Infection and Immunology Flashcards

(332 cards)

1
Q

What is an Abscess?

A

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

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2
Q

What is the aetiology of Abscesses?

A

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)

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3
Q

What is the epidemiology of Abscess?

A

Common and have become more common in the last few years

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4
Q

What are the presenting symptoms of an Abscess?

A
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
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5
Q

What are the signs of an Abscess on physical examination?

A

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
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6
Q

What are the appropriate investigations for Abscess?

A
Bloods:
-FBC: leukocytosis
-CRP/ESR: inflammatory markers
Blood culture: positive for organism 
CT/Ultrasound: visualisation of abscess
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7
Q

What is anaphylaxis?

A

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

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8
Q

What is anaphylaxis characterised by?

A

Rapidly developing life-threatening airway and/or breathing and/or circulation problems
Usually associated with skin and mucosal changes

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9
Q

What is the aetiology of anaphylaxis?

A

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

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10
Q

What are the common allergens?

A

PILFERS

Peanuts 
Insect stings 
Latex 
Fish 
Egg 
Radiological contrast agents 
Shellfish
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11
Q

What is the epidemiology of anaphylaxis?

A

Relatively common

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12
Q

What are the presenting symptoms of anaphylaxis?

A

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

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13
Q

What are the signs of anaphylaxis on physical examination?

A
URTICARIA:
Urticaria 
Reduced BP 
Tachypnoea 
Infected conjunctiva and swollen eyes 
Cyanosis 
Audible wheeze 
Rhinitis 
Increased heart rate 
Airway swelling
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14
Q

What are the appropriate investigations for anaphylaxis? Interpret the results

A

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

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15
Q

What is the management plan for a patient with anaphylaxis?

A
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

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16
Q

What are the possible complications of anaphylaxis?

A

(RDS)
Respiratory failure
Death
Shock

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17
Q

What is the prognosis for patients with anaphylaxis?

A

Good if prompt treatment given

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18
Q

What is Behçet’s disease?

A

A rare disorder that causes blood vessel inflammation throughout the body (vasculitis)

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19
Q

What is the aetiology of Behçet’s disease?

A

Poorly understood but thought to be an autoimmune condition, may also be due to an infectious trigger

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20
Q

What are the risk factors for Behçet’s disease?

A

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

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21
Q

What is the epidemiology of Behçet’s disease?

A

RARE disorder
Genetic link
Commonly affects men and women in 20-30 year group but is more severe in men

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22
Q

What are the presenting symptoms and signs of Behçet’s disease on physical examination?

A

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

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23
Q

What are the appropriate investigations for Behçet’s disease?

A

*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

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24
Q

What is the management of Behçet’s disease?

