* Drowsiness
* Vomiting
* High-pitched crying or fits (common in children)
* Reduced consciousness
* Fever
IMPORTANT: take a good travel history and exposure history and take not of exposure to any of the following
o Rodents (lymphocytic choriomeningitis virus)
o Ticks (Lyme borrelia, Rocky Mountain spotted fever)
o Mosquitoes (West Nile virus)
o Sexual activity (HSV-2, HIV, syphilis)
o Travel
121
Recognise the signs of meningitis on physical examination
• Signs of MENINGISM
o Photophobia
o Neck stiffness
o Kernig's Sign - with the hips flexed, there is pain/resistance on passive knee extension
o Brudzinski's Sign - flexion of the hips when the neck is flexed
```
• Signs of INFECTION
o Fever
o Tachycardia
o Hypotension
o Skin rash
o Altered mental state
```
122
Identify appropriate investigations for meningitis and interpret the results
Bloods
o Two sets of blood cultures
Imaging
o CT scan - exclude mass lesion or raised ICP before LP
```
Lumbar Puncture
o MC&S
o Bacterial meningitis:
• Cloudy CSF
• High neutrophils
• High protein
• Low glucose
o Viral meningitis:
• High lymphocytes
• High protein
• Normal glucose
o TB meningitis:
• Fibrinous CSF
• High lymphocytes
• High protein
• Low glucose
```
123
Generate a management plan for meningitis
IMMEDIATE IV Antibiotics (before LP)
o First choice: 3rd generation cephalosporin (e.g. cefotaxime or ceftriaxone)
o Benzylpenicillin may be used as an initial blind therapy
Dexamethasone IV
o Given shortly before or with the first dose of antibiotics
o Associated with a reduced risk of complications
Resuscitation
o Manage in ITU
o Notify public health services
124
Identify the possible complications of meningitis and its management
* Septicaemia
* Shock
* DIC
* Renal failure
* Seizures
* Peripheral gangrene
* Cerebral oedema
* Cranial nerve lesions
* Cerebral venous thrombosis
* Hydrocephalus
* Waterhouse-Friderichsen Syndrome (bilateral adrenal haemorrhage caused by severe meningococcal infection)
125
Summarise the prognosis for patients with meningitis
* Mortality rate from bacterial meningitis: 10-40% with meningococcal sepsis
* Viral meningitis is self-limiting
126
Define myocarditis
• Acute inflammation and necrosis of cardiac muscle (myocardium)
127
Explain the aetiology / risk factors of myocarditis
* Incidence is difficult to measure accurately
* Coxsackie B virus is most common in Europe and USA
* Chagas disease is most common in South America
128
Summarise the epidemiology of myocarditis
```
• Usually IDIOPATHIC
• Viruses
o Coxsackie B
o EBV
o CMV
o Adenovirus
o Influenza
• Bacteria
o Post-streptococcal
o Tuberculosis
o Diphtheria
• Fungal
o Candidiasis
• Protozoal
o Trypanosomiasis (Chagas disease)
• Helminths
o Trichinosis
• Non-infective
o Systemic: SLE, sarcoidosis, polymyositis
o Hypersensitivity myocarditis: sulphonamides
• Drugs
o Chemotherapy agents (e.g. doxorubicin, streptomycin)
• Others
o Cocaine, heavy metals, radiation
```
129
Recognise the presenting symptoms of myocarditis
```
• Prodromal flu-like illness with:
o Fever
o Malaise
o Fatigue
o Lethargy
• Breathlessness (due to pericardial effusion/myocardial dysfunction)
• Palpitations
• Sharp chest pain (suggesting there is also pericarditis)
```
130
Recognise the signs of myocarditis on physical examination
* Signs of pericarditis
| * Signs of complications (e.g. heart failure, arrhythmia)
131
Identify appropriate investigations for myocarditis and interpret the results
```
• Bloods
o FBC - raised WCC if infective cause
o U&E
o ESR/CRP - raised
o Cardiac enzymes - may be raised
o Tests to identify cause (e.g. viral/bacterial serology, ANA, TFT)
• ECG
o Non-specific T wave and ST changes
o PERICARDITIS: widespread saddle-shaped ST elevation
```
```
• CXR
o May be NORMAL
o May show cardiomegaly
• Pericardial Fluid Drainage
o Measure glucose, protein, cytology, culture and sensitivity
o Helps identify causative organism
• Echocardiography
o Assesses systolic/diastolic function
o Wall motion abnormalities
o Pericardial effusions
• Myocardial Biopsy
o Rarely required
```
132
Define gangrene
* Gangrene: tissue necrosis, either wet with superimposed infection, dry or gas gangrene
* Necrotising Fasciitis: a life-threatening infection that spreads rapidly across fascial planes
133
Explain the aetiology / risk factors of gangrene
```
o Tissue ischaemia and infarction
o Physical trauma
o Thermal injury
o Gas gangrene is caused by Clostridia perfringens
• Necrotising Fasciitis
o Usually polymicrobial involving streptococci, staphylococci, bacterioides and coliforms
• Risk Factors
o Diabetes
o Peripheral vascular disease
o Leg ulcers
o Malignancy
o Immunosuppression
o Steroid use
o Puncture/surgical wounds
```
134
Summarise the epidemiology of gangrene
* Gangrene - relatively COMMON
| * Necrotising fasciitis and gas gangrene - RARE
135
Recognise the presenting symptoms of gangrene
• Gangrene
o Pain
o Discolouration of affected area
o Often affects extremities or areas subject to high pressure
• Necrotising Fasciitis
o Pain
• Often seems SEVERE and out of proportion to the apparent physical signs
o Predisposing event (e.g. trauma, ulcer, surgery)
136
Recognise the signs of gangrene on physical examination
• Gangrene
o Painful area = erythematous region around gangrenous tissue
o Gangrenous tissue = BLACK because of haemoglobin break down products
o Wet Gangrene - tissue becomes boggy with associated pus and a strong odour caused by the activity of anaerobes
o Gas Gangrene - spreading infection and destruction of tissues causes overlying oedema, discolouration and crepitus (due to gas formation by the infection)
• Necrotising Fasciitis
o Area of erythema and oedema
o Haemorrhagic blisters may be present
o Signs of systemic inflammatory response and sepsis (high/low temperature, tachypnoea, hypotension)
137
Identify appropriate investigations for gangrene and interpret the results
* Bloods - FBC, U&Es, glucose, CRP and blood culture
* Wound Swab, Pus/Fluid Aspirate - MC&S
* X-ray of affected area - may show gas produced in gas gangrene
138
Define neutropenic sepsis
• The development of sepsis in a patient with neutropenia.
• Diagnostic criteria:
o Temperature > 38 degrees
o Neutrophil count < 0.5 x 109 /L
• CAUTION: patients can have neutropenic sepsis without a fever because they may be on anti-pyretic medications or steroids
139
Explain the aetiology / risk factors of neutropenic sepsis
• Incidental Neutropenia
o Congenital - ethnic variation, cyclical neutropenia in children (all VERY RARE)
o Acquired
• Decreased/ineffective neutrophil production: bone marrow infiltration, aplastic anaemia, B12/folate deficiency, chemotherapy, radiotherapy
• Accelerated turnover: Felty's syndrome, hypersplenism, malaria
• Others: toxoplasmosis, dengue fever
• Febrile Neutropenia
o DEFINITION: temperature > 38.5 or two consecutive readings of > 38 for two hours and an absolute neutrophil count < 0.5 x 109 /L
140
Summarise the epidemiology of neutropenic sepsis
• Most common in patients with cytotoxic chemotherapy
141
Recognise the presenting symptoms & signs of neutropenic sepsis
```
• Check history for:
o High-risk features: active cancer, recent chemotherapy, use of immunosuppressants or immunosuppressive illness (e.g. HIV)
o Chronic kidney disease
o Recent blood products
o Intravascular devices (e.g. central line)
• Examination findings:
o Signs of infection may be minimal
o Pyrexia
o Features of infective endocarditis
o Lymphadenopathy
o Skin rashes
```
142
Identify appropriate investigations for neutropenic sepsis and interpret the results
* FBC (check neutrophil level)
* Blood cultures (check for sepsis)
* Others - blood film, D-dimer (for DIC), U&Es, creatinine, LFTs
143
Define osteomyelitis
• Infection of the bone leading to inflammation, necrosis and new bone formation. Can be acute, subacute or chronic.
