Infection & Immunology Flashcards

Question 1

Q

Learning objectives

Question 2

Q

Define abscess

Answer

A

• A painful collection of pus, usually caused by bacterial infection.

Question 3

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Explain the aetiology/risk factors of abscesses

Answer

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

Question 4

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Summarise the epidemiology of abscesses

Answer

A

Skin abscesses are relatively common
IV drug use is a major risk factor for skin abscesses
Internal abscesses are less common

Question 5

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Recognise the presenting symptoms and signs of abscesses

Answer

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

Question 6

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Identify appropriate investigations for abscesses

Answer

A

• Ultrasound - can be useful in visualising an abscess

Question 7

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Generate a management plan for abscesses

Answer

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

Question 8

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Identify possible complications of abscesses

Answer

A

• Recurrence

Question 9

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Summarise the prognosis for patients with abscesses

Answer

A

• GOOD with treatment

Question 10

Q

Define anaphylaxis

Answer

A

Acute life-threatening multisystem syndrome caused by sudden release of mast cell and basophil-derived mediators into the circulation

Question 11

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Explain the aetiology / risk factors of anaphylaxis

Answer

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)

Question 12

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Summarise the epidemiology of anaphylaxis

Question 13

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Recognise the presenting symptoms of anaphylaxis

Answer

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)

Question 14

Q

Recognise the signs of anaphylaxis on physical examination

Answer

A

Tachypnoea 
Wheeze 
Cyanosis 
Swollen upper airways and eyes 
Rhinitis 
Conjunctival infection 
Urticarial rash 
Hypotension 
Tachycardia

Question 15

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Identify appropriate investigations for anaphylaxis and interpret the results

Answer

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

Question 16

Q

Generate a management plan for anaphylaxis

Answer

A

ABCDE
High flow oxygen 
IM Adrenaline 
Chlorpheniramine (antihistamine)
Hydrocortisone  
If continued respiratory deterioration, may require bronchodilator therapy 
Monitor pulse oximetry, ECG and BP

Question 17

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Identify the possible complications of anaphylaxis and its management

Answer

A

SHOCK

Organ damage can result from shock

Question 18

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Summarise the prognosis for patients with anaphylaxis

Answer

A

Good with prompt treatment

Question 19

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Define Behcet’s disease

Answer

A

• An inflammatory multisystem disease that often presents with orogenital ulceration and uveitis

Question 20

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Explain the aetiology/risk factors of Behcet’s disease

Answer

A

UNKNOWN cause

* Associated with HLA-B51

Question 21

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Summarise the epidemiology of Behcet’s disease

Answer

A

• More common in Turkey, Greece and Central Asia

Question 22

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Recognise the presenting symptoms and signs of Behcet’s disease

Answer

A

Recurrent ORAL and GENITAL ulceration
Uveitis
Skin lesions (e.g. erythema nodosum)
Arthritis
Thrombophlebitis
Vasculitis
Myo/pericarditis
CNS symptoms
Colitis

Question 23

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Identify appropriate investigations for Behcet’s disease

Answer

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

Question 24

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Define candidiasis

Answer

A

• Infection caused by Candida.

Question 25

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Explain the aetiology/risk factors of candidiasis

Answer

A

•	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

Question 26

Q

Summarise the epidemiology of candidiasis

Answer

A

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

Question 27

Q

Recognise the presenting symptoms and signs of candidiasis

Answer

A

• 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

Question 28

Q

Identify appropriate investigations for candidiasis

Answer

A

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

Question 29

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Define cellulitis

Answer

A

• 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.

Question 30

Q

Explain the aetiology/risk factors of cellulitis

Answer

A

•	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)

Question 31

Q

Summarise the epidemiology of cellulitis

Answer

A

• VERY COMMON

Question 32

Q

Recognise the presenting symptoms of cellulitis

Answer

A

History of cut, scratch or injury
Periorbital Cellulitis - painful swollen red skin around the eye

• Orbital Cellulitis - painful or limited eye movements, visual impairment

Question 33

Q

Recognise the signs of cellulitis on physical examination

Answer

A

•	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

Question 34

Q

Identify appropriate investigations for cellulitis

Answer

A

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)

Question 35

Q

Generate a management plan for cellulitis

Answer

A

• 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

Question 36

Q

Identify possible complications of cellulitis

Answer

A

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

Question 37

Q

Summarise the prognosis for patients with cellulitis

Answer

A

• Good prognosis

Question 38

Q

Define Conjuctivitis

Answer

A

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).

