Infection and Immunology Flashcards
What is an Abscess?
A collection of pus that has built up within the tissue of the body
Can develop anywhere in the body
Most commonly in the skin or inside the body, in an organ or in the spaces between organs
What is the aetiology of Abscesses?
Caused by bacterial infection, parasites, or foreign substances
Bacterial infection is the most common cause, most common causative pathogen is methicillin-resistant Staphylococcus aureus (MRSA)
What is the epidemiology of Abscess?
Common and have become more common in the last few years
What are the presenting symptoms of an Abscess?
Skin abscess: -Swollen, pus-filled lump under the surface of the skin -Symptoms of an infection, such as fever and chills Internal abscess: -Pain in the affected area -Fever -Malaise -Loss of appetite and weight loss
What are the signs of an Abscess on physical examination?
Skin abscess:
- Smooth swelling under skin
- Pain and tenderness
- Warmth and erythema
- White or yellow pus under the skin
Internal abscess:
- Fever
- Pain or swelling in the affected area
- Dependent on the affected area e.g. lung- cough, dyspnoea, liver- jaundice
What are the appropriate investigations for Abscess?
Bloods: -FBC: leukocytosis -CRP/ESR: inflammatory markers Blood culture: positive for organism CT/Ultrasound: visualisation of abscess
What is anaphylaxis?
Acute life-threatening multisystem hypersensivity syndrome caused by sudden release of mast cell- and basophil-derived mediators into the circulation
What is anaphylaxis characterised by?
Rapidly developing life-threatening airway and/or breathing and/or circulation problems
Usually associated with skin and mucosal changes
What is the aetiology of anaphylaxis?
Immunologic: IgE-mediated or immune complex/complement-mediated
Non-immunologic: mast cell or basophil degranulation without the involvement of antibodies (e.g. reactions caused by vancomycin, codeine, ACE inhibitors)
Inflammatory mediators such as histamine cause bronchospasm, increased capillary permeability and
reduced vascular tone, resulting in tissue oedema
What are the common allergens?
PILFERS
Peanuts Insect stings Latex Fish Egg Radiological contrast agents Shellfish
What is the epidemiology of anaphylaxis?
Relatively common
What are the presenting symptoms of anaphylaxis?
Acute onset of symptoms on exposure to allergen (SOB):
Skin (rash, pruritis)
Oedema (lips, face)
Breathing (short of breath, wheezing)
Biphasic reactions occur 1–72 h after the first reaction in up to 20% of patients
What are the signs of anaphylaxis on physical examination?
URTICARIA: Urticaria Reduced BP Tachypnoea Infected conjunctiva and swollen eyes Cyanosis Audible wheeze Rhinitis Increased heart rate Airway swelling
What are the appropriate investigations for anaphylaxis? Interpret the results
The diagnosis of anaphylaxis is made clinically.
1st line:
Serum (mast cell) tryptase (measured within 15 min–3 h after onset of symptoms)= elevated
Histamine levels (measured preferably within 30 min after symptom onset)
Urinary metabolites of histamine (which may remain elevated for several hours after symptom onset)
ABG: elevated lactate
ECG: Non-specific ST ECG changes are common post-adrenaline
What is the management plan for a patient with anaphylaxis?
Oxygen Can Help Anaphylaxis: Oxygen (100%) Chloropheniramine (10mg) Hydrocortisone (100mg) Adrenaline (IM)- 0.5 mL of 1:1,000, can be repeated every 10mins according to response of pulse and BP
Advice: Educate on use of adrenaline pen for IM administration. Provide Medicalert bracelet
What are the possible complications of anaphylaxis?
(RDS)
Respiratory failure
Death
Shock
What is the prognosis for patients with anaphylaxis?
Good if prompt treatment given
What is Behçet’s disease?
A rare disorder that causes blood vessel inflammation throughout the body (vasculitis)
What is the aetiology of Behçet’s disease?
Poorly understood but thought to be an autoimmune condition, may also be due to an infectious trigger
What are the risk factors for Behçet’s disease?
Age: Commonly affects men and women in their 20s and 30s (though can occur at any age)
People from countries in the Middle East and East Asia, including Turkey, Iran, Japan and China, are more likely to develop Behcet’s
Gender: The disease is usually more severe in men
Genes: genetic predisposition
What is the epidemiology of Behçet’s disease?
RARE disorder
Genetic link
Commonly affects men and women in 20-30 year group but is more severe in men
What are the presenting symptoms and signs of Behçet’s disease on physical examination?
Mouth:
-Painful mouth sores (most common sign), begin as raised, round lesions in the mouth that quickly turn into painful ulcers, usually heal in 1-3 weeks, can reoccur
Skin:
Acne-like sores on bodies
-Red, raised and tender nodules on skin, especially on the lower legs
Genitals:
-Red, open sores can occur on the scrotum or the vulva
-Usually painful and can leave scars
Eyes:
-Inflammation in the eye (uveitis) causes redness, pain and blurred vision, typically in both eyes
Joints:
-Joint swelling and pain often affect the knees, ankles, elbows or wrists also might be involved
-Can resolve in 1-3 weeks
Blood vessels:
-Inflammation in veins and arteries can cause redness, pain, and swelling in the arms or legs when a blood clot results
-Inflammation in the large arteries can lead to complications, such as aneurysms and narrowing or blockage of the vessel
Digestive system:
-Abdominal pain
-Diarrhoea
-Bleeding
Brain:
-Headache
-Fever
-Disorientation
-Ataxia
-More severely: stroke
What are the appropriate investigations for Behçet’s disease?
*Pathergy testing:
-subcutaneous skin prick is performed
-formation of pustule within 48 hours
Bloods:
-CRP/ESR: inflammation
-Rheumatoid factor: exclude rheumatoid arthritis
-Anti-neutrophil antibodies: exclude other autoimmune conditions
-HLA-B51
Imaging:
-MR angiography: CNS involvement
-Colonoscopy: from GI symptoms, exclude other pathology, features on colonoscopy are usually distinct, single, deep ulcers
-Upper GI endoscopy
-CT chest/angiography: when haemoptysis occurs to evaluate for pulmonary aneurysm
-Pulmonary angiography
What is the management of Behçet’s disease?
Immunosuppression: corticosteroids
What is candidiasis?
A fungal infection due to any type of Candida (type of yeast)
What is the aetiology of candidiasis?
Candida normally lives on the skin and inside the body, in places such as the mouth, throat, gut, and vagina, without causing any problems. Candida can cause infections if it grows out of control or if it enters deep into the body (bloodstream or internal organs)
Although mucosal disease is common, invasive disease is not, and the primary reason is that Candida species in general are unable to enter intact epithelium
What are the risk factors for candidiasis infections?
Immunosuppressive agents e.g. systemic corticoid steroid use
Current or recent past use of brand spectrum antibiotics
Malabsorption/ malnutrition
HIV infection
Poor oral hygiene (oral candidiasis)
Endocrine disturbances (DM, pregnancy, hypoadrenalism) - reduce effectiveness of immune system
What are the presenting symptoms of candidiasis infections?
Oral: -creamy white/ yellow plaques adherent to oral mucosa -Cracks/ ulcers around the mouth -spotty red areas on the buccal mucosa -burning oral pain -loss of taste -pain while eating or swallowing Vaginal: -vaginal itching or soreness -pain during sexual intercourse -pain/ discomfort when urinating -abnormal vaginal discharge
What are the signs of a candidiasis infection on physical examination?
Rash
Erythema
Visible plaques/ulcers
What are the appropriate investigations for a candidiasis infection?
Superficial smear of the lesion for microscopy: test for candida
Biopsy
Blood culture
FBC: WCC elevated indicates infection
What is Cellulitis?
An acute spreading infection of the skin with visually indistinct borders that principally involves the dermis and subcutaneous tissue
What is Cellulitis usually characterised by?
Erythema Oedema Warmth Tenderness Commonly occurs in an extremity
What is Erysipelas?
A distinct form of superficial cellulitis with notable lymphatic involvement and is raised, sharply demarcating it from uninvolved skin
What is the aetiology of Cellulitis?
Cellulitis develops when micro-organisms gain entry to the dermal and subcutaneous tissues via disruptions in the cutaneous barrier
The most common causative agents are:
-Beta-haemolytic streptococci
-Staphylococcus aureus
What is the epidemiology of Cellulitis?
Cellulitis is a common condition Main risk factors are: -skin break -poor hygiene -poor vascularization of tissue (e.g. diabetes mellitus)
What are the presenting symptoms of Cellulitis?
There may be history of a cut, scratch or injury
Skin discomfort
Periorbital: Painful swollen red skin around eye
Orbital cellulitis: Painful or limited eye movements, visual impairment
What are the signs of Cellulitis on physical examination?
Lesion: -Erythema -Oedema -Warm tender indistinct margins *Pyrexia may signify systemic spread Exclude abscess: Test for fluid thrill or fluctuation- aspirate if pus suspected Periorbital: -Swollen eyelids -Conjunctival injection Orbital cellulitis: -Proptosis (protrusion of the eyeball) -Impaired acuity and eye movement Test for relative afferent pupillary defect, visual acuity and colour vision
What are the appropriate investigations for Cellulitis?
Bloods: WCC, blood culture
Discharge: Culture and sensitivity
Aspiration: As it is often non-purulent, it is not usually necessary
CT/MRI scan: When orbital cellulitis is suspected (to assess the posterior spread of infection)
What is the management of Cellulitis?
Medical:
-Oral penicillins (e.g. flucloxacillin, benzylpenicillin, coamoxiclav)
-Tetracyclines are effective in most community acquired cases
-In the hospital- intravenous use may be necessary
Surgical:
-Orbital decompression may be necessary in orbital cellulitis(emergency)
Abscess: Abscesses can be aspirated, incised and drained or excised completely
What are the complications of Cellulitis?
Sloughing (shedding) of overlying skin Localized tissue damage In orbital cellulitis, there may be permanent vision loss and spread to brain Abscess formation Meningitis Cavernous sinus thrombosis
What is the prognosis of Cellulitis?
Good with treatment
What is conjunctivitis?
Inflammation of the lining of the eyelids and eyeball
What is the aetiology of conjunctivitis?
Caused by: Bacteria Viruses Allergic or immunological reactions Mechanical irritation Medicines
Bacterial and viral conjunctivitis is highly contagious
What are the risk factors for conjunctivitis?
Exposure to infected person Infection in one eye Environmental irritants Allergen exposure Mechanical irritation Chronic contact lens useful Camps/ swimming pools
What are the presenting symptoms of conjunctivitis?
Watery discharge (viral) Ropy/ mucoid discharge, itching (allergic) Purulent discharge (bacterial) Eyelids stuck together in the morning (bacterial and viral)
What are the signs of conjunctivitis on physical examination?
Tender pre-auricular lymphadenopathy (more common in viral than bacterial infection)
Conjunctival follicles- round collections of lymphocytes
What are the appropriate investigations for conjunctivitis?
1st line:
Rapid adenovirus immunoassay- 2 visible lines equal positive
Others:
Cell culture/ Gram stain/ PCR- isolate viral or bacterial strains, amplify DNA
What is Encephalitis?
Inflammation of the brain parenchyma
What is the aetiology for Encephalitis?
In the majority of cases encephalitis is the result of a viral infection. Most common in the UK is HSV.
Other: bacteria (syphilis, staph A), immunocompromised (Cytomegalovirus, toxoplasmosis, Listeria)
What is the epidemiology of Encephalitis?
Annual UK incidence is 7.4 in 100,000
What are the presenting symptoms for Encephalitis?
Usually encephalitis is a mild self-limiting illness.
Subacute onset (hours to days) headache
Fever
Vomiting
Neck stiffness, photophobia, i.e. symptoms of meningism (meningoencephalitis) with behavioural changes
Drowsiness and confusion
There is often a history of seizures
Focal neurological symptoms (e.g. dysphasia and hemiplegia) may be present
It is important to obtain a detailed travel history
What are the signs of Encephalitis on physical examination?
Reduced level of consciousness with deteriorating GCS, seizures, pyrexia.
Signs of meningism: Neck stiffness, photophobia, Kernigs test positive.
Signs of raised intracranial pressure: hypertension, bradycardia, papilloedema.
Focal neurological signs.