• Causative organisms:
o Staphylococcus aureus
o Group A Streptococcus
144
Explain the aetiology/risk factors of osteomyelitis
```
• Bacterial infection from indirect inoculation from skin (e.g. trauma, operative, chronic skin ulcers, haematogenous spread)
• Risk Factors
o Diabetes
o Immunosuppression
o IV drug use
o Prostheses
o Sickle-cell anaemia
```
145
Summarise the epidemiology of osteomyelitis
* Mostly in YOUNG CHILDREN
| * < 20% of cases are in adults
146
Recognise the presenting symptoms of osteomyelitis
* Pain in the affected area
* Fever
* Malaise
* Rigors
* History of preceding skin lesion, sore throat, trauma or operation
* NOTE: infants may not show localising signs
147
Recognise the signs of osteomyelitis on physical examination
* Localised erythema
* Tenderness
* Swelling
* Warmth
* Painful/limited movement of affected limb
* Seropurulent discharge from an associated wound or ulcer
148
Identify appropriate investigations for osteomyelitis
```
• Bloods
o FBC
o Blood culture
o ESR
o CRP
• Swabs of wound or discharge
• Radiographs
• Radioisotope bone scan - shows areas of increased activity
```
149
Define pericarditis
• Inflammation of the pericardium
| o It may be acute, subacute or chronic
150
Explain the aetiology / risk factors of pericarditis
* UNCOMMON
* < 1/100 hospital admissions
* More common in males
151
Summarise the epidemiology of pericarditis
```
• IDIOPATHIC
• Infective
Most common causative organisms:
o Coxsackie B
o Echovirus
o Mumps
o Streptococci
o Fungi
o Staphylococci
o TB
• Connective tissue disease (e.g. sarcoidosis, SLE, scleroderma)
• Post-MI (within 24-72 hrs of MI - occurs in up to 20% of patients)
• Dressler's Syndrome - pericarditis occurring weeks/months after acute MI
• Malignancy - lung, breast, lymphoma, leukaemia, melanoma
• Radiotherapy
• Thoracic surgery
• Drugs (e.g. hydralazine, isoniazid)
```
152
Recognise the presenting symptoms of pericarditis
```
• CHEST PAIN
o Sharp and central
o May radiate to the neck or shoulders
o Worse when coughing and deep inspiration (pleuritic pain)
o Relieved by sitting forward
• Dyspnoea
• Nausea
```
153
Recognise the signs of pericarditis on physical examination
```
• Fever
• Pericardial friction rub
o Heard best at lower left sternal edge, with patient leaning forward during expiration
• Heart sounds may be faint due to a pericardial effusion
• Cardiac Tamponade signs
o Beck's Triad (signs associated with acute cardiac tamponade)
• Raised JVP
• Low Blood Pressure
• Muffled Heart Sounds
o Tachycardia
o Pulsus paradoxus
• Definition: an abnormally large decrease in SBP (> 10 mm Hg drop) and pulse wave amplitude during inspiration
• Constrictive Pericarditis signs
o Kussmaul's sign
o Pulsus paradoxus
o Hepatomegaly
o Ascites
o Oedema
o Pericardial knock (due to rapid ventricular filling)
o AF
```
154
Identify appropriate investigations for pericarditis and interpret the results
• ECG - widespread saddle-shaped ST elevation
• Echocardiogram - assesses pericardial effusion and cardiac function
• Bloods
o FBC
o U&Es
o ESR/CRP
o Cardiac Enzymes (usually normal)
o Other investigations for cause: blood cultures, ASO titres, ANA, rheumatoid factor
• CXR
o Usually normal
o May be globular if there is a pericardial effusion
155
Generate a management plan for pericarditis
```
• Acute - cardiac tamponade is treated with emergency pericardiocentesis
• Medical
o Treat underlying cause
o NSAIDs for pain and fever relief
• Recurrent
o Low-dose steroids
o Immunosuppressants
o Colchicine
• Surgical
o Pericardiectomy is performed in cases of constrictive pericarditis
```
156
Identify the possible complications of pericarditis and its management
* Pericardial effusion
* Cardiac tamponade
* Cardiac arrhythmias
157
Summarise the prognosis for patients with pericarditis
* Depends on the underlying cause
* Viral cases have a GOOD prognosis
* Malignant pericarditis has a POOR prognosis
158
Define peritonitis
• Inflammation of the peritoneal lining of the abdominal cavity. It can be localised to one part of the peritoneum or generalised.
159
Explain the aetiology/risk factors of peritonitis
• Localised Peritonitis
o Appendicitis
o Cholecystitis
o Diverticulitis
o Salpingitis
• Primary Generalised Peritonitis
o Bacterial infection of the peritoneal cavity without an obvious source
• Could be via haematogenous or lymphatic spread or ascending infection from the female genital tract)
o Risk Factors
• Ascites
• Nephrotic syndrome
• Secondary Generalised Peritonitis
o Caused by bacterial translocation from a localised focus
o Could be non-bacterial due to spillage of bowel contents, bile and blood (e.g. perforated peptic ulcer)
160
Summarise the epidemiology of peritonitis
* Primary peritonitis is RARE
* Primary peritonitis is usually seen in adolescent females
* Localised and secondary generalised peritonitis is COMMON in surgical patients
161
Recognise the presenting symptoms of peritonitis
* Do a full SOCRATES for peritonitis
* Inflammation of the parietal peritoneum is usually continuous, sharp, localised, exacerbated by movement and coughing
* Symptoms may be vague in those with liver disease and ascites (due to confusion caused by encephalopathy)
162
Recognise the signs of peritonitis on physical examination
• Check vital signs and look for signs of dehydration or compromised perfusion (e.g. due to sepsis or hypovolaemia)
• Localised Peritonitis
o Tenderness on examination
o Guarding
o Rebound tenderness
• Generalised Peritonitis
o Very unwell
o Systemic signs of toxaemia or sepsis (e.g. fever, tachycardia)
o The patient will lie still
o Shallow breathing
o Rigid abdomen
o Generalised abdominal tenderness
o Reduced bowel sounds (may be absent due to paralytic ileus)
o DRE may show anterior tenderness (suggests pelvic peritonitis)
163
Identify appropriate investigations for peritonitis
```
• Bloods
o FBC
o U&Es
o LFTs
o Amylase
o CRP
o Clotting
o Group & Save or Cross-match
o Blood cultures
o Pregnancy test
o ABG
• Imaging
o Erect CXR (check for air under the diaphragm)
o AXR (check for bowel obstruction)
o USS or CT abdomen
o Laparoscopy
• If Ascites
o Ascitic tap and cell count
o SBP = > 250 neutrophils/mm3
o Gram stain and culture
```
164
Generate a management plan for peritonitis
• Localised Peritonitis
o Depends on CAUSE
o Some causes may require surgery (e.g. appendicitis)
o Some causes can be treated with antibiotics (e.g. salpingitis)
• Generalised Peritonitis
o Patient may be at risk of DEATH from sepsis or shock
o IV fluids
o IV antibiotics
o Urinary catheter
o NG tube
o Central venous line (to monitor fluid balance)
o Laparotomy
• Remove the infected or necrotic tissue
• Treat cause
• Peritoneal lavage
o Primary Peritonitis - should be treated with antibiotics
• Spontaneous Bacterial Peritonitis (SBP)
o Quinolone antibiotics
OR
o Cefuroxime + Metronidazole
165
Identify possible complications of peritonitis
```
• Early
o Septic shock
o Respiratory failure
o Multiorgan failure
o Paralytic ileus
o Wound infection
o Abscesses
• Late
o Incisional hernia
o Adhesions
```
166
Summarise the prognosis for patients with peritonitis
* Localised peritonitis usually resolves with treatment of the underlying cause
* Generalised peritonitis has a much higher mortality (30-50%)
* Primary peritonitis has a good prognosis with antibiotic treatment
* SBP has a mortality > 30% if diagnosis and treatment is delayed
167
Define pneumonia
```
Infection of distal lung parenchyma.