Question 39

Q

Explain the aetiology / risk factors of conjunctivitis

Answer

A

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

Question 40

Q

Summarise the epidemiology of conjunctivitis

Answer

A

Affects 2% annually. Viral is most common

Question 41

Q

Recognise the presenting symptoms of conjunctivitis

Answer

A

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

Question 42

Q

Recognise the signs of conjunctivitis on physical examination

Answer

A

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.

Question 43

Q

Identify appropriate investigations for conjunctivitis and interpret the results

Answer

A

Based on symptoms, microbial culture

Question 44

Q

Define encephalitis

Answer

A

• Inflammation of the brain parenchyma

Question 45

Q

Explain the aetiology / risk factors of encephalitis

Answer

A

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)

Question 46

Q

Summarise the epidemiology of encephalitis

Answer

A

• UK incidence: 7.4/100,000

Question 47

Q

Recognise the presenting symptoms of encephalitis

Answer

A

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

Question 48

Q

Recognise the signs of encephalitis on physical examination

Answer

A

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

Question 49

Q

Identify appropriate investigations for encephalitis and interpret the results

Answer

A

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)

Question 50

Q

Define epididymitis and orchitis

Answer

A

• Inflammation of the epididymis or testes
o 60% of epididymitis is associated with orchitis
o Most cases of orchitis are associated with epididymitis

Question 51

Q

Explain the aetiology/risk factors of epididymitis and orchitis

Answer

A

•	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)

Question 52

Q

Summarise the epidemiology of epididmytis and orchitis

Answer

A

COMMON
Affects all age groups
Most commonly: 20-30 yrs

Question 53

Q

Recognise the presenting symptoms of epididymitis and orchitis

Answer

A

Painful, swollen and tender testis or epididymis
NOTE: less acute onset than testicular torsion
Penile discharge
IMPORTANT: ask about sexual history

Question 54

Q

Recognise the signs of epididymitis and orchitis on physical examination

Answer

A

Swollen and tender epididymis or testis
Scrotum may be erythematous and oedematous
Pyrexia
Walking will be painful
Eliciting a cremasteric reflex may be painful

Question 55

Q

Identify appropriate investigations for epididymitis and orchitis

Answer

A

•	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

Question 56

Q

Generate a management plan for epididymitis and orchitis

Answer

A

•	Medical
o	Antibiotics 
•	Surgical
o	Exploration of testicles if testicular torsion cannot be excluded clinically 
o	Required if an abscess develops

Question 57

Q

Identify possible complications of epididymitis and orchitis

Answer

A

Pain
Abscess
Fournier’s gangrene (if the infection is left untreated and spreads)
Mumps orchitis could cause testicular atrophy and fertility issues

Question 58

Q

Summarise the prognosis for patients with epididymitis and orchitis

Answer

A

GOOD if treated

* May take up to 2 months for the swelling to resolve

Question 59

Q

Define gastroenteritis

Answer

A

• Acute inflammation of the lining of the GI tract, manifested by nausea, vomiting, diarrhoea and abdominal discomfort.

Question 60

Q

Explain the aetiology/risk factors of gastroenteritis

Answer

A

•	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

Question 61

Q

Summarise the epidemiology of gastroenteritis

Answer

A

COMMON

* Serious cause of morbidity and mortality in the developing world

Question 62

Q

Recognise the presenting symptoms of gastroenteritis

Answer

A

• 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

Question 63

Q

Recognise the signs of gastroenteritis on physical

Answer

A

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

Question 64

Q

Identify appropriate investigations for gastroenteritis

Answer

A

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

Answer 63

A

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

Answer 64

A

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

Answer 65

A

• Good prognosis because most cases are self-limiting

Answer 66

A

• Inflammation of the colon due to bacteria, parasites or viruses

Answer 67

A

•	Infection leads to inflammation of the colon
•	Risk Factors
o	Lack of sanitation 
o	Drinking contaminated water 
o	Antibiotic use

Answer 68

A

• Quite COMMON

Answer 69

A

Diarrhoea
Blood and mucus in the stools
Lower abdominal pain
Malaise
Low-grade fever