Minimental examination may reveal cognitive or psychiatric disturbances.
What is Kernigs sign?
Positive when the thigh is flexed at the hip and knee at 90 degree angles, and subsequent extension in the knee is painful (leading to resistance)- indicating the presence of meningitis or subarachnoid haemorrhage
What are the appropriate investigations for Encephalitis?
Blood: FBC (raised lymphocytes), U&E (SIADH may occur), glucose (compare with CSF glucose), viral serology, ABG.
MRI/CT: Excludes mass lesion. HSV produces characteristic oedema of the temporal lobe on MRI.
Lumbar puncture: raised Lymphocytes,monocyte and protein, glucose usually normal. Viral PCR is first line.
EEG: May show epileptiform activity, e.g. spiking activity in temporal lobes
What is Epididymitis and Orchitis?
Epididymitis is characterized by acute unilateral scrotal pain and swelling of less than 6 weeks’ duration.
The pain usually begins at the epididymis and can spread to the entire testicle (epididymo-orchitis)
What is the aetiology of Epididymitis and Orchitis?
- Among sexually active men of all ages, STI pathogens including Chlamydia trachomatis and Neisseria gonorrhoeaeare common causes of epididymitis
- In older men (>35 years), infection may be due to non-sexually transmitted infection with common uropathogens, such as Escherichia coli and Enterococcus faecalis
What is the epidemiology of Epididymitis and Orchitis?
Epididymitis is the most common cause of scrotal pain in adults with an incidence of 25–65 cases per 10,000 adult males per year
Over half of men and boys with epididymitis also have orchitis.
-Isolated orchitis is rare: the commonest cause is mumps infection, although it can also be caused by other viral infections
What are the presenting symptoms of Epididymitis and Orchitis?
Gradual onset (unlike testicular torsion)
Unilateral scrotal pain and swelling
Other symptoms: fever, dysuria
What are the signs of Epididymitis and Orchitis on physical examination?
Diffuse enlargement of the testis
Erythema of the scrotal skin
Swelling for < 6 weeks: otherwise indicates chronic inflammation
What are the appropriate investigations for Epididymitis and Orchitis?
*first catch urine sample
Urethral swab: highly sensitive and specific for documenting urethritis and the presence or absence of gonococcal infection (look for urethral discharge)
Urine dipstick test: positive leukocyte esterase test (urethritis and lower urinary tract infection)
Urine microscopy: WBC
Urine culture: isolate causative organism
Colour duplex ultrasound: done in patients with signs suggestive of abscess formation or possible testicular torsion and infarction; epididymis is enlarged and hyperaemic (increased blood flow)
Consider STI screen
What is the management for Epididymitis and Orchitis?
If <35yrs;
-Doxycycline 100mg/12h (covers chlamydia; treat sexual partners)
-If gonorrhoea suspected add ceftriaxone 500mg IM stat. If >35yrs (mostly non-STI) associated UTI is common:
-Ciprofloxacin 500mg/12h or ofloxacin 200mg/12h
*Antibiotics should be used for 2–4wks
Also: analgesia, scrotal support, drainage of any abscess.
What are the complications of Epididymitis and Orchitis?
(usually of chronic disease, more commonly associated with uropathogen enteric organisms than sexually transmitted organisms) include: Chronic pain Reactive hydrocele Abscess formation Infarction of the testicle Testicular atrophy Reduced fertility
What is the prognosis of Epididymitis and Orchitis?
In men with infectious acute epididymitis, symptoms usually resolve rapidly following the initiation of appropriate antibiotic therapy
RARE CASES: particularly in STIs-epididymal obstruction/testicular atrophy and subsequent infertility problems
What is Gastroenteritis?
Acute inflammation of the lining of the GI tract, manifested by nausea, vomiting, diarrhoea and abdominal discomfort
What is Infectious Colitis?
Inflammation of the colon due to a virus or bacteria
What is the aetiology of Gastroenteritis and Infectious Colitis?
Can be caused by viruses, bacteria, protozoa or toxins contained in contaminated food or water
What are the common causative organisms of Gastroenteritis and Infectious Colitis?
Viral: Rotavirus, adenovirus, astrovirus
Bacterial: Campylobacter jejuni, Escherichia coli, Salmonella, Shigella, Vibrio cholerae, Listeria, Yersinia enterocolitica
Protozoal: Entamoeba histolytica
Toxins: From Staphylococcus aureus, Clostridium botulinum, Bacillus cereus, mushrooms, heavy metals, seafood
Commonly contaminated foods: Improperly cooked meat (S. aureus, C. perfringens), old rice (B. cereus, S. aureus), eggs and poultry (Salmonella), milk and cheeses (Listeria,
Campylobacter), canned food (botulism)
What is the epidemiology of Gastroenteritis and Infectious Colitis?
Common, and often under-reported, a serious cause of morbidity and mortality in the developing world
What are the presenting symptoms of Gastroenteritis and Infectious Colitis?
Sudden onset nausea, vomiting, anorexia
Diarrhoea (bloody or watery)
Abdominal pain or discomfort
Fever and malaise
*Enquire about recent travel, antibiotic use and recent food intake (how cooked, source andwhether anyone else ill)
Time of onset:
-Toxins (early; 1–24 h)
-Bacterial/viral/protozoal (12 h or later)
Effect of toxin:
-Botulinum causes paralysis
-Mushrooms can cause fits, renal or liver failure
What are the signs of Gastroenteritis and Infectious Colitis on physical examination?
Diffuse abdominal tenderness Abdominal distension Bowel sounds are often increased If severe: -Pyrexia -Dehydration -Hypotension -Peripheral shutdown
What are the appropriate investigations for Gastroenteritis and Infectious Colitis?
Blood:
-FBC
-Blood culture (helps identification if bacteriaemia present)
-U&Es: dehydration
Stool:
-Faecal microscopy for polymorphs, parasites, oocysts, culture, electron microscopy (used to diagnose viral infections)
-Analysis for toxins, particularly for pseudomembranous
colitis (Clostridium difficile toxin)
AXR or ultrasound:
-To exclude other causes of abdominal pain
Sigmoidoscopy:
-Often unnecessary unless inflammatory bowel disease needs to be excluded
What is the management for Gastroenteritis and Infectious Colitis?
Bed rest
Fluid and electrolyte replacement with oral rehydration solution (containing glucose and salt)
IV rehydration may be necessary in those with severe vomiting
*Most infections are self-limiting
-Antibiotic treatment is only warranted if severe or the infective agent has been identified (e.g. ciprofloxacin against Salmonella, Shigella, Campylobacter)
Botulism: Botulinum antitoxin IM and manage in ITU.
Public health:
-Often a notifiable disease
-Educate on basic hygiene and cooking
What are the complications of Gastroenteritis and Infectious Colitis?
Dehydration
Electrolyte imbalance
Pre-renal failure
Secondary lactose intolerance (particularly in infants)
Sepsis and shock (particularly Salmonella and Shigella)
Haemolytic uraemic syndrome is associated with toxins from E. coli
Guillian–Barre syndrome may occur weeks after recovery from Campylobacter gastroenteritis
*Botulism: Respiratory muscle weakness or paralysis
What is the prognosis for Gastroenteritis and Infectious Colitis?
Generally good, as the majority of cases are self-limiting
What is Herpes Simplex Virus?
Disease resulting from HSV1 or HSV2 infection
What is the aetiology of Herpes Simplex Virus?
HSV is an alpha-herpes virus with double-stranded deoxyribonucleic acid (dsDNA)
Transmitted via close contact with an individual shedding the virus (e.g. kissing, sexual intercourse)
What is the epidemiology of Herpes Simplex Virus?
90% adults seropositive for HSV1 by 30 years
35% adults >60 years seropositive for HSV2
Over 1/3 world population has recurrent HSV infections
Most common cause of encephalitis
What are the presenting symptoms of Herpes Simplex Virus?
HSV1:
Primary infection often asymptomatic
Usual symptoms:
-Pharyngitis;
-Gingivostomatis, may make eating very painful
-Herpetic whitlow, inoculation of virus into a finger
Recurrent infection/reactivation (herpes labialis/cold sore):
- Prodrome (6 h) peri-oral tingling and burning
- Vesicles appear (48 h duration), ulcerate and crust over -Complete healing 8–10 days
HSV2:
Very painful blisters and rash in genital, perigenital and anal area
Dysuria
Fever and malaise
What are the signs of Herpes Simplex Virus on physical examination?
HSV1:
Primary infection:
-Tender cervical lymphadenopathy
-Erythematous, oedematous pharynx
-Oral ulcers filled with yellow slough (gingivostomatitis)
-Digital blisters/pustules (herpetic whitlow)
Herpes labialis: Perioral vesicles/ulcers/crusting
HSV2:
- Maculopapular rash
- Vesicles and ulcers (external genitalia, anal margin, upper thighs)
- Inguinal lymphadenopathy
- Pyrexia
What are the appropriate investigations for Herpes Simplex Virus?
Usually a clinical diagnosis
Vesicle fluid: Electron microscopy, PCR, direct immunofluorescence, growth of virus in tissue culture
What is Human immunodeficiency virus (HIV)?
A pandemic infectious disease whose impact on societies is without precedent
It is caused by a retrovirus that infects and replicates in human lymphocytes and macrophages, eroding the integrity of the human immune system over a number of years
This results in immune deficiency and a susceptibility to a series of opportunistic and other infections as well as the development of certain malignancies
What is the aetiology of Human immunodeficiency virus (HIV)?
HIV is retrovirus that infects and replicates primarily in human CD4+ T cells and macrophages
It can be transmitted via blood, blood products, sexual fluids, other fluids containing blood, and breast milk
Most individuals are infected with HIV through:
- Sexual contact (most common)
- Before birth or during delivery
- During breastfeeding
- When sharing contaminated needles and syringes (intravenous drug users)
What is the epidemiology of Human immunodeficiency virus (HIV)?
Globally, the HIV incidence rate is believed to have peaked in the late 1990s and to have stabilised subsequently
Transmission among heterosexuals was the largest single route of infection
>40,000,000 adults affected worldwide
What are the presenting symptoms of Human immunodeficiency virus (HIV)?
Three phases:
1. Seroconversion: (4–8 weeks post-infection)
Self-limiting
Fever, night sweats
Generalized lymphadenopathy
Sore throat
Oral ulcers
Rash
Myalgia
Headache
Encephalitis
Diarrhoea
2. Early/asymptomatic: (18 months to 15 +years)
Apparently well -some patients may have persistent lymphadenopathy (>1 cm nodes, at 2 + extrainguinal sites for >3 months)
Progressive minor symptoms, e.g. rash, oral thrush, weight loss, malaise
3. AIDS: Syndrome of secondary diseases reflecting severe immuno deficiency or direct effect
of HIV infection (CD4 cell count <200/mm3)
What are the direct effects of HIV?
Neurological: Polyneuropathy, myelopathy, dementia Lung: Lymphocytic interstitial pneumonitis
Heart: Cardiomyopathy, myocarditis
Haematological: Anaemia, thrombocytopenia
GI: Anorexia, HIV enteropathy (malabsorption and diarrhoea), severe wasting
Eyes: Cotton wool spots
What are the secondary infections arising from HIV immunodeficiency?
Bacterial: Mycobacteria (lungs, GI, skin), e.g. Mycobacterium tuberculosis, staphylococci (skin), Salmonella, capsulated organisms (Streptococcus pneumoniae, Haemophilus influenzae)
Viral: CMV (retinitis, oesophagitis, colitis, pneumonitis, adrenalitis, encephalitis), HSV (encephalitis), varicella zoster virus (VZV) (recurrent shingles), human papillomavirus (HPV) (warts), Epstein–Barr virus (EBV)
Fungal: Pneumocystis pneumonia (PCP), Cryptococcus (meningitis), Candida (oral, airway, genital, oesophageal), invasive aspergillosis
Protozoal: Toxoplasmosis (cerebral abscess, chorioretinitis, encephalitis)
What are the tumours that arise from HIV immunodeficiency?
Kaposis sarcoma (cutaneous or conjunctival vascular tumour caused by human herpesvirus)
Squamous cell carcinoma (particularly cervical or anal)
Non- Hodgkins B-cell lymphoma (brain, GI)
Hodgkins lymphoma
What are the appropriate investigations for Human immunodeficiency virus (HIV)?