It can be categorised in many ways:
Community-acquired
Hospital-acquired/nosocomial
Aspiration pneumonia
Pneumonia in the immunocomprised
Typical
Atypical (Mycoplasma, Chlamydia, Legionella)
```
168
Explain the aetiology/risk factors of pneumonia
```
Community-Acquired
Streptococcus pneumoniae (70%)
Haemophilus influenzia
Moraxella catarrhalis (occurs in COPD patients)
Chlamydia pneumonia
Chlamydia psittaci (causes psittacosis)
Mycoplasma pneumonia
Legionella (air conditioning)
Staphylococcus aureus
Coxiella burnetii (causes Q fever)
TB
```
Hospital-Acquired
Gram-negative enterobacteria (Pseudomonas, Klebsiella)
Anaerobes (due to aspiration pneumonia)
```
Risk factors
Age
Smoking
Alcohol
Pre-existing lung disease (COPD)
Immunodeficiency
Contact with patients with pneumonia
```
169
Summarise the epidemiology of pneumonia
5-11/1000
| Community-acquired pneumonia is responsible for >60,000 deaths per year in the UK
170
Recognise the presenting symptoms of pneumonia
```
Fever
Rigors
Sweating
Malaise
Cough
Sputum
Breathlessness
Pleuritic chest pain
Confusion (in severe cases or in the elderly)
```
```
Atypical Pneumonia Symptoms:
Headache
Myalgia
Diarrhoea/abdominal pain
Dry cough
```
171
Recognise the signs of pneumonia on physical examination
```
Pyrexia
Respiratory distress
Tachypnoea
Tachycardia
Hypotension
Cyanosis
Decreased chest expansion
Dull to percuss over affected area
Increased tactile vocal fremitus over affected area
Bronchial breathing over affected area
Coarse crepitations on affected side
Chronic suppurative lung disease (empyema, abscess) --> clubbing
```
172
Identify appropriate investigations for pneumonia
```
Bloods
FBC - raised WCC
U&Es
LFT
Blood cultures
ABG
Blood Film - Mycoplasma causes red cell agglutination
```
CXR
Lobar or patchy shadowing
Pleural effusion
NOTE: Klebsiella often affects upper lobes
May detect complications (e.g. lung abscess)
Sputum/Pleural Fluid - MC&S
Urine - Pneumococcus and Legionella antigens
Atypical Viral Serology
Bronchoscopy and Bronchoalveolar Lavage - if Pneumocystis carinii pneumonia is suspected, or if pneumonia fails to resolve
173
Generate a management plan for pneumonia
Assess severity using the British Thoracic Society Guidelines
Start empirical antibiotics
Oral Amoxicillin (0 markers)
Oral or IV Amoxicillin + Erythromycin (1 marker)
IV Cefuroxime/Cefotaxime/Co-‐amoxiclav + Erythromycin (> 1 marker)
Add metronidazole if:
Aspiration
Lung
abscess
Empyema
Switch to appropriate antibiotic based on sensitivity
Supportive treatment
Oxygen
IV
fluids
CPAP, BiPAP or ITU care for respiratory failure
Surgical drainage may be needed for lung abscesses and empyema
Discharge planning
If two or more features of clinical instability are present (e.g. high temperature, tachycardia, tachypnoea, hypotension, low oxygen sats) there is a high risk of re-admission and mortality
Consider other causes if pneumonia is not resolving
Prevention
Pneumococcal vaccine
Haemophilus influenzae type B vaccine
These are only usually given to high risk groups (e.g. elderly, splenectomy)
174
Identify the possible complications of pneumonia
```
Pleural effusion
Empyema
Localised suppuration (e.g. abscess)
Symptoms of abscesses:
Swinging fever
Persistent pneumonia
Copious/foul-smelling sputum
Septic shock
ARDS
Acute renal failure
Extra complications of Mycoplasma pneumonia
Erythema multiforme
Myocarditis
Haemolytic anaemia
Meningoencephalitis
Transverse myelitis
Guilliain-Barre syndrome
```
175
Summarise the prognosis for patients with pneumonia
Most resolve within treatment within 1-3 weeks
Severe pneumonia has a high mortality
The CURB-65 score is used to assess the severity of pneumonia:
Confusion <8 AMTS
Urea > 7 mmol/L
Respiratory rate >30/min
Blood pressure: systolic < 90 mmHg or diastolic < 60 mmHg
Age > 65 years
176
Define rheumatic fever
Rheumatic fever is an inflammatory disease that can develop as a complication of inadequately treated strep throat or scarlet fever. Strep throat and scarlet fever are caused by an infection with streptococcus bacteria.
177
Explain the aetiology / risk factors for rheumatic fever
Rheumatic fever is most common in 5- to 15-year-old children, though it can develop in younger children and adults.
Family history. Some people carry a gene or genes that might make them more likely to develop rheumatic fever.
Type of strep bacteria. Certain strains of strep bacteria are more likely to contribute to rheumatic fever than are other strains.
Environmental factors. A greater risk of rheumatic fever is associated with overcrowding, poor sanitation and other conditions that can easily result in the rapid transmission or multiple exposures to strep bacteria.
178
Summarise the epidemiology of rheumatic fever
Rare in developed countries
179
Recognise the presenting symptoms of rheumatic fever
Fever
Painful and tender joints — most often in the knees, ankles, elbows and wrists
Pain in one joint that migrates to another joint
Red, hot or swollen joints
Small, painless bumps (nodules) beneath the skin
Chest pain
Heart murmur
Fatigue
Flat or slightly raised, painless rash with a ragged edge (erythema marginatum)
Jerky, uncontrollable body movements (Sydenham chorea, or St. Vitus' dance) — most often in the hands, feet and face
Outbursts of unusual behavior, such as crying or inappropriate laughing, that accompanies Sydenham chorea
180
Recognise the signs of rheumatic fever on physical examination
Valve stenosis. This narrowing of the valve decreases blood flow.
Valve regurgitation. This leak in the valve allows blood to flow in the wrong direction.
Damage to heart muscle. The inflammation associated with rheumatic fever can weaken the heart muscle, affecting its ability to pump.