Answer 70

A

Diagnosis is largely CLINICAL

* Stool culture may be used to identify the causative organism

Answer 71

A

• Disease resulting from HSV1 or HSV2 infection

Answer 72

A

• 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

Answer 73

A

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

Answer 74

A

• 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

Answer 75

A

• 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)

Answer 76

A

Diagnosis is usually CLINICAL

* Vesicle fluid can be sampled and sent for electron microscopy, PCR

Answer 77

A

• Infection with the human immunodeficiency virus (HIV)

Answer 78

A

• 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

Answer 79

A

• Increasing in incidence in Africa and Asia

Answer 80

A

• 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

Answer 81

A

• 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

Answer 82

A

• Clinical syndrome caused by primary EBV infection

o AKA glandular fever

Answer 83

A

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

Answer 84

A

• COMMON
• TWO age peaks:
o 1-6 yrs
o 14-20 yrs

Answer 85

A

•	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

Answer 86

A

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)

Answer 87

A

• 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)

Answer 88

A

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)

Answer 89

A

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

Answer 90

A

Most make uncomplicated recovery (within 3 weeks)

* Immunodeficiency and death are VERY RARE

Answer 91

A

• Infection of intracardiac endocardial structures (mainly heart valves)

Answer 92

A

• 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)

Answer 93

A

• UK Incidence: 16-22/1 million per year

Answer 94

A

•	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

Answer 95

A

•	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

Answer 96

A

• 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

Answer 97

A

•	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

Answer 98

A

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

Answer 99

A

FATAL if untreated

* 15-30% mortality even WITH treatment

Answer 100

A

•	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

Answer 101

A

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

Answer 102

A

Endemic in the tropics

* 250 million people worldwide

Answer 103

A

•	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

Answer 104

A

Pyrexia
Anaemia (haemolytic)
Hepatosplenomegaly

Answer 105

A

• 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

Answer 106

A

Define breast abscess
•	Abscess formation in breast tissues.
o	TWO main forms:
•	Lactational 
•	Non-Lactational

Answer 107

A

•	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)

Answer 108

A

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

Answer 109

A

Breast discomfort
Painful swelling
Generally unwell and feverish
Non-lactational - tend to present with a history of previous infections with less pronounced systemic upset

Answer 110

A

• 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

Answer 111

A

Ultrasound

* MC&S of pus samples

Answer 112

A

• 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

Answer 113

A

Mammary fistula

* Overlying skin may (rarely) undergo necrosis

Answer 114

A

If untreated, a breast abscess may discharge onto the skin surface
Non-lactational breast abscesses tend to recur

Answer 115

A

• Inflammation of the leptomeningeal (pia and arachnoid mater) coverings of the brain, most commonly due to infection

Answer 116

A

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

Answer 117

A

• UK: 2500 notifications/yr

Answer 118

A

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

Answer 119

A

• 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

Answer 120

A

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

Answer 121

A

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

Answer 122

A

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)

Answer 123

A

Mortality rate from bacterial meningitis: 10-40% with meningococcal sepsis
Viral meningitis is self-limiting

Answer 124

A

• Acute inflammation and necrosis of cardiac muscle (myocardium)

Answer 125

A

Incidence is difficult to measure accurately
Coxsackie B virus is most common in Europe and USA
Chagas disease is most common in South America

Answer 126

A

•	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

Answer 127

A

•	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)

Answer 128

A

Signs of pericarditis

* Signs of complications (e.g. heart failure, arrhythmia)

Answer 129

A

•	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

Answer 130

A

Gangrene: tissue necrosis, either wet with superimposed infection, dry or gas gangrene
Necrotising Fasciitis: a life-threatening infection that spreads rapidly across fascial planes

Answer 131

A

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

Answer 132

A

Gangrene - relatively COMMON

* Necrotising fasciitis and gas gangrene - RARE

Answer 133

A

• 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)

Answer 134

A

• 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)

Answer 135

A

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

Answer 136

A

• 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

Answer 137

A

• 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

Answer 138

A

• Most common in patients with cytotoxic chemotherapy

Answer 139

A

•	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

Answer 140

A

FBC (check neutrophil level)
Blood cultures (check for sepsis)
Others - blood film, D-dimer (for DIC), U&Es, creatinine, LFTs