HIV testing (after discussion and consent):
-e.g. Serum HIV enzyme linked immunosorbent assay: positive/Serum HIV rapid test
-HIV antibodies (usually positive by 12 weeks after exposure)
-PCR for viral RNA or incorporated proviral DNA
Monitor CD4+ count and viral load
Others: (as appropriate)
-For PCP (Pneumocystis pneumonia):CXR bilateral perihilar/ground glass shadowing, bronchoalveolar lavage -Cryptococcal meningitis: Brain CT or MRI, lumbar puncture – cerebrospinal fluid (CSF) microscopy (India ink staining), culture, ELISA for antigen
CMV (colitis): Colonoscopy and biopsy (cytomegalic cells with inclusions)
Toxoplasmosis: Brain CT or MRI shows ring-enhancing lesions
Cryptosporidia/microsporidia: Stool microscopy
What is Incision and drainage of an abscess?
A treatment for abscesses to relieve pain and speed healing
What are the indications for Incision and drainage of an abscess?
The treatment typically used to clear an abscess of pus and start the healing process
Smaller abscesses may not need to be drained to disappear
What are the possible complications of Incision and drainage of an abscess?
Damage to adjacent structures
Bacteremic complications
Spread of infection owing to inadequate drainage (dissemination)
What is infectious mononucleosis?
A clinical syndrome most commonly caused by Epstein Barr virus (EBV) infection, also known as glandular fever
What is the aetiology of infectious mononucleosis?
Epstein Barr virus (EBV), also known as human herpes virus 4, is the aetiological agent in approximately 80% to 90% of cases
Other causes: Herpes virus 6, cytomegalovirus and HSV-1
What are the risk factors for infectious mononucleosis?
Close contact e.g. kissing, sharing eating utensils, sexual behaviour
What is the epidemiology of infectious mononucleosis?
Common (UK annual incidence 1 in 1000)
Has two peaks:
1. 1–6 years (usually asymptomatic)
2. 14–20 years
What are the presenting symptoms of infectious mononucleosis?
Incubation period: 4–8 weeks
May have abrupt onset: sore throat, fever, fatigue, headache, malaise, anorexia, sweating, abdominal pain
What are the signs of infectious mononucleosis on physical examination?
Pyrexia
Oedema and erythema of pharynx, fauces and soft palate, with white/creamy exudate on the tonsils which becomes confluent within 1–2 days, palatal petechiae. Cervical/generalized lymphadenopathy
Splenomegaly (50–60%), hepatomegaly (10–20%).
Jaundice (5–10%)
What are the appropriate investigations for infectious mononucleosis?
1st line:
- Bloods: FBC (leukocytosis), LFT (raised aminotransferases)
- Blood film: Lymphocytosis (>20% atypical lymphocytes)
- Heterophile antibodies: produced in response to EBV infection
- EBV specific antibodies
- Throat swab: exclude streptococcal tonsilitis
Consider: CT of abdomen (splenic rupture)
What is Infective Endocarditis?
Infection involving the endocardial surface of the heart, including the valvular structures, the chordae tendineae, sites of septal defects, or the mural endocardium
What is the aetiology of Infective Endocarditis?
The endocardium can be colonized by virtually any organism, but the most common are:
- Streptococci (40%): Mainly a-haemolytic
- Staphylococci(35%):Staphylococcusaureus
- Enterococci (20%)
Historical sources of bacteraemia should be considered, such as indwelling vascular catheters, recent dental work, and intravenous drug use
RF: prosthetic heart valves, congenial heart disease, valvular disease, IV drug use
What is the epidemiology of Infective Endocarditis?
Incidence 16–22 per million per year, around 50% are over 60 years old
Incidence increases with age
What are the presenting symptoms of Infective Endocarditis?
Fever with sweats/chills/rigors (may be relapsing and remitting) Malaise Fatigue Weight loss Headache Arthralgia Myalgia Dyspnoea Confusion (particularly in elderly) Skin lesions
What are the signs of Infective Endocarditis on physical examination?
Pyrexia, tachycardia, signs of anaemia
Clubbing (if long-standing)
New regurgitant murmur or muffled heart sounds:
Frequency: Mitral > aortic > tricuspid > pulmonary
Splenomegaly
Vasculitic lesions:
-Petechiae particularly on retinae (Roths spots)
-Pharyngeal and conjunctival mucosa
-Janeway lesions (painless palmar macules, which blanch on pressure)
-Oslers nodes (tender nodules on finger/toe pads)
-Splinter haemorrhages (nail-bed haemorrhages)
What are the appropriate investigations for Infective Endocarditis?
Bloods:
-FBC (leukocytosis, normocytic anaemia)
-Raised ESR and CRP
-U&Es: mildly elevated urea
-Rheumatoid factors: may be positive (minor criteria for diagnosis)
-Complement levels: decreased
Blood culture: At least three sets 1h apart: bacteraemia or fungaemia
ECG: progression of the infection may lead to conduction system disease
Imaging:
Echocardiography: Should be performed in all cases of suspected IE, detection of vegetations and valve abscess, diagnosis of prosthetic valve endocarditis and assessment of embolic risk
CT/CXR: valvular abnormalities and vegetations, septic pul- monary emboli: focal lung infiltrates
What is Dukes’ classification of Infective Endocarditis?
Major criteria:
Positive blood culture in two separate sample
-Positive echocardiogram (vegetation, abscess, prosthetic valve dehiscence, new valve regurgitation)
Minor criteria:
- High-grade pyrexia (temperature >38C)
- Risk factors (abnormal valves, IV drug use, dental surgery)
- Positive blood culture, but not major criteria
- Positive echocardiogram, but not major criteria
- Vascular signs
What is the management for Infective Endocarditis?
ABC approach
1. Broad-spectrum antimicrobial therapy is required empirically on clinical suspicion:
-Benzylpenicillin + gentamicin (empirical treatment)
2. Streptococci: Continue as above (alternatives – ceftriaxone, vancomycin)
3. Staphylococci: Flucloxacillin/vancomycin + gentamicin (for prosthetic valves: vancomycin + gentamicin + rifampin)
Enterococci: Ampicillin + gentamicin
Surgery: If poor response or deterioration, urgent valve replacement is indicated.
*Antibiotic prophylaxis for patients with a PMH of infective endocarditis undergoing high risk procedures
What are the complications of Infective Endocarditis?
Valve incompetence Intracardiac fistulae or abscesses Aneurysm formation Heart failure Renal failure Glomerulonephritis Arterial emboli from the vegetations (brain, kidneys, lungs, spleen)
What is the prognosis for Infective Endocarditis?
Fatal if untreated
Even when treated, 15–30% mortality (mortality is greater in older patients)
What is Malaria?
A parasitic infection caused by protozoa of the genus Plasmodium.
Five species are known to infect humans; Plasmodium falciparum is the most life-threatening
What is the aetiology of Malaria?
It is naturally transmitted to humans through a bite by an infected female Anopheles mosquito but may potentially be transmitted by blood transfusion or organ transplantation
What is the epidemiology of Malaria?
It is widely distributed throughout tropical and subtropical regions, and the main burden of disease falls on these areas (93% of all malaria deaths occurred in the African region)
Travellers account for the majority of disease in Western countries
*Pregnant women and children aged under 5 years remain the most susceptible to disease in endemic areas
What are the presenting symptoms of Malaria?
*High degree of clinical suspicion in any feverish traveller (incubation up to 1 year, but usually 1–2 weeks)
*Cyclical symptoms of high fever, flulike symptoms, severe sweating and shivering cold/rigors
Peak temperature may coincide with rupture of the intra-erythrocytic schizonts:
-every 48 h for P. falciprum (malignant tertian)
-every 72 h for P. malariae (benign quartan)
-every 48 h for P. vivax and P. ovale (benign tertian)
What are the signs of Malaria on physical examination?
Pyrexia/rigors
Anaemia
Hepatosplenomegaly
What are the appropriate investigations for Malaria?
Thick/thin blood film (using Fields or Giemsas stain):
- -Test of choice to identify parasite
- Detection of asexual or sexual forms of the parasites inside erythrocytes
- Measure daily for detection and quantitative count of level of intracellular ring forms.
- Has to be negative for 3 days to exclude malaria
- > 2% in P. falciparum malaria is severe
Rapid diagnostic test: immunochromatographic tests detect the presence of malaria antigen or enzyme and typically give a visible band after 15 minutes if positive
Bloods:
- FBC (anaemia, prothrombin time may be moderately prolonged)
- U&Es: usually normal or mildly impaired; renal failure may be present in severe infection
- LFTs: may show elevated bilirubin or elevated aminotransferases
- ABG: In severe malaria, tissue hypoxia due to microvascular obstruction, impaired red cell deformability, anaemia, hypovolaemia, and hypotension can lead to lactic acidosis, which may contribute to impaired level of consciousness
Urinalysis: In severe Plasmodium falciparum infections, massive haemolysis combined with acute tubular necrosis produce acute renal failure with haemoglobinuria and proteinuria
What is mastitis?
Inflammation of the breast with or without infection
What are breast abscesses?
A breast abscess is a localised area of infection with a walled-off collection of pus
It may or may not be associated with mastitis (as a complication)
What are the two types of mastitis with infection?
Lactational
Non-lactational
What is the aetiology for mastitis/ breast abscesses?
Infectious mastitis and breast abscesses are usually caused by bacteria colonising the skin. Cases due to Staphylococcus aureus are by far the most common.
Non-infectious mastitis may result from underlying duct ectasia and infrequently foreign material (e.g. nipple piercing, breast implant)
What is the epidemiology for mastitis/breast abscesses?
The global prevalence of mastitis in lactating women is approximately 1% to 10% but may be higher
Breast abscess develops in 3% to 11% of women with mastitis
What are the presenting symptoms for mastitis/breast abscesses?
Fever
Decreased milk outflow (if lactational)
Breast warmth/ tenderness/ swelling/ redness (erythema)
Flu like symptoms- malaise and myalgia
What are the signs of mastitis/breast abscesses on physical examination?
Breast erythema
UNCOMMON: Breast mass, fistula, nipple inversion/retraction, nipple discharge, lymphadenopathy, extra-mammary lesions
What are the appropriate investigations for mastitis/breast abscesses?
1st line:
-Breast ultrasound-hypoechoic lesion (abscess), may be well circumscribed, irregular, or ill defined
-Diagnostic needle aspiration- purulent fluid indicates a breast abscess
-CMS of nipple discharge or needle aspirate- indicate infection/malignancy
(CMS- cytology, microscopy and sensitivity)
Others: pregnancy test, mammogram, blood culture
What is the management for mastitis/breast abscesses?
The goal of treatment for mastitis is to provide prompt and appropriate management to prevent complications such as a breast abscess. Lactational: -Effective milk removal -Antibiotic therapy -Warm compresses -Symptomatic relief
Non-lactational:
- Antimicrobial therapy (observational period)
- Supportive measures should include analgesia, if necessary.
- For granulomatous mastitis (idiopathic granulomatous inflammation)- glucocorticosteroids
What are the complications of mastitis/breast abscesses?
Breast abscesses (less than 10% of patients with mastitis)
Cessation of breastfeeding (most patients can continue to breastfeed)
Sepsis
Scarring (recurrent infections)
Functional mastectomy (breast that is unable to effectively lactate as a complication of prior tissue destruction from infection or treatment)
What is the prognosis for mastitis/breast abscesses?
When treated promptly and appropriately, most breast infections, including abscess, will resolve without serious complications.
Resolution of mastitis after 2-3 days of appropriate antibiotic therapy is expected among most patients.
Lactational abscesses tend to be easier to treat than non-lactational abscesses- these are multi-factorial and have a greater risk of becoming chronic
What is Meningitis?
Inflammation of the meninges (pia mater and arachnoid) (coverings of the brain) most commonly caused by infection
What is the aetiology of Meningitis?
Infection:
Bacterial:
-Neonates: Group B streptococci, Escherichia coli, Listeria monocytogenes
-Children: Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae
-Adults: *Neisseria meningitidis (meningococcus), Streptococcus pneumoniae, TB
-Elderly: Streptococcus pneumoniae, Listeria monocytogenes
Viral: Enteroviruses, mumps, Herpes simplex V, HIV
Fungal: Cryptococcus (associated with HIV infection)
What are the risk factors for Meningitis?
