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ID Flashcards

1
Q

what causes genital warts?

A

human papillomavirus HPV, especially types 6 & 11.

It is now well established that HPV (primarily types 16,18 & 33) predisposes to cervical cancer.

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2
Q

How is genital warts managed?

A

topical podophyllum or cryotherapy are commonly used as first-line treatments depending on the location and type of lesion
multiple, non-keratinised warts are generally best treated with topical agents
solitary, keratinised warts respond better to cryotherapy

imiquimod is a topical cream that is generally used second line

genital warts are often resistant to treatment and recurrence is common although the majority of anogenital infections with HPV clear without intervention within 1-2 years

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3
Q

What is Amoebiasis?

A

Amoebiasis is caused by Entamoeba histolytica (an amoeboid protozoan) and spread by the faecal-oral route. It is estimated that 10% of the world’s population is chronically infected. Infection can be asymptomatic, cause mild diarrhoea or severe amoebic dysentery. Amoebiasis also causes liver and colonic abscesses.

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4
Q

What are the symptoms of amoebic dysentry?

A

profuse, bloody diarrhoea
there may be a long incubation period
stool microscopy may show trophozoites if examined within 15 minutes or kept warm (known as a ‘hot stool’)
treatment
oral metronidazole
a ‘luminal agent’ (to eliminate intraluminal cysts) is recommended usually as well e.g. diloxanide furoate

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5
Q

What are the symptoms, investigations and management of amoebic liver abscess?

A

usually a single mass in the right lobe (may be multiple). The contents are often described as ‘anchovy sauce’

features
fever
right upper quadrant pain
systemic symptoms e.g. malaise
hepatomegaly

investigations
ultrasound
serology is positive in > 95%

management
oral metronidazole
a ‘luminal agent’ (to eliminate intraluminal cysts) is recommended usually as well e.g. diloxanide furoate

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6
Q

What is Azoles?
What is the mechanism of action and what are the adverse effects?

A

Antifungal
Mechanism of action - Inhibits 14α-demethylase which produces ergosterol

Adverse effects - P450 inhibition, liver toxicity

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7
Q

What is Amphotericin B, what are the mechanisms of actions, what are the adverse effects?

A

An anti-fungal

mechanism of action - Binds with ergosterol forming a transmembrane channel that leads to monovalent ion (K+, Na+, H+ and Cl) leakage

adverse effects - nephrotoxicity, flu-like symptoms, hypokalaemia, hypomagnaseamia

Used for systemic fungal infections

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8
Q

What is Terbinafine?
Mechanism of action and uses?

A

anti fungal
Mechanism of action - inhibits squalene epoxidase

Commonly used in oral form to treat fungal nail infections

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9
Q

what is Griseofulvin? what is the mechanism of action and what are the adverse effects?

A

antifungal

mechanism of action - interacts with microtubules to disrupt mitotic spindle

advers effects - induced P450 system, teratogenic

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10
Q

What is flucytosine and what is the mechanism of action and what are the side effects?

A

anti fungal

mechanism of action - Converted by cytosine deaminase to 5-fluorouracil, which inhibits thymidylate synthase and disrupts fungal protein synthesis

Adverse effects - vomiting

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11
Q

what is capsofungin? what is the mechanism of action and adverse effects?

A

anti fungal

Mechanism of action - inhibits synthesis of beta gluten, a major fungal cell wall component

adverse effects - flushing

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12
Q

what is the mechanism of action of nystatin?

A

Binds with ergosterol forming a transmembrane channel that leads to monovalent ion (K+, Na+, H+ and Cl) leakage

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13
Q

what is strongyloides stercoralis?

A

Strongyloides stercoralis is a human parasitic nematode worm. The larvae are present in soil and gain access to the body by penetrating the skin. Infection with Strongyloides stercoralis causes strongyloidiasis.

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14
Q

what are the features of strongyloides stercoralis?

A

diarrhoea
abdominal pain/bloating
papulovesicular lesions where the skin has been penetrated by infective larvae e.g. soles of feet and buttocks
larva currens: pruritic, linear, urticarial rash
if the larvae migrate to the lungs a pneumonitis similar to Loeffler’s syndrome may be triggered

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15
Q

what is the treatment for stongyloides stericoralis?

A

Ivermectin and albendazole

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16
Q

what indicated to a campylobacter infection over others?

A

it is characterised by a prodrome - headache, fatugue, myalgic

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17
Q

what is campylobacter?