Answer 141

A

• 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

Answer 142

A

•	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

Answer 143

A

Mostly in YOUNG CHILDREN

* < 20% of cases are in adults

Answer 144

A

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

Answer 145

A

Localised erythema
Tenderness
Swelling
Warmth
Painful/limited movement of affected limb
Seropurulent discharge from an associated wound or ulcer

Answer 146

A

•	Bloods
o	FBC 
o	Blood culture 
o	ESR 
o	CRP 
•	Swabs of wound or discharge 
•	Radiographs
•	Radioisotope bone scan - shows areas of increased activity

Answer 147

A

• Inflammation of the pericardium

o It may be acute, subacute or chronic

Answer 148

A

UNCOMMON
< 1/100 hospital admissions
More common in males

Answer 149

A

•	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)

Answer 150

A

•	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

Answer 151

A

•	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

Answer 152

A

• 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

Answer 153

A

•	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

Answer 154

A

Pericardial effusion
Cardiac tamponade
Cardiac arrhythmias

Answer 155

A

Depends on the underlying cause
Viral cases have a GOOD prognosis
Malignant pericarditis has a POOR prognosis

Answer 156

A

• Inflammation of the peritoneal lining of the abdominal cavity. It can be localised to one part of the peritoneum or generalised.

Answer 157

A

• 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)

Answer 158

A

Primary peritonitis is RARE
Primary peritonitis is usually seen in adolescent females
Localised and secondary generalised peritonitis is COMMON in surgical patients

Answer 159

A

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)

Answer 160

A

• 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)

Answer 161

A

•	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

Answer 162

A

• 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

Answer 163

A

•	Early
o	Septic shock 
o	Respiratory failure 
o	Multiorgan failure 
o	Paralytic ileus 
o	Wound infection 
o	Abscesses 
•	Late
o	Incisional hernia 
o	Adhesions

Answer 164

A

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

Answer 165

A

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)

Answer 166

A

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

Answer 167

A

5-11/1000

Community-acquired pneumonia is responsible for >60,000 deaths per year in the UK

Answer 168

A

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

Answer 169

A

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

Answer 170

A

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

Answer 171

A

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)

Answer 172

A

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

Answer 173

A

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

Answer 174

A

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.

Answer 175

A

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.

Answer 176

A

Rare in developed countries

Answer 177

A

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

Answer 178

A

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)

Answer 179

A

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.

Answer 180

A

• Joint inflammation resulting from intra-articular infection. Also known as SEPTIC ARTHRITIS.

Answer 181

A

•	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

Answer 182

A

• Most common in CHILDREN and the ELDERLY

Answer 183

A

• 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

Answer 184

A

Painful, hot, swollen
Immobile joint
Erythema
Severe pain prevents passive movement
Pyrexia
Look for signs of aetiology

Answer 185

A

• 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

Answer 186

A

• 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

Answer 187

A

•	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)

Answer 188

A

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

Answer 189

A

Parotid or salivary gland enlargement
Dry eyes
Dry mouth or tongue
Signs of associated conditions

Answer 190

A

•	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

Answer 191

A

• 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

Answer 192

A

UNKNOWN
Tissue damage may be caused by vascular immune complex deposition
Could be due to a combination of hormonal, genetic and exogenous factors

Answer 193

A

COMMON
1-2/1000
More common in the YOUNG
More common in AFRO-CARIBBEAN and CHINESE
9 x more common in FEMALES

Answer 194

A

•	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

Answer 195

A

•	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

Answer 196

A

•	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

Answer 197

A

• 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

Answer 198

A

Age of onset: 30-60 yrs

* 3 x more common in FEMALES

Answer 199

A

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

Answer 200

A

• 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)

Answer 201

A

• Inflammation of the thyroid gland.

Answer 202

A

• 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)

Answer 203

A

True incidence is UNKNOWN
15-20 x more common in WOMEN
Usually occurs in 30-50 yrs

Answer 204

A

•	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

Answer 205

A

•	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

Answer 206

A

• 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

Answer 207

A

Thyroid hormone over-replacement –> bone loss + tachycardia
Hyperlipidaemia
Hashimoto’s encephalopathy
Myxoedema coma

Answer 208

A

• GOOD PROGNOSIS with early diagnosis and levothyroxine replacement

Answer 209

A

• Inflammation due to infection of the tonsils.