Close communities (e.g. dormitories) Basal skull fractures Mastoiditis Sinusitis Inner ear infections Alcoholism Immunodeficiency Splenectomy Sickle cell anaemia CSF shunts Intracranial surgery
What is the epidemiology of Meningitis?
Variation according to geography, age, social conditions
Viral meningitis is one of the most common infections of the CNS
What are the presenting symptoms of Meningitis?
ASK ABOUT TRAVEL HISTORY *Severe headache *Photophobia *Neck stiffness or backache Irritability Drowsiness Vomiting Fever Clouding of consciousness High-pitched crying or fits (common in children)
What are the signs of Meningitis on physical examination?
Signs of meningism: -Photophobia -Neck stiffness Signs of infection: -Fever -Tachycardia -Hypotension -Skin rash (petechiae with meningococcal septicaemia) -Altered mental state
What are the appropriate investigations for Meningitis?
Blood: Two sets of blood cultures (do not delay antibiotics)
Imaging:
-CT scan to exclude a mass lesion or increased intracranial pressure before LP, (may lead to cerebral herniation during subsequent CSF removal)
*A CT scan of the head must be done before LP in patients with:
-Immunodeficiency
-History of CNS disease
-Reduced consciousness
-Fit
-Focal neurologic deficit
-Papilloedema
Lumbar puncture: Send CSF for MCS and Gram staining (Streptococcus pneumoniae: Gram-positive diplococcic, Neisseria Meningitidis: gram-negative diplococcic)
Bacterial: Cloudy CSF, raised neutrophils, raised protein, reduced glucose (CSF: serum glucose ratio of <0.5)
Viral: raised Lymphocytes, raised protein BUT normal glucose
*TB: Fibrinous CSF, raised lymphocytes, raised protein, reduced glucose
What is the management for Meningitis?
Immediate IV/IM antibiotics if meningitis suspected (before lumbar puncture or CT)
Antibiotics:
Benzylpenicillin may be given as initial blind therapy
Amoxicillin + gentamicin
Add vancomycin and if necessary rifampicin
If anaphylaxis to penicillin or cephalosporins- use chloramphenicol
Steroids:
IV (10 mg for 4 days) given shortly before or with first dose of antibiotics to reduce complications
Avoid dexamethasone in patients with HIV
Resuscitation: Patient is best managed in ITU
Prevention (only applicable to meningococcal meningitis): Notify public health services and consult a consultant in communicable disease control, vaccination for meningococcal serogroups A and C
What are the complications for Meningitis?
Septicaemia Shock DIC-disseminated intravascular coagulation, which is the inappropriate clotting of blood within the vessels Renal failure Fits Peripheral gangrene Cerebral oedema Cranial nerve lesions Cerebral venous thrombosis Hydrocephalus Water- house–Friderichsen syndrome (bilateral adrenal haemorrhage)
What is the prognosis of Meningitis?
Mortality rate from bacterial meningitis is high (10–40% with meningococcal sepsis)
In developing countries mortality rate often higher
Viral meningitis self-limiting
What is Myocarditis?
Acute inflammation and necrosis of cardiac muscle (myocardium) in the absence of the predominant acute or chronic ischaemia characteristic of coronary artery disease
What is the aetiology of Myocarditis?
Usually unknown (idiopathic)
Infection:
-Viruses: e.g. Coxsackie B, echovirus, EBV, CMV
-Bacterial: e.g. post-streptococcal, tuberculosis, -diphtheria, Lyme disease
-Fungal: e.g. candidiasis.
-Protozoal: e.g. trypanosomiasis (Chagas disease)
Non-infective:
-Systemic disorders (e.g. SLE, sarcoidosis, polymyositis)
-Hypersensitivity myocarditis (e.g. sulphonamides)
Drugs:
-Chemotherapy agents (e.g. doxorubicin, streptomycin) Others: Cocaine abuse, heavy metals, radiation
What is the epidemiology of Myocarditis?
True incidence is unknown, as many cases are not detected at the time of acute illness
Coxsackie B virus is a common cause in Europe and the USA but in South America Chagas disease is the common cause
*Patients with myocarditis tend to be younger (<50 years) than those presenting with more common cardiac conditions such as acute coronary syndrome
What are the presenting symptoms of Myocarditis?
Prodromal ‘flu-like’ illness Fever Malaise Fatigue Lethargy Breathlessness (pericardial effusion/myocardial dysfunction) and orthopnoea Palpitations Sharp chest pain (suggesting associated pericarditis)
What are the signs of Myocarditis on physical examination?
Atrial and ventricular arrhythmias
Sinus tachycardia
S3 gallop
Signs of concurrent pericarditis:
-Pericardial friction rub (best heard lower left sternal edge, with patient leaning forward in expiration)
-Heart sounds may be faint in the presence of an effusion
What are the appropriate investigations for Myocarditis?
12 lead ECG: anyone who resents with chest pain, Non-specific T wave and ST changes, widespread saddle-shaped ST elevation in pericarditis
Bloods:
- FBC (raised WCC in infective causes)
- U&Es, BNP, raised ESR or CRP, cardiac enzymes e.g. creatinine kinase, troponin (may be elevated)
- To identify the cause (viral or bacterial serology, antistreptolysin O titre, ANA, serum ACE, TFT)
CXR: May be normal or show cardiomegaly with or without pulmonary oedema (frequently reveals bilateral pulmonary infiltrates in the setting of myocarditis-induced CHF)
Echocardiography: Assesses systolic/diastolic function, wall motion abnormalities, pericardial effusion: global and regional left ventricular motion abnormalities and dilatation
Myocardial biopsy: Rarely required, show histological findings of myocardial cellular infiltrates ± myocardial necrosis
What is Necrotising fasciitis?
A life-threatening subcutaneous soft-tissue infection that may extend to the deep fascia, but not into the underlying muscle
What is the aetiology of Necrotising fasciitis?
Type I necrotising fasciitis is a polymicrobial infection of subcutaneous tissue (such as Bacteroides plus Escherichia coli or non-group A streptococcus with or without Staphylococcus aureus)
Type II necrotising fasciitis is a monomicrobial infection of subcutaneous tissue most commonly caused by Streptococcus pyogenes (group A streptococci)
What are the predisposing risk factors for Necrotising fasciitis?
Diabetes mellitus Peripheral vascular disease Immunocompromising conditions or immunosuppression (corticosteroids) Chronic renal or hepatic insufficiency Chickenpox or herpes zoster Intravenous drug use
What is the epidemiology of Necrotising fasciitis?
Type I (due to mixed anaerobic-facultative anaerobic infections) is more common than type II necrotising fasciitis
What are the presenting symptoms/signs of Necrotising fasciitis on physical examination?
Anaesthesia or severe pain over the site of cellulitis indicates necrotising fasciitis Examination of the skin overlying the area of cellulitis may reveal vesicles or bullae Grey discolouration of skin Oedema Location: about half of cases occur in the extremities, with the remainder concentrated in the perineum, trunk, and head and neck areas Systemic signs of infection: -Fever -Nausea and vomiting -Palpitations -Tachycardia -Tachypnoea -Hypotension -Light headedness
What are the appropriate investigations for Necrotising fasciitis?
Bloods:
- FBC: abnormally high or low WCC
- U&Es: hyponatraemia is a non-specific finding
- Urea and Creatinine: may be elevated
- CRP: elevation (non-specific)
- Creatinine kinase: elevated
- Serum lactate: elevated
Blood and tissue cultures: positive; may indicate polymicrobial or monomicrobial aetiology
ABG: hypoxaemia, acidosis
CT/MRI: oedema extending along fascial plane and/or soft tissue gas
Surgical exploration: surgical consultation for inspection, exploration, and drainage of infected tissue should be obtained in every case of suspected necrotising fasciitis
What is neutropenic sepsis?
A potentially life-threatening complication of anti-cancer and other immunosuppressive drug treatment
It is defined as a temperature of greater than 38°C or any symptoms and/or signs of sepsis, in a person with an absolute neutrophil count of 0.5 x 109/L or lower
What is sepsis?
A syndrome defined as life-threatening organ dysfunction due to a dysregulated host response to infection
What is neutropenia?
The risk of clinically significant infection and sepsis increases as the neutrophil count decreases to less than 0.5 x 109/L
What is the aetiology of neutropenic sepsis?
It is a common complication of chemotherapy- often more common in patients with haematological malignancies than in patients with solid tumours
Risk: greatest with the first treatment, also cumulative with ongoing cycles of therapy
What are the risk factors for neutropenic sepsis?
Infants and people over 60 years of age are at higher risk
Corticosteroids (additional immunosuppression)
Co-morbidities: diabetes mellitus, liver disease, renal disease; poor nutritional status
Full dose intensity chemotherapy
Concurrent radiotherapy
Prior episodes of neutropenia following chemotherapy
What is the epidemiology of neutropenic sepsis?
The most common life-threatening complication of cancer therapy
Higher incidence in patients with heamatological malignancy
What are the presenting symptoms of neutropenic sepsis?
Symptoms or signs indicating possible infection:
Dysuria
Dyspnoea
Diarrhoea
Cough
Nausea or vomiting
Chills, shivers and/or a temperature greater than 38°C
What are the signs of neutropenic sepsis on physical examination?
Clinical features of possible sepsis: -Fever -Rigors -Tachycardia -Hypotension *people with sepsis may present with non-specific, non-localized clinical features: -general malaise -agitation -behavioural change In addition, neutropenia may cause changes in behaviour, mental state, or cognition which is independent from the onset of sepsis
What are the appropriate investigations for neutropenic sepsis?
Bloods:
-FBC: absolute neutrophil count (ANC) <500
-U&Es: normal or elevated, indicator of renal dysfunction
-LFTs: albumin <35 g/L (also a RF for neutropenic sepsis), total bilirubin and aminotransferases elevated
Blood cultures: positive for pathogen
CXR: infiltrates in pneumonia
Others:
-Stool and urine culture
-Lumbar puncture: for patients with suspected CNS infection
-Viral assay
-CT of chest, abdomen and pelvis: infiltrates of pneumonia
What is osteomyelitis?
An inflammatory condition of bone caused by an infecting organism, most commonly Staphylococcus aureus
What is the aetiology of osteomyelitis?
May be caused from haematogenous spread, direct inoculation of micro-organisms into bone, or from a contiguous (touching) focus of infection
What is the most common pathogen implicated in osteomyelitis?
Staphylococcus aureus
What are the risk factors for osteomyelitis?
Penetrating injuries e.g. open fractures Surgical site infections Intravenous drug misuse Diabetes Mellitus- diabetic foot Periodontal abscess of the mandible
What is the epidemiology of osteomyelitis?
Greater incidence in men than women
Risk increased with age particularly over 50
What are the presenting symptoms of osteomyelitis?
Malaise
Fatigue
Vague symptoms: non-specific pain at site of infection, low grade fever
Local inflammation, erythema or swelling
What are the signs of osteomyelitis on physical examination?
Local inflammation, erythema or swelling Reduced range of movement Reduced sensation (particularly in diabetic foot)
What are the appropriate investigations for osteomyelitis?
Bloods:
-Raised WCC
-Raised ESR/CRP
Plain x-rays of affected areas: osteopenia, bone destruction (lytic lesions)- ‘fallen leaf’ sign
Ultrasound: look for signs of associated septic arthritis and infection (collections, subperiosteal abscesses)
CT: bone destruction
Radionuclide scan: increased uptake at infected sites
Histology: organisms or inflammatory cells, dead cells
What is Pericarditis?
Inflammation of the pericardium, may be acute, subacute or chronic
What is the criteria for acute Pericarditis?
New-onset inflammation lasting <4-6 weeks
What is the aetiology of Pericarditis?
Can be idiopathic or due to an underlying systemic condition (e.g., systemic lupus erythematosus)
As many as 90% of cases are either idiopathic or due to viral infections or systemic autoimmune conditions
What are the risk factors for Pericarditis?