An irregular and chaotic beating of the upper chambers of the heart (atrial fibrillation)
An inability of the heart to pump enough blood to the body (heart failure)
181
Identify appropriate investigations for rheumatic fever and interpret the results
Major signs and symptoms are strongly associated with ARF and include carditis (swelling of the heart), arthritis (pain, redness and swelling of one or more joints), Sydenham’s chorea (strange movements of the body and face), erythema marginatum (painless skin pigmentation), and subcutaneous nodules (small lumps under the skin). Minor signs and symptoms are used to help support the diagnosis. These include fever, arthralgia (generalised joint aches), blood tests that suggest general illness, and changes seen on heart electrocardiogram.
A combination of these signs and symptoms, plus a positive test for recent group A streptococcus infection is required to confirm ARF diagnosis.
182
Define infective arthritis
• Joint inflammation resulting from intra-articular infection. Also known as SEPTIC ARTHRITIS.
183
Explain the aetiology/risk factors of infective arthritis
```
• May be idiopathic
• In most cases there is systemic infection allowing for haematogenous spread
• Risk Factors
o Recent orthopaedic procedures
o Osteomyelitis
o Diabetes
o Immunosuppression
o Alcoholism
• Common causative organisms:
o Bacteria
• All ages
Staphylococcus aureus
TB
• < 4 yrs
Streptococcus pneumoniae
Streptococcus pyogenes
Neisseria meningitidis
Gram-negative rods
• 16-40 yrs
Neisseria gonorrhoeae
o Viruses
• Rubella
• Mumps
• Hepatitis B
• Parvovirus B19
o Fungi
• Candida
```
184
Summarise the epidemiology of infective arthritis
• Most common in CHILDREN and the ELDERLY
185
Recognise the presenting symptoms of infective arthritis
• Fever
• Excruciating joint pain
• Joint redness, swelling and loss of joint function
• Usually a monoarthropathy (usually affecting one large joint)
o NOTE: it may cause a polyarthropathy in the immunosuppressed
• Tuberculous arthritis develops more slowly and is more chronic
186
Recognise the signs of infective arthritis on physical examination
* Painful, hot, swollen
* Immobile joint
* Erythema
* Severe pain prevents passive movement
* Pyrexia
* Look for signs of aetiology
187
Identify appropriate investigations for septic arthritis
• Joint Aspiration (IMPORTANT)
o In infective arthritis, the aspirate will be grossly purulent
o Send synovial fluid for MC&S
• Microscopy - rule out crystal arthritis
o PCR may be used if a viral cause is suspected
• Bloods
o FBC - high WCC, high neutrophils
o High CRP and ESR
o Blood cultures - MC&S
o Viral serology may be useful
• Plain Joint Radiographs
o Affected joint may look normal initially
o Can show signs of damage following the infection
• MRI Scan
o Useful for detecting osteomyelitis
188
Define Sjogren's syndrome
• Characterised by inflammation and destruction of exocrine glands (usually salivary and lacrimal glands).
o NOTE: when associated with other autoimmune diseases, Sjogren's syndrome is termed secondary
189
Explain the aetiology/risk factors of Sjogren's syndrome
```
• UNKNOWN
• Genetic associations:
o HLA-B8
o HLA-DR3
• Associated autoimmune diseases:
o Rheumatoid arthritis
o Scleroderma
o SLE
o Polymyositis
o Organ-specific autoimmune diseases (e.g. PBC, autoimmune hepatitis, myasthenia gravis)
```
190
Recognise the presenting symptoms of Sjogren's syndrome
* Fatigue
* Fever
* Weight loss
* Depression
* Dry eyes (keratoconjunctivitis sicca) - they will be gritty and sore
* Dry mouth - leads to secondary dysphagia
* Dry upper airways - leads to a dry cough and recurrent sinusitis
* Dry skin or hair
* Dry vagina - may cause dyspareunia
* Reduced GI mucus secretions leads to reflux oesophagitis, gastritis and constipation
191
Recognise the signs of Sjogren's syndrome on physical examination
* Parotid or salivary gland enlargement
* Dry eyes
* Dry mouth or tongue
* Signs of associated conditions
192
Identify appropriate investigations for Sjogren's syndrome
```
• Bloods
o High ESR
o High amylase (if salivary glands involved)
• Autoantibodies
o Rheumatoid factor
o ANA
o Anti-ENA (extractable nuclear antigens)
• Schirmer's Test
```
o A strip of filter paper is placed under the eyelid
o Positive for Sjogren's syndrome if < 10 mm of the strip is wet after 5 mins
• Fluorescein/Rose Bengal Stains
o May show punctate or filamentary keratitis
• Other Investigations
o Reduced parotid salivary flow rate
o Reduced uptake or clearance on isotope scan
• Biopsy - of salivary or labial glands
193
Define SLE
• Multi-system inflammatory autoimmune disorder
• 4/11 of the diagnostic criteria of the American College of Rheumatology provides high sensitivity and specificity for the diagnosis of SLE: SOAP BRAIN MD
o Serositis
o Oral ulcers
o Arthritis (non-erosive)
o Photosensitivity
o Bloods (haemolytic anaemia/leukopaenia/thrombocytopaenia)
o Renal disease (urine casts/proteinuria)
o ANA
o Immunological disorder (anti-dsDNA/anti-Sm/anti-phospholipid)
o Neurological disease (psychosis/seizures)
o Malar rash
o Discoid rash
194
Explain the aetiology/risk factors of SLE
* UNKNOWN
* Tissue damage may be caused by vascular immune complex deposition
* Could be due to a combination of hormonal, genetic and exogenous factors
195
Summarise the epidemiology of SLE
* COMMON
* 1-2/1000
* More common in the YOUNG
* More common in AFRO-CARIBBEAN and CHINESE
* 9 x more common in FEMALES
196
Recognise the presenting symptoms and signs of SLE
```
• General Symptoms
o Fever
o Fatigue
o Weight loss
o Lymphadenopathy
o Splenomegaly
• Raynaud's phenomenon
• Oral ulcers
• Skin Rash
o Malar rash
o Discoid lupus (red scaly patches)
o Atypical rashes (e.g. photosensitivity, vasculitis, urticaria, purpura)
```
• Systemic Involvement
o Musculoskeletal - arthritis, tendonitis, myopathy
o Heart - pericarditis, myocarditis, arrhythmias, Libman-Sacks endocarditis
o Lung - pleurisy, pleural effusion, basal atelectasis, restrictive lung defects
o Neurological - headache, stroke, cranial nerve palsies, confusion, chorea
o Psychiatric - depression, psychosis
o Renal - glomerulonephritis
197
Identify appropriate investigations for SLE
```
• Bloods
o FBC
o U&E
o LFT
o Raised ESR
o Normal CRP
o Clotting
o Complement
• Autoantibodies
o Anti-dsDNA (60%)
o Rheumatoid factor (30-50%)
o Anti-ENA
o Anti-RNP
o Anti-SM
o Anti-Ro
o Anti-La
o Anti-histone
o Anti-cardiolipin
• Urine - haematuria, proteinuria, red cell casts
• Joints - plain radiographs
• Heart and Lungs - CXR, ECG, echocardiogram, CT
• Kidneys - renal biopsy (if glomerulonephritis suspected)
• CNS - MRI scan, lumbar puncture
```