Answer 210

A

• 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

Answer 211

A

VERY COMMON

* Usually in children and young adults

Answer 212

A

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

Answer 213

A

• 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

Answer 214

A

Throat swabs and rapid antigen tests can be performed (but are NOT recommended)
Swabs may not be able to distinguish between infection and colonisation

Answer 215

A

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

Answer 216

A

Mycobacterium tuberculosis is an intracellular organism

It survives after being phagocytosed by macrophages

Answer 217

A

Annual mortality = 3 million (95% in developing countries)
Annual UK incidence = 6000
Asian immigratns are the highest risk group in the UK

Answer 218

A

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

Answer 219

A

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

Answer 220

A

• 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)

Answer 221

A

•	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

Answer 222

A

VERY COMMON
1-3% of GP consultations
The majority of women will have a UTI in their lifetime
MUCH more common in FEMALES

Answer 223

A

•	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)

Answer 224

A

Fever
Abdominal or loin tenderness
Foul-smelling urine
Distended bladder (occasionally)
Enlarged prostate (if prostatitis)

Answer 225

A

• 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

Answer 226

A

• 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)

Answer 227

A

•	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

Answer 228

A

• GOOD prognosis with appropriate treatment

Answer 229

A

• 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

Answer 230

A

• 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

Answer 231

A

15% of general population experience urticaria at some point in life
Acute is much more common than chronic urticaria

Answer 232

A

• 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

Answer 233

A

Usually clinical

* Tests may be required for chronic urticaria (e.g. FBC, ESR/CRP, patch testing, IgE tests)

Answer 234

A

• 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

Answer 235

A

VZV is a herpes ds-DNA virus
Highly contagious
Transmission by aerosol inhalation or direct contact with vesicular secretions

Answer 236

A

Chicken pox peak incidence: 4-10 yrs
Shingles peak incidence: > 50 yrs
90% of adults are VZV IgG positive

Answer 237

A

• 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

Answer 238

A

•	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

Answer 239

A

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

Answer 240

A

•	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

Answer 241

A

•	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

Answer 242

A

Depends on complications

* Worse in pregnancy, elderly and immunocompromised

Answer 243

A

•	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

Answer 244

A

• 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

Answer 245

A

RARE

* Takayasu’s arteritis is most common in JAPANESE FEMALES

Answer 246

A

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

Answer 247

A

• 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)

Answer 248

A

• Hepatitis caused by infection with the RNA viruses, hepatitis A or hepatitis E virus, that follow an acute course without progression to chronic carriage

Answer 249

A

• 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

Answer 250

A

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

Answer 251

A

•	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

Answer 252

A

Pyrexia
Jaundice
Tender hepatomegaly
Spleen may be palpable
ABSENCE of stigmata of chronic liver disease (although some spider naevi may appear transiently)

Answer 253

A

• 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

Answer 254

A

• 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

Answer 255

A

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

Answer 256

A

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%

Answer 257

A

• 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

Answer 258

A

• 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

Answer 259

A

Common
1-2 million deaths annually
Common in Southeast Asia, Africa and Mediterranean countries
HDV is also found worldwide

Answer 260

A

•	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

Answer 261

A

• 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

Answer 262

A

•	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

Answer 263

A

• 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)

Answer 264

A

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

Answer 265

A

Adults: 10% of infections become chronic

* Of the chronic infections, 20-30% will develop cirrhosis

Answer 266

A

• Hepatitis caused by infection with hepatitis C virus (HCV), often following a chronic course (in 80% of cases)

Answer 267

A

• 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

Answer 268

A

COMMON

* Different genotypes of HCV have different geographical prevalence

Answer 269

A

90% of acute infections are ASYMPTOMATIC
10% become jaundiced with mild flu-like illness
May be diagnosed after incidental abnormal LFT

Answer 270

A

• 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)

Answer 271

A

• 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

Answer 272

A

• 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

Answer 273

A

Fulminant hepatic failure
Chronic carriage of HCV
Hepatocellular carcinoma
Less common: porphyria cutanea tarda, cryoglobulinaemia, glomerulonephritis

Answer 274

A

80% of exposed will progress to chronic carriage

* Of these, 20-30% will develop cirrhosis over 10-20 years

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Infection & Immunology Flashcards

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