A

Immunosuppression: corticosteroids

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25
What is candidiasis?
A fungal infection due to any type of Candida (type of yeast)
26
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
27
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
28
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 ```
29
What are the signs of a candidiasis infection on physical examination?
Rash Erythema Visible plaques/ulcers
30
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
31
What is Cellulitis?
An acute spreading infection of the skin with visually indistinct borders that principally involves the dermis and subcutaneous tissue
32
What is Cellulitis usually characterised by?
``` Erythema Oedema Warmth Tenderness Commonly occurs in an extremity ```
33
What is Erysipelas?
A distinct form of superficial cellulitis with notable lymphatic involvement and is raised, sharply demarcating it from uninvolved skin
34
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
35
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) ```
36
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
37
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 ```
38
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)
39
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
40
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 ```
41
What is the prognosis of Cellulitis?
Good with treatment
42
What is conjunctivitis?
Inflammation of the lining of the eyelids and eyeball
43
What is the aetiology of conjunctivitis?
``` Caused by: Bacteria Viruses Allergic or immunological reactions Mechanical irritation Medicines ``` Bacterial and viral conjunctivitis is highly contagious
44
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 ```
45
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) ```
46
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
47
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
48
What is Encephalitis?
Inflammation of the brain parenchyma
49
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)
50
What is the epidemiology of Encephalitis?
Annual UK incidence is 7.4 in 100,000
51
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
52
What are the signs of Encephalitis on physical examination?
Reduced level of consciousness with deteriorating GCS, seizures, pyrexia. Signs of meningism: Neck stiffness, photophobia, Kernig’s test positive. Signs of raised intracranial pressure: hypertension, bradycardia, papilloedema. Focal neurological signs. Minimental examination may reveal cognitive or psychiatric disturbances.
53
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
54
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
55
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)
56
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
57
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
58
What are the presenting symptoms of Epididymitis and Orchitis?
Gradual onset (unlike testicular torsion) Unilateral scrotal pain and swelling Other symptoms: fever, dysuria
59
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
60
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
61
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.
62
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 ```
63
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
64
What is Gastroenteritis?
Acute inflammation of the lining of the GI tract, manifested by nausea, vomiting, diarrhoea and abdominal discomfort
65
What is Infectious Colitis?
Inflammation of the colon due to a virus or bacteria
66
What is the aetiology of Gastroenteritis and Infectious Colitis?
Can be caused by viruses, bacteria, protozoa or toxins contained in contaminated food or water
67
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)
68
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
69
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
70
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 ```
71
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
72
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
73
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
74
What is the prognosis for Gastroenteritis and Infectious Colitis?
Generally good, as the majority of cases are self-limiting
75
What is Herpes Simplex Virus?
Disease resulting from HSV1 or HSV2 infection
76
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)
77
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
78
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
79
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
80
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
81
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
82
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)
83
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
84
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)
85
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
86
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)
87
What are the tumours that arise from HIV immunodeficiency?
Kaposi’s sarcoma (cutaneous or conjunctival vascular tumour caused by human herpesvirus) Squamous cell carcinoma (particularly cervical or anal) Non- Hodgkin’s B-cell lymphoma (brain, GI) Hodgkin’s lymphoma
88
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
89
What is Incision and drainage of an abscess?
A treatment for abscesses to relieve pain and speed healing
90
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
91
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)
92
What is infectious mononucleosis?
A clinical syndrome most commonly caused by Epstein Barr virus (EBV) infection, also known as glandular fever
93
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
94
What are the risk factors for infectious mononucleosis?
Close contact e.g. kissing, sharing eating utensils, sexual behaviour
95
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
96
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
97
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%)
98
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)
99
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
100
What is the aetiology of Infective Endocarditis?
The endocardium can be colonized by virtually any organism, but the most common are: 1. Streptococci (40%): Mainly a-haemolytic 2. Staphylococci(35%):Staphylococcusaureus 3. 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
101
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
102
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 ```
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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 (Roth’s spots) -Pharyngeal and conjunctival mucosa -Janeway lesions (painless palmar macules, which blanch on pressure) -Osler’s nodes (tender nodules on finger/toe pads) -Splinter haemorrhages (nail-bed haemorrhages)
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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
105
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 >38􏰂C) - Risk factors (abnormal valves, IV drug use, dental surgery) - Positive blood culture, but not major criteria - Positive echocardiogram, but not major criteria - Vascular signs
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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
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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) ```
108
What is the prognosis for Infective Endocarditis?
Fatal if untreated | Even when treated, 15–30% mortality (mortality is greater in older patients)
109
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
110
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
111
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
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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)
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What are the signs of Malaria on physical examination?
Pyrexia/rigors Anaemia Hepatosplenomegaly
114
What are the appropriate investigations for Malaria?
Thick/thin blood film (using Field’s or Giemsa’s 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
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What is mastitis?
Inflammation of the breast with or without infection
116
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)
117
What are the two types of mastitis with infection?
Lactational | Non-lactational
118
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)
119
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
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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
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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
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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
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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
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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)
125
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
126
What is Meningitis?
Inflammation of the meninges (pia mater and arachnoid) (coverings of the brain) most commonly caused by infection
127
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)
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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 ```
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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
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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) ```
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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 ```
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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
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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
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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) ```
135