Viral or bacterial infection (viral is most common):
-Commonly coxsackie B, echovirus, mumps virus, streptococci, fungi, staphylococci, TB
Systemic autoimmune conditions e.g. rheumatoid arthritis and SLE
Malignancy
Metabolic disorders
Cardiac surgery (4 weeks after coronary artery bypass graft)
Transmural MI:
-post-myocardial infarction (24–72 h)
-Dresslers syndrome (weeks to months after acute MI)
What is the epidemiology of Pericarditis?
Acute pericarditis is more common in adults (typically between 20 to 50 years old) and in men
Uncommon- the clinical incidence is <1 in 100 hospital admissions
What are the presenting symptoms of Pericarditis?
Chest pain (most common- 85% of cases)
-Sharp, stabbing, pleuritic, or aching, and can mimic the pain of myocardial ischaemia or infarction
**Almost all patients report relief of pain with sitting up or leaning forward
-Pain radiates to neck or shoulders
-Aggravated by coughing, deep inspiration and lying flat
Others: Dyspnoea, nausea
What are the signs of Pericarditis on physical examination?
Fever
Pericardial friction rub (best heard lower left sternal edge, with patient leaning forward in expiration)
Heart sounds may be faint in the presence of an effusion
What are the signs of Constrictive Pericarditis (chronic) on physical examination?
Raised JVP with inspiration (Kussmauls sign)
Pulsus paradoxus: an abnormally large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration (<10 mmHg)
Hepatomegaly
Ascites
Oedema
Pericardial knock (rapid ventricular filling)
AF
What is Constrictive Pericarditis?
Impedes (delays) normal diastolic filling and can be a medium to late complication of acute pericarditis
What are the appropriate investigations for Constrictive Pericarditis?
*ECG: Widespread ST elevation that is saddle-shaped (most useful diagnostic test)
Bloods:
-Troponin: elevated
-ESR and CRP: elevated consistent with inflammation
-Urea: elevated suggest a urea cause
-FBC: elevated leukocytes
Pericardial fluid/blood culture: positive if infectious cause
(and viral serology, ANA, rheumatoid factor)
CXR: Usually normal unless a large pericardial effusion is present >300 mL effusion: water-bottle-shaped enlarged cardiac silhouette
Chest CT: Pericardial calcification can be seen in constrictive pericarditis:
-pericardial thickness, calcification
-deformed ventricular contours
-dilatation of the inferior vena cava
-angulation of the ventricular septum (lateral CXR or CT)
What is Peritonitis?
Inflammation of the peritoneum usually caused by infection from bacteria or fungi
Left untreated, peritonitis can rapidly spread into the blood (sepsis) and to other organs, resulting in multiple organ failure and death
What is the aetiology of Peritonitis?
The two main types:
- Primary spontaneous peritonitis, an infection that develops in the peritoneum
- Secondary peritonitis, which usually develops when an injury or infection in the abdominal cavity allows infectious organisms into the peritoneum
What is the epidemiology of Peritonitis?
Both types of peritonitis are life-threatening
The death rate from peritonitis depends on many factors, but can be as high as 40% in those who also have cirrhosis
As many as 10% may die from secondary peritonitis
What are the risk factors for Peritonitis?
The most common risk factors for primary spontaneous peritonitis include:
- Liver disease with cirrhosis: buildup of abdominal fluid (ascites) that can become infected
- Kidney failure getting peritoneal dialysis
Common causes of secondary peritonitis include:
- A ruptured appendix, diverticulum, or stomach ulcer
- Digestive diseases such as Crohn’s disease and diverticulitis
- Pancreatitis
- Pelvic inflammatory disease
- Perforations of the bowel, stomach, intestine, gallbladder, or appendix
- Surgery
- Trauma to the abdomen
What are the presenting symptoms of Peritonitis?
Abdominal pain or tenderness
Rigors
Fever
Not passing any urine (or passing less volume than usual)
Difficulty passing gas or having a bowel movement
Vomiting
*may have fluid in the abdominal cavity= ascites
What is Spontaneous bacterial peritonitis?
An infection of ascitic fluid that cannot be attributed to any intra-abdominal, ongoing inflammatory, or surgically correctable condition
It is one of the most frequently encountered bacterial infections in patients with cirrhosis
What are the signs of Peritonitis on physical examination?
Abdominal pain or tenderness Signs of ascites: flank dullness, shifting dullness, fluid wave, and auscultatory percussion Signs of sepsis may be present: -Hypothermia -Hypotension -Tachycardia
What are the appropriate investigations for Peritonitis?
Bloods:
-FBC: leukocytosis, anaemia (if worsens may be a GI bleed)
-Creatinine: elevated hepatorenal syndrome may be present
-LFTs: May be useful in determining if patient has liver disease: liver enzymes and bilirubin elevated; albumin decreased
Blood cultures: growth of causative organism
Peritoneal fluid analysis:
- culture
- pH
- WCC
CT scan of abdomen: demonstrates diffuse ascites; excludes pneumoperitoneum in patients with secondary peritonitis
What is the management for Peritonitis?
Patients who appear otherwise well with no signs of sepsis, encephalopathy, or GI bleeding may be started on oral antibiotics: quinolone or a cephalosporin such as cefixime- continue for 5 to 10 days
Patients who have signs of sepsis, encephalopathy, or GI bleeding should be started on empirical broad-spectrum antibiotics active against both gram-negative and gram-positive organisms
Typical choice of antibiotic would be:
-cephalosporin, ciprofloxacin
-or a broad-spectrum penicillin with a beta-lactamase inhibitor, such as ampicillin/sulbactam
Surgery: necessary to remove infected tissue, treat the underlying cause of the infection, and prevent the infection from spreading, especially if peritonitis is due to a ruptured appendix, stomach or colon
What are the possible complications of Peritonitis?
HIGH RISK: sepsis/septic shock
HIGH RISK: renal dysfunction/impairment
Medium: worsening ascites
Risk of paracentesis:
-Bleeding e.g. intraperitoneal haemorrhage
-Persistent leak at the site of the paracentesis
-Bowel perforation
What is the prognosis of Peritonitis?
One year reoccurrence in primary spontaneous peritonitis however the mortality rate has decreased
*renal dysfunction was found to be the most important independent predictor of mortality
What is pneumonia?
Infection of distal lung parenchyma
How can be pneumonia be classified?
- Community-acquired, hospital-acquired or nosocomial (originating in hospital)
- Aspiration pneumonia, pneumonia in the immunocompromised
- Typical and atypical (Mycoplasma, Chlamydia, Legionella)
- Location: lobar
What is the aetiology of pneumonia?
Community-acquired:
-Streptococcus pneumoniae (70%)
-Haemophilus influenzae and Moraxella catarrhalis (COPD)
-Chlamydia pneumonia and Chlamydia psittaci (contact with birds/parrots)
-Mycoplasma pneumonia (periodic epidemics)
-Legionella (anywhere with air conditioning)
-Staphylococcus aureus (recent influenza infection, IV drug users)
Hospital-acquired:
-Gram-negative enterobacteria (Pseudomonas, Klebsiella), anaerobes (aspiration pneumonia)
What are the risk factors for pneumonia?
Age (over 65 years) Smoking (or exposure) Alcohol Poor oral hygiene Pre-existing lung disease e.g. COPD Immunodeficiency (chronic renal/liver disease, diabetes mellitus) Contact with pneumonia
What is the epidemiology of pneumonia?
Incidence 5–11 in 1000 (25–44 in 1000 in elderly)
Community- acquired causes >60 000 deaths/year in the UK
What is the most common causative organism of Pneumonia?
Streptococcus pneumoniae
What are the presenting symptoms of pneumonia?
Fever
Cough with increasing sputum production(yellow, green or rusty in S. pneumoniae)
Rigors, sweating (night sweats)
Malaise
Breathlessness and pleuritic chest pain
Confusion (severe cases, elderly, Legionella).
What are the signs of pneumonia on physical examination?
Inspection: -Pyrexia -Respiratory distress -Tachypnoea -Tachycardia -Hypotension -Cyanosis Resp examination: -Reduced chest expansion -Dullness to percussion -Increased tactile vocal fremitus -Bronchial breathing (inspiration phase lasts as long as expiration phase) -Coarse crepitations on affected side *Chronic suppurative lung disease (empyema, abscess): Clubbing
What are the presenting symptoms of atypical pneumonia?
Headache, myalgia, diarrhoea/abdominal pain
What system is used to decide whether to treat a patient with pneumonia in the community or in the hospital?
CURB-65 mortality risk score C- Confusion U- Urea > 7mmol/L* R- Respiratory rate > 30 B- BP = SBP < 90 mmHg OR DBP < 60 mmHg 65- age >65 years *Urea may not be easily measured in community
What are the appropriate investigations for pneumonia?
CXR: new consolidation (repeat 6–8 weeks)
Pulse oximetry: low arterial oxygen saturation < 94%
ABG: low arterial oxygen saturation
Sputum/pleural fluid: Microscopy, culture and sensitivity, acid-fast bacilli
Urine: Pneumococcus and Legionella antigens
Bloods:
-FBC: leukocytosis (abnormal WCC)
-CRP: elevated
-U&Es: Low sodium
-Blood culture: CMS
-LFTs: usually normal
*When pneumonia fails to resolve or when there is clinical progression: Bronchoscopy (and bronchoalveolar lavage)
What is the acid-fast bacilli test for?
A type of bacteria that causes tuberculosis
What is the management for pneumonia?
- Assess severity
- Start antibiotics:
-Oral amoxicillin
-Oral or IV amoxicillin and erythromycin
-IV cefuroxime/cefotaxime/co-amoxiclav and erythromycin
*switch to appropriate antibiotic as per sensitivity - Supportive therapy:
-Oxygen (maintain PO2 > 8 kPa, start with 28% O2 in COPD to avoid hypercapnia)
-Parenteral fluids for dehydration or shock, analgesia, chest physiotherapy
-CPAP, BiPAP or ITU care for respiratory failure
-surgical drainage may be needed for empyema/abscesses - Discharge planning:
Presence of two or more features of clinical instability (pyrexia, heart rate, respiratory rate and low BP, oxygen saturation, mental status and oral intake) predict a significant chance of re-admission or mortality
What are the complications of pneumonia?
Pleural effusion Empyema (pus in the pleural cavity) Lung abscess (especially staphylococcal, Klebsiella pneumonia- rare) Septic shock ARDS Acute renal failure Septic schock Heart failure
What is the prognosis of pneumonia?
For patients admitted to hospital, mortality rate ranges from 5% to 15%, but increases to 20% to 50% in patients requiring admission to the intensive care unit (ICU)
Patients treated in the community generally have a good prognosis
What is Rheumatic Fever?
An inflammatory (autoimmune) multisystem disorder, occurring following group A b-haemolytic streptococci (GAS) throat infection
What is the aetiology of Rheumatic Fever?
Streptococcal pharyngeal infection is required, and genetic susceptibility may be present for the autoimmune response to be triggered
What is the epidemiology of Rheumatic Fever?
Peak incidence: between 5-15 years. More common in the Far East, Middle East, eastern Europe and South America
The mean incidence is 19/100 000.
Despite the decline in incidence over time in the West, the incidence rates remain relatively high in non-Western countries
What are the presenting symptoms of Rheumatic Fever?
2–5 weeks after GAS infection- recent sore throat General: Fever Malaise Anorexia Joints: Painful, swollen, reduced movement/function Cardiac: Breathlessness, chest pain, palpitations
What are the signs of Rheumatic Fever on physical examination?
Duckett Jones criteria: Positive diagnosis if at least two major criteria, or one major plus two minor criteria are present
Major criteria:
- Arthritis: Migratory or fleeting polyarthritis with swelling, redness and tenderness of large joints
- Carditis: New murmur, e.g. Carey Coombs murmur (mid-diastolic murmur due to mitral valvulitis), pericarditis, pericardial effusion or rub, cardiomegaly, cardiac failure, ECG changes
- Chorea (Sydenhams): Rapid, involuntary, irregular movements with flowing or dancing quality. May be accompanied by slurred speech. More common in females
- Nodules: Small firm painless subcutaneous nodules seen on extensor surfaces, joints and tendons.