198
Define systemic sclerosis
```
• Rare connective tissue disease characterised by widespread small blood vessel damage and fibrosis in skin and internal organs
• Also known as scleroderma
• It is a spectrum of diseases:
o Pre-Scleroderma
• Raynaud's phenomenon
• Nail-fold capillary changes
• Antinuclear antibodies
o Diffuse Cutaneous Systemic Sclerosis (40%)
• Raynaud's phenomenon
• Followed by skin changes with truncal involvement
• Tendon friction
• Joint contracture
• Early lung disease
• Heart, GI and renal disease
• Nail-fold capillary dilatation
o Limited Cutaneous Systemic Sclerosis (60%)
• Previously known as CREST Syndrome because of its FIVE characteristic features:
Calcinosis
Raynaud's phenomenon
(O)esophageal dysmotility
Sclerodactyly
Telangiectasia
o Scleroderma sine Scleroderma
• Internal organ disease with NO skin changes
```
199
Explain the aetiology/risk factors of systemic sclerosis
• UNKNOWN
• Genetic and environmental factors
• Pathogenesis is unclear
• Activated monocytes, macrophages and lymphocytes may interact with:
o Endothelial cells --> endothelial cell damage, platelet activation, narrowing of blood vessels
o Fibroblasts --> lay down collagen in the dermis
200
Summarise the epidemiology of systemic sclerosis
* Age of onset: 30-60 yrs
| * 3 x more common in FEMALES
201
Recognise the presenting symptoms and signs of systemic sclerosis
* Skin - Raynaud's phenomenon
* Hands
o Initially swollen painful fingers
o Later, they become thickened, tight, shiny and bound to underlying structures
o Changes in pigmentation
o Finger ulcers
• Face
o Microstomia (puckering of the skin around the mouth)
o Telangiectasia
• Lung - pulmonary fibrosis ---> pulmonary hypertension
• Heart - pericarditis or pericardial effusion, myocardial fibrosis, heart failure, arrhythmias
• GI - dry mouth, oesophageal dysmotility, reflux oesophagitis, gastric paresis
• Kidneys - hypertensive renal crisis, chronic renal failure
• Neuromuscular - trigeminal neuralgia, muscular wasting, weakness
• Others - hypothyroidism, impotence
202
Identify appropriate investigations for systemic sclerosis
• Autoantibodies
o Antinuclear
o Anti-centromere (70% of limited cutaneous systemic sclerosis cases)
o Anti-topoisomerase II (anti-Scl-70) - 30% of diffuse cutaneous systemic sclerosis cases
o Anti-nucleolar
o Anti-RNA polymerase
• Lungs - CXR, pulmonary function tests, CT scan
• Heart - ECG, echocardiography
• GI - endoscopy, barium studies
• Kidneys - U&Es, creatinine clearance
• Neuromuscular - electromyography, biopsy
• Joints - radiography
• Skin - biopsy (rarely needed)
203
Define thyroiditis
• Inflammation of the thyroid gland.
204
Explain the aetiology/risk factors of thyroiditis
• Hashimoto's thyroiditis - an autoimmune condition. The most common cause of hypothyroidism in the UK.
• Other types of thyroiditis:
o de Quervain's thyroiditis
o Postpartum thyroiditis
o Drug-induced thyroiditis
o Acute or infectious thyroiditis
o Riedel's thyroiditis
• Pathogenesis of Hashimoto's thyroiditis
o Aggressive destruction of thyroid cells by the immune system
o Environmental triggers have been hypothesised (e.g. smoking, infection)
205
Summarise the epidemiology of thyroiditis
* True incidence is UNKNOWN
* 15-20 x more common in WOMEN
* Usually occurs in 30-50 yrs
206
Recognise the presenting symptoms and signs of thyroiditis
```
• Symptoms of hypothyroidism
o Fatigue
o Constipation
o Dry skin
o Weight gain
o Cold intolerance
o Menstrual irregularities
o Depression
o Hair loss
• Symptoms caused by rapid enlargement of the thyroid gland
o Dyspnoea
o Dysphagia
o Tenderness
```
207
Identify appropriate investigations for thyroiditis
```
• Based on clinical observations
• Histology: diffuse lymphocytic and plasma cell infiltration with formation of lymphoid follicles
• TSH - raised
• Antibodies:
o Anti-TPO antibodies
o Anti-thyroglobulin antibodies
• Thyroid ultrasound
• Radionuclide isotope scanning
```
208
Generate a management plan for thyroiditis
• Pharmacological
o Thyroid hormone replacement - oral levothyroxine sodium
o Titrate dose based on patient's needs
• Surgical
o Considered if there is a large goitre that is causing symptoms due to compression of surrounding structures or if there is a malignant nodule
209
Identify possible complications of thyroiditis
* Thyroid hormone over-replacement --> bone loss + tachycardia
* Hyperlipidaemia
* Hashimoto's encephalopathy
* Myxoedema coma
210
Summarise the prognosis for patients with thyroiditis
• GOOD PROGNOSIS with early diagnosis and levothyroxine replacement
211
Define tonsillitis
• Inflammation due to infection of the tonsils.
212
Explain the aetiology/risk factors of tonsillitis
• Usually VIRAL (e.g. common cold or influenza)
• Can be bacterial (caused by group A streptococci)
• Risk Factors
o Immune deficiency
o Family history of tonsillitis or atopy
213
Summarise the epidemiology of tonsillitis
* VERY COMMON
| * Usually in children and young adults
214
Recognise the presenting symptoms of tonsillitis
* Pain in the throat
* Painful swallowing
* Pain may be referred to ears
* Abdominal pain (in small children)
* Headache
* Loss of voice or changes in voice
215
Recognise the signs of tonsillitis on physical examination
• Red throat
• Swollen tonsils, which may have white flecks of pus
• High temperature (sometimes)
• Swollen lymph nodes
• Classic streptococcal tonsilitis features:
o Acute onset
o Headache
o Abdominal pain
o Dysphagia
• Examination:
o Intense erythema of tonsils and pharynx
o Yellow exudate
o Tender, enlarged anterior cervical glands
216
Identify appropriate investigations for tonsillitis
* Throat swabs and rapid antigen tests can be performed (but are NOT recommended)
* Swabs may not be able to distinguish between infection and colonisation
217
Define Tuberculosis
Granulomatous disease caused by Mycobacterium tuberculosis
Primary TB: initial infection may be pulmonary or more rarely gastro
Miliary TB: results from haematogenous dissemination of TB
Post-Primary TB: caused by reinfection or reactivation
218
Explain the aetiology/risk factors of tuberculosis
Mycobacterium tuberculosis is an intracellular organism
| It survives after being phagocytosed by macrophages
219
Summarise the epidemiology of tuberculosis
Annual mortality = 3 million (95% in developing countries)
Annual UK incidence = 6000
Asian immigratns are the highest risk group in the UK
220
Recognise the symptoms and signs of tuberculosis
```
Primary TB:
Mostly Asymptomatic
Fever
Malaise
Cough
Wheeze
Erythema Nodosum
Phlyctenular conjuctivits
```
```
Miliary TB:
Fever
Weight loss
Meningitis
Yellow caseous tubercles spread to other organs