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
136
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
137
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
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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
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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) ```
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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
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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
142
What is Necrotising fasciitis?
A life-threatening subcutaneous soft-tissue infection that may extend to the deep fascia, but not into the underlying muscle
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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)
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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 ```
145
What is the epidemiology of Necrotising fasciitis?
Type I (due to mixed anaerobic-facultative anaerobic infections) is more common than type II necrotising fasciitis
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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 ```
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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
148
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
149
What is sepsis?
A syndrome defined as life-threatening organ dysfunction due to a dysregulated host response to infection
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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
151
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
152
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
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What is the epidemiology of neutropenic sepsis?
The most common life-threatening complication of cancer therapy Higher incidence in patients with heamatological malignancy
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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
155
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 ```
156
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
157
What is osteomyelitis?
An inflammatory condition of bone caused by an infecting organism, most commonly Staphylococcus aureus
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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
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What is the most common pathogen implicated in osteomyelitis?
Staphylococcus aureus
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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 ```
161
What is the epidemiology of osteomyelitis?
Greater incidence in men than women | Risk increased with age particularly over 50
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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
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What are the signs of osteomyelitis on physical examination?
``` Local inflammation, erythema or swelling Reduced range of movement Reduced sensation (particularly in diabetic foot) ```
164
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
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What is Pericarditis?
Inflammation of the pericardium, may be acute, subacute or chronic
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What is the criteria for acute Pericarditis?
New-onset inflammation lasting <4-6 weeks
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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
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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) -Dressler’s syndrome (weeks to months after acute MI)
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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
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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
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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
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What are the signs of Constrictive Pericarditis (chronic) on physical examination?
Raised JVP with inspiration (Kussmaul’s 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
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What is Constrictive Pericarditis?
Impedes (delays) normal diastolic filling and can be a medium to late complication of acute pericarditis
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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)
175
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
176
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
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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
178
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
179
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
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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
181
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 ```
182
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
183
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
184
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
185
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
186
What is pneumonia?
Infection of distal lung parenchyma
187
How can be pneumonia be classified?
1. Community-acquired, hospital-acquired or nosocomial (originating in hospital) 2. Aspiration pneumonia, pneumonia in the immunocompromised 3. Typical and atypical (Mycoplasma, Chlamydia, Legionella) 4. Location: lobar
188
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)
189
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 ```
190
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
191
What is the most common causative organism of Pneumonia?
Streptococcus pneumoniae
192
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).
193
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 ```
194
What are the presenting symptoms of atypical pneumonia?
Headache, myalgia, diarrhoea/abdominal pain
195
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 ```
196
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)
197
What is the acid-fast bacilli test for?
A type of bacteria that causes tuberculosis
198
What is the management for pneumonia?
1. Assess severity 2. Start antibiotics: -Oral amoxicillin -Oral or IV amoxicillin and erythromycin -IV cefuroxime/cefotaxime/co-amoxiclav and erythromycin *switch to appropriate antibiotic as per sensitivity 3. 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 4. 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
199
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 ```
200
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
201
What is Rheumatic Fever?
An inflammatory (autoimmune) multisystem disorder, occurring following group A b-haemolytic streptococci (GAS) throat infection
202
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
203
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
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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 ```
205
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 (Sydenham’s): 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)
206
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
207
What is septic arthritis?
Joint inflammation resulting from intra-articular (occurring within a joint) infection
208
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
209
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
210
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 ```
211
What is the epidemiology of septic arthritis?
Most common in children and the elderly
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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)
213
How does tuberculous arthritis present?
More insidious onset and is chronic
214
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
215
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
216
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
217
What are the risk factors for Sjögren's syndrome?
``` Pre-existing conditions: -Systemic lupus erythematosus (SLE) -Rheumatoid arthritis -Systemic sclerosis (scleroderma) Family Hx ```
218
What class of HLA is associated with Sjögren's syndrome?
HLA Class 2 markers
219
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%
220
What are the presenting symptoms of Sjögren's syndrome?
Fatigue Dry eyes Dry mouth
221
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) ```
222
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)
223
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
224
What is Systemic lupus erythematosus (SLE)?
A chronic multi-system inflammatory autoimmune disorder that most commonly affects women during their reproductive years
225
What is the aetiology of SLE?
Combination of hormonal, genetic (HLA clustering) and exogenous factors (drugs)
226
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
227
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
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What are the musculoskeletal signs of SLE on physical examination?
Arthritis Tendonitis Myopathy Avascular necrosis of femoral head
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What are the cardiac signs of SLE on physical examination?
``` Pericarditis Myocarditis Arrhythmias Libman–Sacks endocarditis (non-infective mitral valve disease) Aortic valve lesions ```
230
What are the respiratory signs of SLE on physical examination?
Pleuritis Pleural effusions Basal atelectasis Restrictive lung defects
231
What are the neurological signs of SLE on physical examination?
``` Headache Stroke Cranial nerve palsies Confusion Chorea (abnormal involuntary movement disorder) Fits Peripheral neuropathy ```
232
What are the psychological signs of SLE on physical examination?
Depression | Psychosis
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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)