- Erythema marginatum (20% cases): Transient erythematous rash with raised edges, seen on trunk and proximal limbs. They may form crescent- or ring-shaped patches
Minor criteria:
- Pyrexia
- PMH rheumatic fever
- Arthralgia (only if arthritis is not present as major criteria)
- Recent streptococcal infection (supported by positive throat cultures or raised antistreptolysin O titre)
- Elevated inflammatory markers (ESR, CRP or WCC)
- Prolonged PR and QT intervals on ECG (only if carditis not present as major criteria)
What are the appropriate investigations for Rheumatic Fever?
Bloods:
-FBC (elevated WCC)
-Elevated ESR/CRP
-Elevated or rising antistreptolysin O titre
*Throat swab: Culture for GAS, rapid streptococcal antigen test
ECG:
-Prolonged PR interval is a minor criterion of acute rheumatic fever
-Features of pericarditis
-Arrhythmias
Echocardiogram:
-Pericardial effusion
-Myocardial thickening or dysfunction
-Valvulardysfunction
CXR: may demonstrate cardiomegaly and/or congestive cardiac failure
What is septic arthritis?
Joint inflammation resulting from intra-articular (occurring within a joint) infection
What is the aetiology of septic arthritis?
May be idiopathic, although in most cases, there is systemic infection allowing for haematogenous spread
Other causes are orthopaedic procedures, osteomyelitis, diabetes, immunosuppression, alcoholism
What are the common pathogens that cause septic arthritis?
Bacteria:
-Staphylococcus aureus, Mycobacterium tuberculosis (all ages)
-Strepotococcus pneumoniae, Strepotococcus pyogenes, Neisseria meningitidis (<4 years)
Mainly Neisseria gonorrhoea (16–40 years)
Viruses:
-Rubella
-Mumps
-Hepatitis B
Fungi: Candida
What are the risk factors for septic arthritis?
Underlying joint disease such as rheumatoid arthritis, osteoarthritis Joint prostheses Intravenous drug abuse Diabetes (increased risk of infection) Alcoholism
What is the epidemiology of septic arthritis?
Most common in children and the elderly
What are the presenting symptoms of septic arthritis?
Fever
Excruciating joint pain, redness, swelling and loss of joint function
Usually affecting single large joint- (polyarthritis in the immunosuppressed)
How does tuberculous arthritis present?
More insidious onset and is chronic
What are the signs of septic arthritis on physical examination?
Painful, hot, swollen and immobile joint with overlying erythema
Severe pain prevents passive movement
Pyrexia
Look for signs of aetiology- type of infective organism
What are the appropriate investigations for septic arthritis?
**Joint aspiration: Grossly purulent- send synovial fluid for cytology and microscopy
Bloods:
-FBC (raised WCC and neutrophils)
-raised CRP and ESR
-blood cultures for CMS
Plain joint radiographs:
Affected joint may initially be normal- assess joint damage in later films
MRI scan: Useful in detecting associated osteomyelitis
What is Sjögren’s syndrome?
A systemic autoimmune disorder characterised by the presence of dry eyes (keratoconjunctivitis sicca) and dry mouth (xerostomia) because of lymphocytic infiltration into the lacrimal and salivary glands
What are the risk factors for Sjögren’s syndrome?
Pre-existing conditions: -Systemic lupus erythematosus (SLE) -Rheumatoid arthritis -Systemic sclerosis (scleroderma) Family Hx
What class of HLA is associated with Sjögren’s syndrome?
HLA Class 2 markers
What is the epidemiology of Sjögren’s syndrome?
The most common of all systemic autoimmune rheumatic diseases.
Female-to-male ratio of 9:1
Population prevalence of between 0.5% and 1.56%
What are the presenting symptoms of Sjögren’s syndrome?
Fatigue
Dry eyes
Dry mouth
What are the signs of Sjögren’s syndrome on physical examination?
Vasculitis: skin rash Peripheral neuropathy (1/3rd of patients) Enlarged salivary glands Burning mouth (reduced salivary flow)
What are the appropriate investigations for Sjögren’s syndrome?
Schirmer’s test: positive
Antibodies to the ribonucleoproteins 60 kD Ro and La
Sialometry: decreased salivary flow
Parotid sialography: (x-ray with radioactive contrast) gross distortion of the normal pattern of parotid ductules
Minor salivary gland biopsy: mononuclear cell infiltrates
Angiography: for vasculitis (aneurysm, or smooth, tapering vessel stenosis)
Urinalysis: may show abnormal levels of phosphate, calcium, potassium, glucose (renal tubular acidosis)
What is Schirmer’s test?
Quantitatively measures tears- filter paper is placed in the lower conjunctival sac
The test is positive if less than 5 mm of paper is wetted after 5 minutes
What is Systemic lupus erythematosus (SLE)?
A chronic multi-system inflammatory autoimmune disorder that most commonly affects women during their reproductive years
What is the aetiology of SLE?
Combination of hormonal, genetic (HLA clustering) and exogenous factors (drugs)
What is the epidemiology of SLE?
Common- prevalence is 1–2 in 1000
More common in young people (15–45 years)
9 times more common in females
Disease is much more common and severe in those of African and Asian descent
What are the presenting symptoms of SLE?
General: Fever, fatigue, weight loss, lymphadenopathy, splenomegaly
Oral ulcers
Raynaud’s phenomenon
Alopecia: Hair thinning
Skin:
-Malar (butterfly) rash- primarily affects the cheeks and the bridge of the nose
-Photosensitive rash (appears after sun exposure)
-Discoid rash: erythematous raised patches
What are the musculoskeletal signs of SLE on physical examination?
Arthritis
Tendonitis
Myopathy
Avascular necrosis of femoral head
What are the cardiac signs of SLE on physical examination?
Pericarditis Myocarditis Arrhythmias Libman–Sacks endocarditis (non-infective mitral valve disease) Aortic valve lesions
What are the respiratory signs of SLE on physical examination?
Pleuritis
Pleural effusions
Basal atelectasis
Restrictive lung defects
What are the neurological signs of SLE on physical examination?
Headache Stroke Cranial nerve palsies Confusion Chorea (abnormal involuntary movement disorder) Fits Peripheral neuropathy
What are the psychological signs of SLE on physical examination?
Depression
Psychosis
What are the renal signs of SLE on physical examination?
Symptoms of glomerulonephritis:
- Hypertension
- Proteinuria (<3 g/24 h);
- Haematuria (microscopic or macroscopic, especially IgA nephropathy)
- Nephrotic syndrome -proteinuria
- Nephritic syndrome (haematuria, proteinuria, subcutaneous oedema, oliguria, hypertension, uraemia)
What are the appropriate investigations for SLE?
Bloods:
- FBC: anaemia, leukopenia, thrombocytopenia
- Activated PTT (prolonged)
- Elevated urea and creatinine
- Elevated ESR and CRP (latter is sometimes normal)
- Complement
- Antinuclear antibody (ANA) and Antiphospholipid antibodies : positive
Urine: Haematuria, proteinuria, microscopy (for casts). Joints: Plain radiographs: inflammation, non-erosive arthritis
Heart and lung: CXR (pleural effusion, infiltrates, cardiomegaly), ECG, echocardiogram, CT scan
Kidney: Renal biopsy (if glomerulonephritis suspected)
CNS: MRI scan, lumbar puncture
What is systemic sclerosis (scleroderma)?
A multi-system, autoimmune disease, characterised by functional and structural abnormalities of small blood vessels, fibrosis of skin and internal organs, and production of auto-antibodies
What is the aetiology of systemic sclerosis?
Unknown.
Genetic and environmental factors (e.g. vinyl chloride, epoxy resins) have been suggested
-Endothelial cells: endothelial cell damage, platelet activation, myointimal cell proliferation and narrowing of blood vessels
-Fibroblasts: lay down collagen in the dermis
What is the epidemiology of systemic sclerosis?
Age of onset 30–60 years
Three times more common in females
Annual incidence is one in 10 000
What are the presenting symptoms of systemic sclerosis?
Fatigue Initially swollen oedematous painful fingers Changes in pigmentation and finger ulcers Dry mouth Nausea, vomiting, anorexia Impotence Dyspnoea Dry cough
What are the skin signs of systemic sclerosis on physical examination?
Raynauds phenomenon
Initially swollen oedematous painful fingers
Later they become thickened, tight, shiny and bound to underlying structures
Changes in pigmentation
What are the facial signs of systemic sclerosis on physical examination?
Microstomia (puckering and furrowing of perioral skin)
Telangiecstasia (widened venules cause threadlike red lines on the skin)
What are the respiratory signs of systemic sclerosis on physical examination?
Pulmonary fibrosis leading to pulmonary hypertension
Dry crackles at lung bases
What are the cardiac signs of systemic sclerosis on physical examination?
Pericarditis or pericardial effusion
Myocardial fibrosis
Heart failure or arrhythmias
What are the GI signs of systemic sclerosis on physical examination?
Oesophageal dysmotility (dysphagia) Reflux oesophagitis Gastric paresis (nausea, vomiting, anorexia) Watermelon stomach Small bowel pseudo-obstruction Colonic hypomotility (constipation) Anal incontinence Angiodysplasia (small vascular malformation of the gut.)
What are the renal signs of systemic sclerosis on physical examination?
Hypertensive renal crisis
Chronic renal failure
What are the neuromuscular signs of systemic sclerosis on physical examination?
Trigeminal neuralgia
Muscular wasting or weakness
What are the appropriate investigations for systemic sclerosis?
*Serum auto-antibodies: positive ANA in more than 90% of patients
Bloods: may be normal, occasionally anaemic, elevated ESR and CRP, elevated serum urea and creatinine with scleroderma renal crisis
Serum muscle enzymes: elevated in scleroderma myopathy, muscle biopsy
Lung: CXR, pulmonary function tests (interstitial lung disease), CT scan
Heart: ECG, echocardiography (pulmonary HTN)
GI: Endoscopy, barium studies (diminished muscle tone), gastric/oesophageal scintigraphy
Kidney: U&E and measurement of creatinine clearance
Neuromuscular: Electromyography, nerve conduction studies, biopsy
Joints: Radiography (for subcutaneous calcification, flexion deformities)
What is Thyroiditis?
An autoimmune-mediated lymphocytic inflammation of the thyroid gland resulting in a destructive thyroiditis with release of thyroid hormone and transient thyrotoxicosis (hyperthyroidism)
This is frequently followed by a hypothyroid phase and full recovery
What is the aetiology of Thyroiditis?
Painless (lymphocytic) thyroiditis is part of the spectrum of autoimmune thyroid disease and considered by many to be a variant presentation of Hashimoto’s thyroiditis
It has been associated with HLA-DR3 and DR5
What is the epidemiology of Thyroiditis?
The condition is twice as likely to occur in women and can occur in all age groups, although the mean age of onset is in the 30s
Postnatal thyroiditis occurs after 7% of pregnancies
Also seen in patients treated with cytokines or biological agents
What are the risk factors for Thyroiditis?
Postnatal period Receiving immune-modulatory therapy Lithium therapy PMH of Type 1 DM and other autoimmune conditions Weaker RF: -Female sex -FH
What are the presenting symptoms of Thyroiditis?
Features of hyperthyroidism:
- Heat intolerance
- Nervousness
- Palpitations
- Weight loss
- Excessive fatigue
What are the signs of Thyroiditis on physical examination?
Small non-tender goitre
Features of hyperthyroidism (tachycardia) and then features of hypothyroidism (cold intolerance, poor concentration, weight gain)
What are the appropriate investigations for Thyroiditis?
Thyroid function tests:
- TSH: low TSH suggests thyrotoxicosis; elevated in hypothyroid phase
- Serum free T4 and T3: elevated in the thyrotoxic phase; low in the hypothyroid phase
- Thyroid Peroxidase antibodies: confirm autoimmune aetiology: frequently positive
- TSH-r antibodies: *distinguish between Graves’
4,6 or 24 hour radioiodine uptake: very low, usually <1% (Uptake elevated or within the normal range in Graves’ disease and toxic multinodular goitre)
Total T3/T4 ratio: when radioiodine uptake is contraindicated: distinguish thyroiditis from Graves’ disease and toxic nodular goitre: LOW
Others:
- Thyroid biopsy: rarely necessary, lymphocytic infiltrate
- techniteum 99pertechnetate: uptake scan
- serum thyroglobulin: elevated
- Colour flow doppler ultrasound: reduced flow (widely available but uncommonly used)
What is the management of Thyroiditis?