A

Campylobacter is the commonest bacterial cause of infectious intestinal disease in the UK. The majority of cases are caused by the Gram-negative bacillus Campylobacter jejuni. It is spread by the faecal-oral route and has an incubation period of 1-6 days.

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18
Q

what are the features of campylobacter ?

A

prodrome: headache malaise
diarrhoea: often bloody
abdominal pain: may mimic appendicitis

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19
Q

what is the management of campylobacter?

A

usually self-limiting
the BNF advises treatment if severe or the patient is immunocompromised. Antibiotics are recommended if severe symptoms (high fever, bloody diarrhoea, or more than eight stools per day) or symptoms have lasted more than one week
the first-line antibiotic is clarithromycin
ciprofloxacin is an alternative although the BNF states that ‘Strains with decreased sensitivity to ciprofloxacin isolated frequently’

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20
Q

what is the onset of symptoms in salmonella and e.coli infections?

A

48-72 hours

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21
Q

what are the complications of campylobacter?

A

Guillain-Barre syndrome may follow Campylobacter jejuni infections
reactive arthritis
septicaemia, endocarditis, arthritis

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22
Q

What is the most common organism found in central line infections?

A

Staphylococcus epidermidis

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23
Q

what are some basic facts about staphylococci?

A

Gram-positive cocci
facultative anaerobes
produce catalase

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24
Q

what are the main two subtypes of staphylococci?

A

Staoh aureus - coagulase positive, causes skin infections (e.g. cellulitis), abscesses, oestomyelitis, toxic shock syndrome.

Staph epidermidis - coagulase negative, cause of central line infections and infective endocarditis

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25
Q

what is leptospirosis?

A

Leptospirosis is caused by the spirochaete Leptospira interrogans (serogroup L. icterohaemorrhagiae), classically being spread by contact with infected rat urine.
common in sewage workers, farmers, vets

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26
Q

what are the features of leptospirosis?

A

the early phase is due to bacteraemia and lasts around a week
may be mild or subclinical
fever
flu-like symptoms
subconjunctival suffusion (redness)/haemorrhage

second immune phase may lead to more severe disease (Weil’s disease)
acute kidney injury (seen in 50% of patients)
hepatitis: jaundice, hepatomegaly
aseptic meningitis

Bilateral calf and sacral myalgia is commonly seen

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27
Q

what are the investigations of leptospirosis?

A

serology: antibodies to Leptospira develop after about 7 days
PCR
culture
growth may take several weeks so limits usefulness in diagnosis
blood and CSF samples are generally positive for the first 10 days
urine cultures become positive during the second week of illness

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28
Q

How is Leptospirosis managed?

A

high dose ben pen or doxycycline

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29
Q

what kind of virus is Epstein-barr virus?

A

Herpes viruses

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30
Q

What malignancies are associated with EBV?

A

Burkitt’s lymphoma*
Hodgkin’s lymphoma
nasopharyngeal carcinoma
HIV-associated central nervous system lymphomas

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31
Q

Aciclovir

Mechanism of action:
Indications
Adverse effects

A

Antiviral

MOA: Guanosine analog, phosphorylated by thymidine kinase which in turn inhibits the viral DNA polymerase

indications : HSV, VZV

Adverse effects: Crystalline nephropathy

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32
Q

Ganciclovir

Mechanism of action:
Indications
Adverse effects

A

Antiviral

Mechanism of action : Guanosine analog, phosphorylated by thymidine kinase which in turn inhibits the viral DNA polymerase

indications: CMV

adverse effects: Myelosuppression/agranulocytosis

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33
Q

Ribavirin

Mechanism of action:
Indications
Adverse effects

A

antiviral

mechanism of action:
Guanosine analog which inhibits inosine monophosphate (IMP) dehydrogenase, interferes with the capping of viral mRNA

Indications: Chronic hepatitis C, RSV

adverse effects: Haemolytic anaemia

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34
Q

Amantadine

Mechanism of action:
Indications
Adverse effects

A

anti-viral

mechanism - Inhibits uncoating (M2 protein) of virus in cell. Also releases dopamine from nerve endings