```
```
Post-primary TB
Fever/night sweats
Malaise
Weight loss
Breathlessness
Cough
Sputum
Haemoptysis
Pleuritic chest pain
Signs of pleural effusion
Collapse
Consolidation
Fibrosis
```
Non-pulmonary TB - occurs mainly in the immunocompromised
Lymph nodes - suppuration of cervical lymph nodes leading to abscesses or sinuses
CNS - meningitis, tuberculoma
Skin - lupus vulgaris (jelllylike reddish-brown glistening plaques)
Heart - pericardial effusion, constrictive pericarditis
```
GI
Subacute obstruction
Change in bowel habit
Weight loss
Peritonitis
Ascites
```
```
Genitourinary
UTI symptoms
Renal failure
Epididymitis
Endometrial or tubal involvement
Infertility
```
Adrenal insufficiency
Bone/Joint - osteomyelitis, arthiritis, vertebral collapse (Pott's disease), spinal cord compression from an abscess
221
Identify appropriate investigations from tuberculosis
Sputum/Pleural Fluid/Bronchial Washings -MC&S
Note: culturing TB takes a long time (around 6 weeks)
Tuberculin Tests
Positive if the patient has had previous exposure to M.tuberculosis or BCG
Mantoux Test
A purified protein derivative is injected intradermally
Erythema occurs after 72 hours
```
Heaf Test
Place a drop of PPD on the forearm
Fire a spring-loaded needle gun
Check again after 3-7 days
Graded according to papula size and vesiculation
```
Interferon Gamma Tests
Useful in latent TB
Exposure of host T cells to TB antigens leads to release of interferon
CXR
Primary Infection - Peripheral consolidation & Hilar lymphadenopathy
Miliary Infection - Fine shadowing
Post-Primary - Upper lobe shadowing, Streaky fibrosis and cavitation, Calcification, Pleural effusion, Hilar lymphadenopathy
HIV Testing
CT, lymph nodes, pleural biopsy, sampling of other affected systems
222
Define urinary tract infection
• The presence of a pure growth of > 105 organisms per mL of fresh MSU
• Sub-Classification
o Lower UTI - affecting the urethra (urethritis), bladder (cystitis) or prostate (prostatitis)
o Upper UTI - affecting the renal pelvis (pyelonephritis)
• NOTE: the laboratory classification mentioned above isn't a complete necessity for the diagnosis of UTI - 1/3 women with symptoms of UTI will have negative MSU
• Other Classification
o Uncomplicated UTI - normal renal tract and function
o Complicated UTI - abnormal renal/genitourinary tract, voiding difficulty/obstruction, reduced renal function, impaired host defences, virulent organism (e.g. S. aureus)
223
Explain the aetiology/risk factors of urinary tract infection
```
• MOST UTIs are caused by Escherichia coli
• Other causative organisms:
o Staphylococcus saprophyticus
o Proteus mirabilis
o Enterococci
• Atypical organisms that can cause UTI (usually in immunocompromised individuals):
o Klebsiella
o Candida albicans
o Pseudomonas aeruginosa
• Risk Factors
o FEMALE
o Sexual intercourse
o Exposure to spermicide
o Pregnancy
o Menopause
o Immunosuppression
o Catheterisation
o Urinary tract obstruction
o Urinary tract malformation
```
224
Summarise the epidemiology of urinary tract infections
* VERY COMMON
* 1-3% of GP consultations
* The majority of women will have a UTI in their lifetime
* MUCH more common in FEMALES
225
Recognise the presenting symptoms of urinary tract infections
```
• Cystitis
o Frequency
o Urgency
o Dysuria
o Haematuria
o Suprapubic pain
• Prostatitis
o Flu-like symptoms
o Low backache
o Few urinary symptoms
o Swollen or tender prostate on PR
• Acute Pyelonephritis
o High fever
o Rigors
o Vomiting
o Loin pain and tenderness
o Oliguria (if AKI)
```
226
Recognise the signs of urinary tract infection on physical examination
* Fever
* Abdominal or loin tenderness
* Foul-smelling urine
* Distended bladder (occasionally)
* Enlarged prostate (if prostatitis)
227
Identify appropriate investigations for urinary tract infection
• Urine Dipstick
o Positive leucocyte esterase and nitrites
• Urine Microscopy
o Presence of leucocytes indicates infection
• Urine Culture
o To exclude diagnosis or if the patient failed to respond to empirical antibiotics
• Ultrasound
o Rule out obstruction
• Bloods
o FBC
o U&Es - check renal function
o CRP
o Blood cultures - if systemically unwell and risk of urosepsis
228
Generate a management plan for urinary tract infection
• Empirical treatment of uncomplicated UTI: TRIMETHOPRIN or NITROFURANTOIN
o Treat for 3-6 days
o NOTE: men with UTI may need a longer course of antibiotics
• Alternative Treatments: Co-amoxiclav or Cefalexin
• Prophylactic antibiotics may be used in certain circumstances (e.g. recurrent cystitis associated with sexual intercourse)
229
Identify possible complications of urinary tract infection
```
• Ascending infection can lead to:
o Pyelonephritis
o Perinephric and intrarenal abscess
o Hydronephrosis or pyonephrosis
o AKI
o Sepsis
• Prostatic involvement (e.g. prostatitis) in men with UTIs is common
```
230
Summarise the prognosis for urinary tract infection
• GOOD prognosis with appropriate treatment
231
Define urticaria
• Itchy, red, blotchy rash resulting from swelling of the superficial part of the skin. Angiooedema occurs when the deep tissues, the lower dermis and subcutaneous tissues are involved and become swollen.
o AKA hives
232
Explain the aetiology/risk factors of urticaria
• Caused by activation of mast cells in the skin, resulting in the release of histamines
• The cytokine release leads to capillary leakage, which causes swelling of the skin and vasodilation --> erythematous appearance
• Possible Triggers:
o ACUTE urticaria
• Allergies (foods, bites, stings)
• Viral infections
• Skin contact with chemicals
• Physical stimuli
o CHRONIC urticaria
• Chronic spontaneous urticaria - medication, stress, infections
• Autoimmune
233
Summarise the epidemiology of urticaria
* 15% of general population experience urticaria at some point in life
* Acute is much more common than chronic urticaria
234
Recognise the presenting symptoms and signs of urticaria
• Central itchy white papule or plaque surrounded by erythematous flare
• Lesions vary in size and shape
• May be associated with swelling of the soft-tissues of the eyelids, lips and tongue (angiooedema)
• Individual lesions are usually transient
• Timescales:
o Acute - symptoms develop quickly but normally resolve within 48 hrs
o Chronic - rash persists for > 6 weeks
235
Identify appropriate investigations for urticaria
* Usually clinical
| * Tests may be required for chronic urticaria (e.g. FBC, ESR/CRP, patch testing, IgE tests)
236
Define varicella zoster
• Primary infection is called varicella (chickenpox). Reactivation of the dormant virus (found in dorsal root ganglia), causes zoster (shingles).