Thyrotoxic phase:
- Treatment may not be necessary for asymptomatic patients
- In symptomatic thyrotoxicosis: beta-blockers will ameliorate the tachycardia and tremulousness (or calcium-channel blocker)
- If not responding to treatment: systemic corticosteroids
Hypothyroid phase:
- Again may not be needed
- In moderate to severe: levothyroxine is given to normalise serum TSH concentrations
- In permanent hypothyroidism: levothyroxine should be continued indefinitely
Recurrent thyroiditis: Up to 11% of patients with sporadic painless thyroiditis will have recurrent thyroiditis
-Although it is rarely done, such patients may elect to have their thyroid gland ablated with radioiodine or surgically removed between episodes when they are euthyroid
What are the complications of Thyroiditis?
Arrhythmias: AF
Exacerbation of co-morbidities particularly ismchaemic heart disease and congestive heart failure (lower risk)
More likely to develop permanent hypothyroidism
Can also develop Graves’ disease, recurrent hyperthyroidism
What is the prognosis of Thyroiditis?
Most patients recover normal thyroid function:
- 6% remain permanently hypothyroid
- 1/3 have persistent goitre or thyroid peroxidase (TPO) antibodies
- Recurrent episodes are common postnatally (69%) but may also occur in up to 11% of patients with sporadic disease
What is tonsillitis?
An acute infection of the parenchyma of the palatine tonsils
What is the aetiology of tonsillitis?
Tonsillitis is usually viral but the most common bacterial pathogen is Group A beta-haemolytic streptococci.
Local inflammatory pathways result in oropharyngeal swelling, oedema, erythema, and pain
RF: contact with infected people in enclosed spaces
What is the epidemiology of tonsillitis?
Acute tonsillitis is more common in children between the ages of 5-15 years.
More common in winter and early spring although can occur at any time of the year
What are the presenting symptoms of tonsillitis?
Sudden onset of sore throat Headache Fever Pain on swallowing Presence of cough or runny nose Tonsillar enlargement Associated nausea and vomiting
What are the signs of tonsillitis on physical examination?
Tonsillar exudate (purulent “discharge/pus milky looking”)
-particularly when caused by Group A beta-haemolytic streptococci
Tonsillar erythema
Tonsillar enlargement
Enlarged anterior cervical lymph nodes
What are the appropriate investigations for tonsillitis?
Throat culture
Rapid streptococcal antigen test
Bloods: WCC, CRP, ESR
*Important to establish whether the patient has acute tonsillitis and not another cause of sore throat (retropharyngeal abscess or infectious mononucleosis)
What is the management of tonsillitis?
Analgesia
Antibiotics- penicillin is still first choice
Corticosteroids (dexamethasone)
Tonsillectomy may be considered for patients who have recurrent symptoms of tonsillitis and no other explanation for recurrent symptoms
What are the complications of tonsillitis?
Scarlet fever (diffuse erythematous rash from delayed skin reactivity produced by Streptococcus species)
Acute sinusitis
Acute Otitis media
What are the features of the rash produced by Scarlet fever?
The rash blanches with pressure and has multiple small papules.
It generally starts on the head and neck, and is associated with circumoral (around mouth) pallor and a strawberry tongue.
It subsequently spreads to the trunk, sparing the palms and soles, and is more marked over the skin folds
What is the prognosis for a patient with tonsillitis?
Acute tonsillitis is an acute, self-limiting infective condition that normally resolves completely within 1 week.
In vulnerable people tonsillitis may run a more severe course. Antibiotics and/or admission to hospital for a limited period of time may be advisable
Some patients may also develop recurrent tonsillitis; tonsillectomy may be considered in these cases
What is Tuberculosis?
An infectious granulomatous disease caused by Mycobacterium tuberculosis
*notifiable disease
What is the aetiology of TB?
M. tuberculosis is an intracellular organism (also known as acid-fast bacilli, AFB) which survives after being phagocytosed by macrophages
*predominantly in the upper lobes
What is the epidemiology of TB?
According to WHO, TB is the 9th leading cause of death worldwide, and is the leading cause of death from a single infectious agent
Both the very young (age <5 years) and older people are at increased risk for progression to disease
*Incidence in Asian immigrants >30 times native UK white population
What are the risk factors for TB?
Exposure to infection Birth in a high rid country e.g. Asia, Latin America, and Africa HIV Immunosuppressive medication IV drug use Malnutrition
What are the pulmonary presenting symptoms for TB?
*TB is a multi-system disease- but can be LATENT Primary TB: -Mostly asymptomatic* -May have fever -Malaise -Cough -Wheeze Miliary TB: -Fever -Weight loss -Meningitis -Yellow caseous tubercles spread to other organs (e.g. in bone and kidney may remain dormant for years) Post-primary TB: -Fever/night sweats -Malaise -Weight loss -Breathlessness -Cough, sputum, haemoptysis -Pleuritic pain
What are the signs of TB on physical examination?
Signs of pleural effusion, collapse, consolidation, fibrosis (abnormal chest auscultation and percussion)
Wheeze
Erythema nodosum and phlyctenular conjunctivitis (allergic manifestations)
What are the other features of TB?
Lymph nodes: Suppuration (acute onset of tender) cervical lymph nodes leading to abscesses or sinuses, which discharge pus and spread to skin (scrofuloderma).
CNS: Meningitis, tuberculoma
Skin: Lupus vulgaris (jellylike reddish-brown glistening plaques)
Heart: Pericardial effusion, constrictive pericarditis
Gastrointestinal: Subacute obstruction, change in bowel habit, weight loss, peritonitis, ascites
Genitourinary: UTI symptoms, renal failure, epididymitis, endometrial or tubal involvement, infertility
Adrenal: Insufficiency
Bone/joints: Osteomyelitis, arthritis, paravertebral abscesses and vertebral collapse (Potts disease), spinal cord compression from abscesses.
What are the appropriate investigations for TB?
*CXR: fibronodular opacities in upper lobes with or without cavitation (hilar lymphadenopathy)
Sputum smear: positive for acid-fast bacilli (AFB)
Sputum culture: positive for Mycobacterium tuberculosis
DNA or RNA amplification tests for rapid diagnosis: +ve
Bloods:
-Latent: exposure of host T cells to TB antigens causes release of interferon
-Active: Raised WCC, low Hb
Bronchoscopy and bronchoalveolar lavage: positive for AFB
*Gastric aspirate if unable to produce sputum
What is a urinary tract infection (UTI)?
An inflammatory reaction of the urinary tract epithelium in response to pathogenic micro-organisms, most commonly bacteria
What is the aetiology of a UTI?
UTIs result from pathogenic organisms gaining access to the urinary tract and not being effectively eliminated
The bacteria ascend the urethra and generally have an intestinal origin; therefore, Escherichia coli causes most UTIs in men and women
What are the classifications of UTIs?
Uncomplicated: normal renal tract structure and function
Complicated: structural/functional abnormality of genitourinary tract, eg obstruction, catheter, stones, neurogenic bladder, renal transplant
What are the risk factors for a UTI?
- Increased bacterial inoculation:
- Sexual activity
- Urinary incontinence
- Faecal incontinence
- Constipation - Increased binding of uropathogenic bacteria:
- Spermicide use
- Reduced oestrogen
- Menopause - Reduced urine flow:
- Dehydration
- Obstructed urinary tract - Increased bacterial growth:
- Diabetes Mellitus
- Immunosuppression
- Obstruction
- Stones
- Catheter
- Renal tract malformation
- Pregnancy
What is the epidemiology of UTIs?
All patient-care settings identify UTI as the most common infection
The ratio of UTI occurrence between institutionalised women and men is almost equal (2 to 3:1), unlike the ratio for younger women and men (25:1)
What are the presenting symptoms of a UTI?
Cystitis: Frequency, dysuria, urgency, suprapubic pain, polyuria, haematuria.
Acute pyelonephritis: Fever, rigor, vomiting, loin pain/tenderness, costovertebral pain, associated cystitis symptoms, septic shock
Prostatitis:
-Pain: perineum, rectum, scrotum, penis, bladder, lower back.
Fever, malaise, nausea, urinary symptoms, swollen or tender prostate on PR*
What are the types of lower UTIs?
Bladder (cystitis)
Prostate (prostatitis)
What are the types of upper UTIs?
Pyelonephritis = infection of kidney/renal pelvis
What are the signs of a UTI on physical examination?
Fever
Abdominal or loin tenderness
Check for a distended bladder, enlarged (tender) prostate
*If vaginal discharge, consider Pelvic inflammatory disease
What are the appropriate investigations for a UTI?
Dipstick urinalysis: positive leukocyte esterase and/or nitrite (avoid using in pregnant women)
*(MSU) Urine culture and microscopy: leukocytes and/or bacteria (≥10^2 CFU/mL)- Use in pregnant women, men, children
Bloods: (if systemically unwell) FBC, U&E, CRP, and blood culture (positive in only 10–25% of pyelonephritis)
Imaging:
-Consider USS (rules out obstruction) and referral to urology for assessment in men with upper UTI; failure to respond to treatment; recurrent UTI (>2/year); pyelonephritis; persistent haematuria
-CT renal tract: perirenal abscess, urinary calculi, or tumours
-CT Kidneys, Ureter and Bladder: urinary tract stone, abscess
*consider urogram for those who have voiding dysfunction without a clearly identifiable cause such as BPH or failure to treatment
What is the overall management of a UTI?
The goal of treatment: eradication of bacteria through antibiotics
There are different guidelines for the different populations that can be affected by UTIs
What is the management of a UTI in a non-pregnant woman?
If 3 or more symptoms (or 1 severe) of cystitis, and no vaginal discharge: treat empirically with 3-day course of trimethoprim, or nitrofurantoin (if eGFR >30)
- If first-line empirical treatment fails, culture urine and treat according to antibiotic sensitivity.
- In upper UTI, take a urine culture and treat initially with a broad-spectrum antibiotic according to local guidelines/sensitivities, eg co-amoxiclav.
What is the management of a UTI in a pregnant woman?
*Get expert help
UTI in pregnancy is associated with preterm delivery and intrauterine growth restriction
Asymptomatic bacteriuria should be confirmed on a second sample
Treat with an antibiotic- local guidance advice for antibiotic choice (avoid ciprofloxacin, trimethoprim in 1st trimester, nitrofurantoin in 3rd trimester)
Confirm eradication.
What is the management of a UTI in a man?
Treat lower UTI with a 7-day course of trimethoprim or nitrofurantoin (if eGFR >30)
- If symptoms suggest prostatitis (pain in pelvis, genitals, lower back, buttocks) consider a longer (4-week) course of a fluoroquinolone (eg ciprofloxacin) due to ability to penetrate prostatic fluid
- If upper or recurrent UTI, refer for urological investigation
What is the management of a UTI in a patient with a catheter?
All catheterized patients are bacteriuric
Send MSU only if symptomatic (symptoms of UTI may be non-specific/atypical)
Possible symptoms:
Fever, flank/ suprapubic pain, change in voiding pattern, vomiting, confusion, sepsis
-Change long-term catheter before starting an antibiotic.
-Where possible use a narrow-spectrum antibiotic according to culture sensitivity.
What are the complications of UTIs?
Prostatitis
Pyelonephritis
*Renal function impairment: RF include prostatitis, obstruction, the presence of stones, and the presence of indwelling catheters
*Sepsis
What is the prognosis for a UTI?
In the absence of a complicated UTI, antibiotic therapy is more effective and results in fewer failures
Younger patients have a better prognosis
Older patients often have a complicated UTI
What is Urticaria?
A skin condition characterised by erythematous, blanching, oedematous, non-painful, pruritic lesions that typically resolve within 24 hours and leave no residual markings
What is the aetiology of Acute Urticaria?
Many cases of acute urticaria are allergic in nature and caused by an IgE-mediated reaction
The most common agents involved are drugs (e.g., penicillins, sulfonamides, muscle relaxants, diuretics, NSAIDs) and foods (e.g., milk, eggs, peanuts, tree nuts, finfish, shellfish). Insect bites can also lead to acute urticaria
Non-IgE-mediated mechanisms can also be responsible and these cases tend to involve certain drugs (e.g., NSAIDs, opioids, vancomycin), radiocontrast dye, or acute viral infections (especially in children)
What is the aetiology of Chronic Urticaria?