indications - Influenza, Parkinson’s disease

adverse effects - Confusion, ataxia, slurre

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35
Q

Oseltamivir

mechanism of action
indications

A

antiviral

mechanism of action - inhibits neuraminidase

Indications - influenza

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36
Q

Foscarnet

mechanisms of action
indications
adverse effects

A

Foscarnet

Mechanism of action - Pyrophosphate analog which inhibits viiral DNA polymerase

Indications - CMV, HSV if not responding to aciclovir

Adverse effects - Nephrotoxicity, hypocalcaemia, hypomagnasaemia, seizures

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37
Q

Interferon - a

mechanisms of action
indications
adverse effects

A

antiviral

mechanism of action - Human glycoproteins which inhibit synthesis of mRNA

indications - Chronic hepatitis B & C, hairy cell leukaemia

Adverse effects - Flu-like symptoms, anorexia, myelosuppression

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38
Q

Cidofovir

mechanism of action
indications
adverse effects

A

antiviral

mechanism of action - Acyclic nucleoside phosphonate, and is therefore independent of phosphorylation by viral enzymes (compare and contrast with aciclovir/ganciclovir)

indications - CMV retinitis in HIV

Adverse effects - nephrotoxicity

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39
Q

what are the anti-retroviral agent used in HIV ?

A

Nucleoside analogue reverse transcriptase inhibitors (NRTI)
examples: zidovudine (AZT), didanosine, lamivudine, stavudine, zalcitabine

Protease inhibitors (PI)
inhibits a protease needed to make the virus able to survive outside the cell
examples: indinavir, nelfinavir, ritonavir, saquinavir

Non-nucleoside reverse transcriptase inhibitors (NNRTI)
examples: nevirapine, efavirenz

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40
Q

what is lyme disease?

A

Lyme disease is caused by the spirochaete Borrelia burgdorferi and is spread by ticks

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41
Q

What are the early features of Lyme disease?

A

Early features (within 30 days)

erythema migrans
‘bulls-eye’ rash is typically at the site of the tick bite
typically develops 1-4 weeks after the initial bite but may present sooner
usually painless, more than 5 cm in diameter and slowlly increases in size
present in around 80% of patients.

systemic features
headache
lethargy
fever
arthralgia

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42
Q

What are the later features of Lyme disease?

A

Later features (after 30 days)

cardiovascular
heart block
peri/myocarditis

neurological
facial nerve palsy
radicular pain
meningitis

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43
Q

what are the investigations of Lyme disease?

A

NICE recommend that Lyme disease can be diagnosed clinically if erythema migrans is present
erythema migrans is therefore an indication to start antibiotics
enzyme-linked immunosorbent assay (ELISA) antibodies to Borrelia burgdorferi are the first-line test
if negative and Lyme disease is still suspected in people tested within 4 weeks from symptom onset, repeat the ELISA 4-6 weeks after the first ELISA test. If still suspected in people who have had symptoms for 12 weeks or more then an immunoblot test should be done
if positive or equivocal then an immunoblot test for Lyme disease should be done

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44
Q

how do you manage asymptomatic tick bites?

A

tick bites can be a relatively common presentation to GP practices, and can cause significant anxiety
if the tick is still present, the best way to remove it is using fine-tipped tweezers, grasping the tick as close to the skin as possible and pulling upwards firmly. The area should be washed following.
NICE guidance does not recommend routine antibiotic treatment to patients who’ve suffered a tick bite

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45
Q

How is Lyme disease managed?

A

doxycycline if early disease (amoxicillin can be used if doxy is contraindicated)

ceftriaxone if disseminated disease

Jarisch-Herxheimer reaction is sometimes seen after initiating therapy: fever, rash, tachycardia after first dose of antibiotic (more commonly seen in syphilis, another spirochaetal disease)

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46
Q

What is Trypanosmiasis?

A

Two main form of this protozoal disease are recognised - African trypanosomiasis (sleeping sickness) and American trypanosomiasis (Chagas’ disease).

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47
Q

what are the features of African Trypanosomiasis?

A

Two forms of African trypanosomiasis, or sleeping sickness, are seen - Trypanosoma gambiense in West Africa and Trypanosoma rhodesiense in East Africa. Both types are spread by the tsetse fly. Trypanosoma rhodesiense tends to follow a more acute course.

Trypanosoma chancre - painless subcutaneous nodule at site of infection
intermittent fever
enlargement of posterior cervical lymph nodes
later: central nervous system involvement e.g. somnolence, headaches, mood changes, meningoencephalitis

The reversal of the sleep wake cycle is typical of trypanosomiasis (African sleeping sickness) and can be accompanied by behavioural changes.

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48
Q

How is African trypanosomiasis managed?

A

early disease: IV pentamidine or suramin
later disease or central nervous system involvement: IV melarsoprol

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49
Q

what is American typanosomiasis?