o NOTE: varicella zoster is also known as herpes zoster
237
Explain the aetiology/risk factors of varicella zoster
* VZV is a herpes ds-DNA virus
* Highly contagious
* Transmission by aerosol inhalation or direct contact with vesicular secretions
238
Summarise the epidemiology of varicella zoster
* Chicken pox peak incidence: 4-10 yrs
* Shingles peak incidence: > 50 yrs
* 90% of adults are VZV IgG positive
239
Recognise the presenting symptoms of varicella zoster
• Chickenpox
o Prodromal malaise
o Mild pyrexia
o Sudden appearance of intensely itchy spreading rash mainly affecting face and trunk
o Vesicles weep and crust over
o New vesicles appear
o Contagious from 48 hrs before the rash until after the vesicles have all crusted over (7-10 days)
• Shingles
o May occur after a period of stress
o Tingling/hyperaesthesia in a dermatomal distribution
• Dermatomal because the rash remains dormant in the dorsal root ganglia and reactivation makes the virus travel down the sensory axon to produce a dermatomal shingles rash
o Painful skin lesions
o Recovery: 10-14 days
240
Recognise the signs of varicella zoster on physical examination
```
• Chickenpox
o Maculopapular rash
o Areas of weeping and crusting
o Skin excoriation (from scratching)
o Mild pyrexia
• Shingles
o Vesicular maculopapular rash
o Dermatomal distribution
o Skin excoriation
```
241
Identify appropriate investigations for varicella zoster
* Usually CLINICAL diagnoses
* Vesicle fluid may be sent for electron microscopy viral PCR (RARELY necessary)
* Chicken pox in an adult with previous history of varicella infection may require HIV testing
242
Generate a management plan for varicella zoster
```
• Chickenpox
o Children - treat symptoms
o Adults - consider aciclovir
• Shingles
o Aciclovir, valaciclovir, famciclovir
• Prevention
o Varicella Zoster Ig (VZIG) - may be considered in immunosuppressed or pregnant
```
243
Identify possible complications of varicella zoster
```
• Chickenpox
o Secondary infection
o Scarring
o Pneumonia
o Encephalitis
o Congenital varicella syndrome
• Shingles
o Postherpetic neuralgia
o Zoster ophthalmicus (rash in the ophthalmic division of the trigeminal nerve)
```
o Ramsay-Hunt syndrome
• DEFINITION: reactivation of VZV in the geniculate ganglion causing zoster of the ear and facial nerve palsy. Vesicles may be seen behind the pinna of the ear or in the ear canal
o Sacral zoster
o Motor zoster
244
Summarise the prognosis for patients with varicella zoster
* Depends on complications
| * Worse in pregnancy, elderly and immunocompromised
245
Define vasculitis
```
• Vasculitis is the inflammation and necrosis of blood vessels.
o Primary vasculitides are classified based on the MAIN VESSEL SIZE affected:
• LARGE
Giant cell arteritis
Takayasu's aortitis
• MEDIUM
Polyarteritis nodosa
Kawasaki's disease
• SMALL
Churg-Strauss syndrome
Microscopic polyangiitis
Wegner's granulomatosis
Henoch-Schonlein purpura
Mixed essential cryoglobulinaemia (MEC)
Relapsing polychondritis
```
246
Explain the aetiology/risk factors of vasculitides
• UNKNOWN
• Suggested autoimmune origin
• Immune complex deposition in the walls of blood vessels leads to inflammation
• Risk Factors
o Hepatitis B - polyarteritis nodosa
o Hepatitis C - mixed essential cryoglobulinaemia
o pANCA - microscopic polyangiitis + Churg-Strauss
o c-ANCA - Wegner's granulomatosis
247
Summarise the epidemiology of vasculitides
* RARE
| * Takayasu's arteritis is most common in JAPANESE FEMALES
248
Recognise the presenting symptoms and signs of vasculitides
Large vessel vasculitides have classic clinical patterns based on the vessels affected (e.g. GCA and loss of vision/headache)
Medium and small vessel vasculitides are characterised by multiorgan involvement and have less specific clinical features
• Possible Features of ALL Vasculitides
o General: fever, malaise, night sweats, weight loss
o Skin: rash
o Joint: arthralgia, arthritis
o GI: abdominal pain, haemorrhage, diarrhoea
o Kidneys: glomerulonephritis, renal failure
o Lungs: dyspnoea, cough ,chest pain, haemoptysis, haemorrhage
o CVS: pericarditis, coronary arteritis, myocarditis
o CNS: mononeuritis multiplex, infarctions
o Eyes: retinal haemorrhage, cotton wool spots
• Features Characteristics of Specific Vasculitides
o GCA: loss of vision, jaw claudication, headache, scalp tenderness
o Polyarteritis Nodosa: microaneurysms, thrombosis, infarctions, hypertension, testicular pain
o Henoch-Schonlein Purpura: purpura, arthritis, gut symptoms, glomerulonephritis, IgA deposition
o Wegner's Granulomatosis: granulomatous vasculitis of upper and lower respiratory tract, nasal discharge, ulceration and deformity, haemoptysis, sinusitis, glomerulonephritis, saddle nose
249
Identify appropriate investigations for vasculitides
• Bloods
o FBC - normocytic anaemia, high platelets, high neutrophils
o High ESR/CRP
• Autoantibodies - e.g. cANCA in Wegner's
• Urine - haematuria, proteinuria, red cell casts (if glomerulonephritis)
• CXR - diffuse, nodular or flitting shadows, atelectasis
• Biopsy - renal, lung, temporal artery (in GCA)
• Angiography - to identify aneurysms (in PAN)
250
Define viral hepatitis A and E
• Hepatitis caused by infection with the RNA viruses, hepatitis A or hepatitis E virus, that follow an acute course without progression to chronic carriage
251
Explain the aetiology/risk factors of viral hepatitis A and E
• HAV = picornavirus
• HEV = calicivirus
• Transmission = faecal-oral route
• Both viruses replicate within hepatocytes and are secreted into bile
• Liver inflammation and hepatocyte necrosis is caused by the immune response
• Infected cells are targeted by CD8+ T cells and NK cells
• Histological features:
o Inflammatory cell infiltration of portal tracts
o Zone 3 necrosis
o Bile duct proliferation
252
Summarise the epidemiology of viral hepatitis A and E
* HAV is endemic in the developing world
* Infection often occurs sub-clinically
* Better sanitation in the developed world means that it is less common, age of exposure is higher and, hence, patients are more likely to be symptomatic
* HEV is endemic in Asia, Africa and Central America
253
Recognise the presenting symptoms of viral hepatitis A and E
```
• Incubation period of HAV and HEV: 3-6 weeks
• Prodromal period symptoms:
o Malaise
o Anorexia
o Fever
o Nausea and vomiting
• Hepatitis symptoms:
o Dark urine
o Pale stools
o Jaundice lasting around 3 weeks
o Occasionally, itching and jaundice may last several weeks in HAV infection
```
254
Recognise the signs of viral hepatitis A and E on physical examination
* Pyrexia
* Jaundice
* Tender hepatomegaly
* Spleen may be palpable
* ABSENCE of stigmata of chronic liver disease (although some spider naevi may appear transiently)
255
Identify appropriate investigations for viral hepatitis A and E
• Bloods
o LFTs - high AST, ALT, ALP and bilirubin
o High ESR
o Low albumin + high platelets (if severe)
• Vital Serology
o Hepatitis A:
• Anti-HAV IgM (during acute illness, disappears after 3-5 months)
• Anti- HAV IgG (recovery phase and lifelong persistence)
o Hepatitis E:
• Anti-HEV IgM (raised 1-4 weeks after onset)
• Anti-HEV IgG
• Urinalysis
o Positive for bilirubin
o Raised urobilinogen
256
Generate a management plan for viral hepatitis A and E
• There is no specific management other than bed rest and symptomatic treatment (e.g. antipyretics, antiemetics or cholestyramine (for severe pruritus))
• Prevention and Control
o Public Health - safe water, sanitation and food hygiene
o These are notifiable diseases
o Immunisation is available for HAV
• Passive immunisation with IM human immunoglobulin (effective for a short time)
• Active immunisation with attenuated HAV vaccine offers safe and effective immunity for those travelling to endemic areas and high-risk individuals