Approximately 40% of cases are thought to be autoimmune in nature, while many cases are idiopathic
individuals with acute or chronic urticaria experience spontaneous and unpredictable lesions
What is the epidemiology of Urticaria?
The life-time prevalence for acute urticaria is approximately 20%.
While the majority of these cases are acute and self-limiting events, roughly 30% of people will go on to experience prolonged symptoms
Acute urticaria is more common in children and adolescents than in adults, while chronic urticaria more typically affects adults
In chronic urticaria, women are affected more often than men
What are the presenting symptoms/signs of Urticaria?
Erythematous oedematous lesions that may be distributed on any part of the body
Typically pruritic, although occasionally patients may report a painful or burning sensation
Generally resolve within 24h
Swelling of the face, tongue or lips (up to 40% of cases of urticaria have associated angio-oedema)
*Urticarial lesions blanch when palpated:
Non-blanching lesions should raise suspicion for vasculitis
What are the appropriate investigations for Urticaria?
Mainly for chronic urticaria
Bloods:
-FBC: may provide evidence of occult infection, anaemia, or findings suggestive of chronic illness
-Metabolic profile: May provide evidence of chronic illness, such as hepatitis or nephritis
-ESR and CRP: non-specific elevation
-anti-Ig E antibodies: reassures both the patient and the physician that there are no exogenous factors causing the condition
-Antithyroid/antinuclear antibodies: exclude thyroid/rheumatic causes of chronic illness
Skin biopsy: may show urticarial vasculitis in setting of atypical urticarial lesions
What is Varicella Zoster?
Primary infection is called varicella (chickenpox)
Reactivation of the dormant virus in the dorsal root ganglia, causes zoster (shingles)
What is the aetiology of Varicella Zoster?
VZV is an herpes ds-DNA virus
Highly contagious, transmission is by aerosol inhalation or direct contact with the vesicular secretions
What is the epidemiology of Varicella Zoster?
Chickenpox peak incidence occurs at 4–10 years
Shingles peak incidence occurs at >50 years
About 90% of adults are VZV IgG positive (previously infected)
What are the presenting symptoms of Varicella Zoster?
*Incubation period 14–21 days
Chickenpox:
-Prodromal malaise
-Mild pyrexia
-Sudden appearance of intensely itchy spreading rash affecting the face and trunk more than the extremities, the oropharynx, conjunctivae and genitourinary tract
-As vesicles weep and crust over, new vesicles appear
-Contagious from 48 h before the rash and until all the vesicles have crusted over (within 7–10 days)
Shingles:
-May occur after a period of stress
-Tingling/hyperaesthesia in a dermatomal distribution, followed by painful skin lesions
Recovery in 10–14 days
What are the signs of Varicella Zoster on physical examination?
Chickenpox (disseminated varicella):
-Macular papular rash evolving into crops of vesicles with areas of weeping (exudate) and crusting (vesicles, macules, papules and crusts may all be present at one time)
-Skin excoriation (from scratching)
-Mild pyrexia
Shingles:
-Vesicular macular papular rash, in a dermatomal distribution
-Skin excoriation
What are the appropriate investigations for Varicella Zoster?
*Clinical diagnosis: typical vesicular rash at different stages, with pruritus, fever, malaise
Others:
-Vesicle fluid: Electron microscopy, direct immunofluorescence, cell culture, viral PCR (all
rarely necessary)
-Chickenpox: Consider HIV testing especially in adults with prior history of varicella infection
What is Vasculitides?
Vasculitis is the inflammation and necrosis of blood vessels (autoimmune disorders)
What is the classification of primary vasculitides?
Large: Giant cell arteritis (GCA), Takayasus aortitis (TA).
Medium: Polyarteritis nodosa (PAN), Kawasakis disease (KD)
Small: Churg–Strauss syndrome (CSS), microscopic polyangiitis (MP), Wegeners granulomatosis (WG)
What is eosinophilic granulomatosis with polyangiitis?
A rare autoimmune condition that causes inflammation of small and medium-sized blood vessels in persons with a history of airway allergic hypersensitivity (atopy). Also called Churg–Strauss syndrome (small)
What is granulomatosis with polyangiitis?
Inflammation of the blood vessels in your nose, sinuses, throat, lungs and kidneys. Formerly called Wegener’s granulomatosis (small)
What is the aetiology of Vasculitides?
Unknown- thought to be of autoimmune origin
Immune complex deposition in vessel walls triggers classical complement activation and inflammation
What infection is Polyarteritis nodosa associated with?
Hepatitis B infection
What is the epidemiology of Vasculitides?
Annual incidence of small vessel vasculitis is 1 in 10000
TA is more common in Japanese young females, PAN may affect any age (M:F is 2 : 1)
What are the presenting symptoms of Vasculitides?
Constitutional symptoms (whole body): malaise, fever, arthralgia, myalgia- may develop these months before specific signs
- The large vessel vasculitides have classical clinical patterns resulting from the vessels affected
- Medium and small vessel vasculitides are characterized by multiorgan involvement with less specific clinical features
What are the presenting symptoms/signs of Large Vessel Vasculitides on physical examination?
Headache and tenderness (GCA)
Visual changes
Upper extremity or jaw claudication
Asymmetric brachial pulses
What are possible features of all types of Vasculitides?
General: Fever, night sweats, malaise, weight loss
Skin: Rash (vasculitic, purpuric, maculopapular)
Joint: Arthralgia or arthritis
GI: Abdominal pain, haemorrhage from mucosal ulceration, diarrhoea
Kidney: Glomerulonephritis, renal failure
Lung: Dyspnoea, cough, chest pain, haemoptysis, lung haemorrhage
CVS: Pericarditis, coronary arteritis, myocarditis, heart failure, arrhythmias
CNS: Mononeuritis multiplex, infarctions, meningeal involvement
Eyes: Retinal haemorrhage, cotton wool spots
What are features of Takayasus aortitis (TA)?
Constitutional upset Head or neck pain Tenderness over affected arteries (aorta and the major branches) Dizziness and fainting Reduced peripheral pulses Hypertension
What are features of Polyarteritis nodosa?
Microaneurysms Thrombosis Infarctions (e.g. causing GI perforations) Hypertension Testicular pain
What are features of granulomatosis with polyangiitis?
Granulomatous vasculitis of upper and lower respiratory tract Nasal discharge Ulceration and deformity Haemoptysis Sinusitis Corneal thinning Glomerulonephritis
What are features of eosinophilic granulomatosis with polyangiitis?
Asthma
Eosinophilia
What are features of microscopic polyangiitis?
Non-specific with multiple organs affected
Glomerulonephritis with no glomerular Ig deposits
What are the appropriate investigations for Vasculitides?
Bloods: FBC (normocytic anaemia, raised platelets, raised neutrophils), raised ESR/CRP, elevated urea and creatinine (glomerulonephritis)
Autoantibodies: *anti-neutrophil cytoplasmic autoantibodies (ANCA)
Urine: Haematuria, proteinuria. Red cell casts
CXR: Diffuse, nodular or flitting shadows. Atelectasia (collapse of lung tissue with loss of volume)
Biopsy: Renal, lung (transbronchial), temporal artery (in GCA)
Angiography: To identify aneurysms (in PAN)
What is the management for Varicella Zoster?
Chickenpox (primary infection):
- Children: Treat symptoms (calamine lotion, analgesia, antihistamines)
- Adults: Consider acyclovir if within 24 h of rash onset especially if elderly, smoker, immunocompromised or pregnant (especially second or third trimester)
Shingles (reactivation):
- Aciclovir, valaciclovir or famciclovir if within 72 h of appearance of the rash if elderly, immunocompromised or ophthalmic involvement.
- Low-dose amitriptyline may benefit those with moderate/severe discomfort
- Simple analgesia (paracetamol)
Prevention:
- VZIG(immunoglobulin blood product that is offered to individuals at high risk of severe chickenpox) may be indicated in the immunosuppressed and in pregnant women exposed to varicella zoster
- Chickenpox vaccine is licensed in the United Kingdom, but no guidelines available for appropriate use
What are the complications of Varicella Zoster?
Chickenpox:
- Secondary infection e.g. Pneumonia, encephalitis, cerebellar syndrome, congenital varicella syndrome
- Scarring
Shingles:
- Postherpetic neuralgia
- Zoster opthalmicus (rash involves opthalmic division of trigeminal nerve)
- Ramsay Hunts syndrome (bilateral facial weakness)
- Sacral zoster may lead to urinary retention
- Motor zoster (muscle weakness of myotome at similar level as involved dermatome)
What is the prognosis of Varicella Zoster?
Depends on the complications
Worse in pregnancy, the elderly and immunocompromised
What is Viral hepatitis?
An infection with the RNA viruses, hepatitis A (HAV) or hepatitis E virus (HEV), that is not associated with chronic liver disease
What is the aetiology of Viral hepatitis?
Both are small non-enveloped single-stranded linear RNA viruses of 7500 nucleotides, with transmission by the faecal–oral route
Both viruses replicate in hepatocytes and are secreted into bile (resistant to bile lysis due to lack of a lipid envelope)
Liver inflammation and hepatocyte necrosis is caused by the immune response, with targeting of infected cells by CD8+ T cells and natural killer cells
Transmitted via close contact with an infected person or by contact with contaminated food or water products
What is the epidemiology of Viral hepatitis?
HAV is endemic in Asia, Africa and Central America, infection often occurs sub-clinically
In the developed world, better sanitation means that seroprevalence is lower, age of exposure is older and hence is more likely to be symptomatic
What are the presenting symptoms of Viral hepatitis?
Incubation period for HAV or HEV is 3–6 weeks
Prodromal period:
-Malaise, anorexia (distaste for cigarettes in smokers), fever, nausea and vomiting
Hepatitis:
-Prodrome followed by dark urine, pale stools and jaundice lasting 3 weeks
-Occasionally, itching and jaundice last several weeks in HAV infection (owing to cholestatic hepatitis)
What are the signs of Viral hepatitis on physical examination?
Pyrexia
Jaundice
Tender hepatomegaly- spleen may be palpable (20%)
*Absence of stigmata of chronic liver disease, although a few spider naevi may appear, transiently
What are the appropriate investigations for Viral hepatitis?
Bloods:
-LFTs: SIGNIFCANTLY ELEVATED AST and ALT, raised bilirubin, raised AlkPhos)
-Elevated ESR
-In severe cases, reduced albumin and elevated platelets
Viral serology:
-Hepatitis A: Anti-HAV IgM (during acute illness, disappearing after 3–5 months)
-Anti-HAV IgG (recovery phase and lifelong persistence)
-Hepatitis E: Anti-HEV IgM (“ 1–4 weeks after onset of illness)
-Anti-HEV IgG. Hepatitis B and C viral serology is also necessary to rule out these infections
Urinalysis: Positive for bilirubin, raised urobilinogen
What is the management for Viral hepatitis?
No specific management but there is post prophylactic exposure:
-Active or passive immunisation is available for protection following exposure to hepatitis A virus
Bed rest and symptomatic treatment (e.g. antipyretics, antiemetics)
Colestyramine for severe pruritus
What are the prevention measures for Viral hepatitis?
Public health:
-Safe water
-Sanitation
-Food hygiene standards
*Both are notifiable diseases
-Personal hygiene and sensible dietary precautions when travelling
Immunization (HAV only):
-Passive immunization with IM human immunoglobulin is only effective for a short period
-Active immunization with attenuated HAV vaccine offers safe and effective immunity for those travelling to endemic areas, high-risk individuals (e.g. residents of institutions)
What are the complications of Viral hepatitis?
Fulminant hepatic failure develops in 0.1% cases of HAV, 1 or 2% of HEV but up to 20% in pregnant women
Cholestatic hepatitis with prolonged jaundice and pruritus may develop after HAV infection
Post-hepatitis syndrome: Continued malaise for weeks to months
What is the prognosis of Viral hepatitis?
Recovery is usual within 3–6 weeks
Occasionally, a relapse during recovery
There are no chronic sequelae
*Fulminant hepatic failure carries an 80% mortality (greater risk in pregnant women)