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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
235
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
236
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
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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
238
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 ```
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What are the skin signs of systemic sclerosis on physical examination?
Raynaud’s phenomenon Initially swollen oedematous painful fingers Later they become thickened, tight, shiny and bound to underlying structures Changes in pigmentation
240
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)
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What are the respiratory signs of systemic sclerosis on physical examination?
Pulmonary fibrosis leading to pulmonary hypertension | Dry crackles at lung bases
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What are the cardiac signs of systemic sclerosis on physical examination?
Pericarditis or pericardial effusion Myocardial fibrosis Heart failure or arrhythmias
243
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.) ```
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What are the renal signs of systemic sclerosis on physical examination?
Hypertensive renal crisis | Chronic renal failure
245
What are the neuromuscular signs of systemic sclerosis on physical examination?
Trigeminal neuralgia | Muscular wasting or weakness
246
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)
247
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
248
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
249
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
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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 ```
251
What are the presenting symptoms of Thyroiditis?
Features of hyperthyroidism: - Heat intolerance - Nervousness - Palpitations - Weight loss - Excessive fatigue
252
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)
253
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)
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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
255
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
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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
257
What is tonsillitis?
An acute infection of the parenchyma of the palatine tonsils
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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
259
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
260
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 ```
261
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
262
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)
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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
264
What are the complications of tonsillitis?
Scarlet fever (diffuse erythematous rash from delayed skin reactivity produced by Streptococcus species) Acute sinusitis Acute Otitis media
265
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
266
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
267
What is Tuberculosis?
An infectious granulomatous disease caused by Mycobacterium tuberculosis *notifiable disease
268
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
269
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
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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 ```
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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 ```
272
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)
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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 (Pott’s disease), spinal cord compression from abscesses.
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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
275
What is a urinary tract infection (UTI)?
An inflammatory reaction of the urinary tract epithelium in response to pathogenic micro-organisms, most commonly bacteria
276
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
277
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
278
What are the risk factors for a UTI?
1. Increased bacterial inoculation: - Sexual activity - Urinary incontinence - Faecal incontinence - Constipation 2. Increased binding of uropathogenic bacteria: - Spermicide use - Reduced oestrogen - Menopause 3. Reduced urine flow: - Dehydration - Obstructed urinary tract 4. Increased bacterial growth: - Diabetes Mellitus - Immunosuppression - Obstruction - Stones - Catheter - Renal tract malformation - Pregnancy
279
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)
280
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*
281
What are the types of lower UTIs?
Bladder (cystitis) | Prostate (prostatitis)
282
What are the types of upper UTIs?
Pyelonephritis = infection of kidney/renal pelvis
283
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
284
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
285
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
286
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.
287
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.
288
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
289
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.
290
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
291
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
292
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
293
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)
294
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
295
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
296
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
297
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
298
What is Varicella Zoster?
Primary infection is called varicella (chickenpox) | Reactivation of the dormant virus in the dorsal root ganglia, causes zoster (shingles)
299
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
300
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)
301
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
302
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
303
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
304
What is Vasculitides?
Vasculitis is the inflammation and necrosis of blood vessels (autoimmune disorders)
305
What is the classification of primary vasculitides?
Large: Giant cell arteritis (GCA), Takayasu’s aortitis (TA). Medium: Polyarteritis nodosa (PAN), Kawasaki’s disease (KD) Small: Churg–Strauss syndrome (CSS), microscopic polyangiitis (MP), Wegener’s granulomatosis (WG)
306
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)
307
What is granulomatosis with polyangiitis?
Inflammation of the blood vessels in your nose, sinuses, throat, lungs and kidneys. Formerly called Wegener's granulomatosis (small)
308
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
309
What infection is Polyarteritis nodosa associated with?
Hepatitis B infection
310
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)
311
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
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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
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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
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What are features of Takayasu’s aortitis (TA)?
``` Constitutional upset Head or neck pain Tenderness over affected arteries (aorta and the major branches) Dizziness and fainting Reduced peripheral pulses Hypertension ```
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What are features of Polyarteritis nodosa?
``` Microaneurysms Thrombosis Infarctions (e.g. causing GI perforations) Hypertension Testicular pain ```
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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 ```
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What are features of eosinophilic granulomatosis with polyangiitis?
Asthma | Eosinophilia
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What are features of microscopic polyangiitis?
Non-specific with multiple organs affected | Glomerulonephritis with no glomerular Ig deposits
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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)
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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
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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 Hunt’s syndrome (bilateral facial weakness) - Sacral zoster may lead to urinary retention - Motor zoster (muscle weakness of myotome at similar level as involved dermatome)
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What is the prognosis of Varicella Zoster?
Depends on the complications | Worse in pregnancy, the elderly and immunocompromised
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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
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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
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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
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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)
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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
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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
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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
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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)
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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
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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)