257
Identify the possible complications of viral hepatitis A and E
* Fulminant hepatic failure (in a very small proportion of patients but is more common in pregnant women)
* Cholestatic hepatitis with prolonged jaundice and pruritus can develop after HAV infection
* Post-hepatitis syndrome: continued malaise for weeks to months
258
Summarise the prognosis for patients with viral hepatitis A and E
* Recovery is usually within 3-6 weeks
* Occasionally patients may relapse during recovery
* There is no chronic sequelae
* Fulminant hepatic failure has a mortality of 80%
259
Define viral hepatitis B and D
• Hepatitis caused by infection with hepatitis B virus (HBV), which may follow an acute or chronic course
o Chronic is defined as viraemia and hepatic inflammation continuing for > 6 months
• Hepatitis D virus (HDV) is a defective virus, that may only co-infect with HBV or superinfect people who are already carriers of HBV
260
Explain the aetiology/risk factors for viral hepatitis B and D
• HBV is an enveloped, partially double-stranded DNA virus
• Transmission: sexual contact, blood and vertical transmission (from mother to baby)
• Various viral proteins are produced such as:
o Core antigen (HBcAg)
o Surface antigen (HBsAg)
o e antigen (HBeAg)
• This is a marker of high infectivity
• HDV is a single-stranded RNA virus coated with HBsAg
• Antibody and cell-mediated immune response to viral replication leads to liver inflammation and hepatocyte necrosis
• Histology can show mild to severe inflammation and changes to cirrhosis
• Risk Factors
o IV drug use
o Unscreened blood and blood products
o Infants of HBeAg-positive mothers
o Sexual contact with HBV carriers
o Younger individuals (particularly babies) are more likely to become chronic carriers
o Genetic factors are associated with varying rates of viral clearance
261
Summarise the epidemiology of viral hepatitis B and D
* Common
* 1-2 million deaths annually
* Common in Southeast Asia, Africa and Mediterranean countries
* HDV is also found worldwide
262
Recognise the presenting symptoms of viral hepatitis B and D
```
• Incubation period: 3-6 months
• 1-2 week prodrome consisting of:
o Malaise
o Headache
o Anorexia
o Nausea and vomiting
o Diarrhoea
o RUQ pain
o Serum-sickness type illness (e.g. fever, arthralgia, polyarthritis, urticaria, maculopapular rash)
• Jaundice develops with dark urine
• Recovery: 4-8 weeks
• 1% develop fulminant liver failure
• Chronic carriage may be diagnosed after routine LFT testing or if cirrhosis or decompensation develops
```
263
Recognise the signs of viral hepatitis B and D on physical examination
• Acute
o Jaundice
o Pyrexia
o Tender hepatomegaly
o Splenomegaly
o Cervical lymphadneopathy (in 10-20% of patients)
o Occasionally: urticaria and maculopapular rash
• Chronic
o May be no findings
o May have signs of chronic liver disease or decompensation
264
Identify appropriate investigations for viral hepatitis B and D
```
• Viral Serology
o Acute HBV:
• HBsAg positive
• IgM anti-HBcAg
o Chronic HBV:
• HBsAg positive
• IgG anti-HBcAg
• HBeAg positive or negative
o HBV Cleared or Vaccinated against HBV:
• Anti-HBsAg antibody positive
• IgG anti-HBcAg
o HDV infection:
• Detected by IgM or IgG against HDV
• PCR is used for detection of HDV
• LFTs
o High: AST, ALT, ALP, bilirubin
• Clotting
o High PT (in severe disease)
• Liver Biopsy
```
265
Generate a management plan for viral hepatitis B and D
• Prevention: blood screening, safe sex, instrument sterilisation
• Passive immunisation
o Hepatitis B immunoglobulin following acute exposure and to neonates born to HBeAg-positive mothers (in addition to active immunisation)
• Active immunisation
o Recombinant HBsAg vaccine for individuals at risk and neonates born to HB
• Acute HBV Hepatitis
o Symptomatic treatment (antipyretics, antiemetics and cholestyramine) and bed rest
o Notifiable disease
• Chronic HBV
o Interferon alpha (standard or pegylated)
• Side-effects: flu-like symptoms such as fever, chills, myalgia, headaches, bone marrow suppression and depression
o Nucleoside/nucleotide analogues (adefovir, entecavir, telbivudine, tenofovir)
266
Identify the possible complications of viral hepatitis B and D
* 1% get fulminant hepatic failure
* Chronic HBV infection (10% of adults, much higher in neonates)
* Cirrhosis
* HCC
* Extrahepatic immune complex disorders (e.g. glomerulonephritis, polyarteritis nodosa)
* Superinfection with HDV may lead to acute liver failure or more rapidly progressive disease
267
Summarise the prognosis of patients with viral hepatitis B and D
* Adults: 10% of infections become chronic
| * Of the chronic infections, 20-30% will develop cirrhosis
268
Define viral hepatitis C
• Hepatitis caused by infection with hepatitis C virus (HCV), often following a chronic course (in 80% of cases)
269
Explain the aetiology/risk factors of viral hepatitis C
• HCV is a small, enveloped, single-stranded RNA virus
• RNA viruses have poor fidelity of replication and mutation rates are high
• So, there are lots of HCV genotypes (which can co-exist in a single patient)
• Transmission: PARENTERAL
o Sexual transmission
o Vertical transmission
• At risk patients:
o Recipients of blood and blood products
o IV drug users
o Non-sterile acupuncture
o Tattooing
o Haemodialysis
o Health care workers
• Pathology/Pathogenesis of HCV
o The virus is not thought to be directly hepatotoxic
o It is the humoral and cell-mediated responses to the viral infection that leads to hepatic inflammation and necrosis
o Liver biopsy shows:
• Chronic hepatitis
• Lymphoid follicles in portal tracts
• Fatty change
• Cirrhosis may be present
270
Summarise the epidemiology of viral hepatitis C
* COMMON
| * Different genotypes of HCV have different geographical prevalence
271
Recognise the presenting symptoms of viral hepatitis C
* 90% of acute infections are ASYMPTOMATIC
* 10% become jaundiced with mild flu-like illness
* May be diagnosed after incidental abnormal LFT
272
Recognise the signs of viral hepatitis C on physical examination
• May be NO SIGNS
• There may be signs of chronic liver disease (if long-standing HCV infection)
• Extra-hepatic manifestations (rare) include:
o Skin rash
o Renal dysfunction (due to glomerulonephritis)
273
Identify appropriate investigations for viral hepatitis C
• Bloods
o HCV Serology
• Anti-HCV antibodies - IgM (acute) or IgG (past exposure or chronic)
o Reverse-transcriptase PCR
• Allows detection and genotyping of HCV
o LFT
• Acute infection: High ALT, AST and bilirubin
• Chronic infection: 2-8 x elevation of AST + ALT (often fluctuates over time)
• Liver Biopsy
o Assess the degree of inflammation and liver damage
o NOTE: transaminase (AST and ALT) levels bear little correlation to histological changes
o Useful for diagnosing cirrhosis
274
Generate a management plan for viral hepatitis C
• Prevention
o Screen blood, blood products and organ donors
o Needle exchange schemes for IV drug users
o Instrument sterilisation
o NO VACCINE AVAILABLE
• Medical
o Acute - mainly supportive (antipyretics, antiemetics, cholestyramine)
o Chronic
• Pegylated interferon-
• Ribavirin (guanosine nucleotide analogue)
• Duration:
HCV Genotype 1 or 4: 24-48 weeks
HCV Genotype 2 or 3: 12-24 weeks
o Regular US of the liver may be needed if the patient has cirrhosis
275
Identify the possible complications of viral hepatitis C
* Fulminant hepatic failure
* Chronic carriage of HCV
* Hepatocellular carcinoma
* Less common: porphyria cutanea tarda, cryoglobulinaemia, glomerulonephritis
276
Summarise the prognosis for patients with viral hepatitis C
* 80% of exposed will progress to chronic carriage
| * Of these, 20-30% will develop cirrhosis over 10-20 years