A

American trypanosomiasis, or Chagas’ disease, is caused by the protozoan Trypanosoma cruzi. The vast majority of patients (95%) are asymptomatic in the acute phase although a chagoma (an erythematous nodule at site of infection) and periorbital oedema are sometimes seen. Chronic Chagas’ disease mainly affects the heart and gastrointestinal tract
myocarditis may lead to dilated cardiomyopathy (with apical atophy) and arrhythmias
gastrointestinal features includes megaoesophagus and megacolon causing dysphagia and constipation

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50
Q

how is American trypanosomiasis managed?

A

treatment is most effective in the acute phase using azole or nitroderivatives such as benznidazole or nifurtimox
chronic disease management involves treating the complications e.g., heart failure

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51
Q

How is TB managed?

A

Initial phase - first 2 months (RIPE)
Rifampicin
Isoniazid
Pyrazinamide
Ethambutol (the 2006 NICE guidelines now recommend giving a ‘fourth drug’ such as ethambutol routinely - previously this was only added if drug-resistant tuberculosis was suspected)

Continuation phase - next 4 months
Rifampicin
Isoniazid

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52
Q

how is latent TB managed?

A

The treatment for latent tuberculosis is 3 months of isoniazid (with pyridoxine) and rifampicin OR 6 months of isoniazid (with pyridoxine)

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53
Q

How is meningeal TB managed?

A

Patients with meningeal tuberculosis are treated for a prolonged period (at least 12 months) with the addition of steroids

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54
Q

who is directly observed therapy indicated in TB?

A

Directly observed therapy with a three times a week dosing regimen may be
indicated in certain groups, including:
homeless people with active tuberculosis
patients who are likely to have poor concordance
all prisoners with active or latent tuberculos

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55
Q

What are the complications of TB management?

A

Immune reconstitution disease
occurs typically 3-6 weeks after starting treatment
often presents with enlarging lymph nodes

Drug adverse effects
rifampicin
potent liver enzyme inducer
hepatitis, orange secretions
flu-like symptoms

isoniazid
peripheral neuropathy: prevent with pyridoxine (Vitamin B6)
hepatitis, agranulocytosis
liver enzyme inhibitor

pyrazinamide
hyperuricaemia causing gout
arthralgia, myalgia
hepatitis

ethambutol
optic neuritis: check visual acuity before and during treatment

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56
Q

what kind of bacteria is gonorrhoea ?

A

Gram-negative diplococcus Neisseria gonorrhoeae.

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57
Q

what is the incubation period or gonorrhoea?

A

2-5 days

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58
Q

what are the features of gonorrhoea?

A

males: urethral discharge, dysuria
females: cervicitis e.g. leading to vaginal discharge
rectal and pharyngeal infection is usually asymptomati

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59
Q

How is Gonorrhoea managed?

A

ciprofloxacin used to be the treatment of choice. However, there is increased resistance to ciprofloxacin (around 36% in the UK) and therefore cephalosporins are now more widely used
there was a change in the 2019 British Society for Sexual Health and HIV (BASHH) guidelines. Previously the first-line treatment was IM ceftriaxone + oral azithromycin. The new first-line treatment is a single dose of IM ceftriaxone 1g (i.e. no longer add azithromycin). If sensitivities are known (and the organism is sensitive to ciprofloxacin) then a single dose of oral ciprofloxacin 500mg should be given
if ceftriaxone is refused (e.g. needle-phobic) then oral cefixime 400mg (single dose) + oral azithromycin 2g (single dose) should be used

60
Q

What is the bacteria which causes BV?

A

predominately anaerobic organisms such as Gardnerella vaginalis.

61
Q

what are the features of BV

A

vaginal discharge: ‘fishy’, offensive
asymptomatic in 50%

62
Q

what criteria is used for diagnosing BV?

A

Amsel’s criteria for diagnosis of BV - 3 of the following 4 points should be present

thin, white homogenous discharge
clue cells on microscopy: stippled vaginal epithelial cells
vaginal pH > 4.5
positive whiff test (addition of potassium hydroxide results in fishy odour)

63
Q

How is BV managed?

A

asymptomatic - treatment not required

symptomatic - metronidazole 5-7 days
relapse rate > 50% in 3 months
single dose of 2g of metro can be used

if pregnant - increased risk of preterm labour, low birth rate, and chorioamnionitis, late miscarriage

64
Q

what are examples of tetracyclines?

A

doxycycline
tetracycline

65
Q

how do tetracyclines work?

A

protein synthesis inhibitors
binds to 30S subunit blocking binding of aminoacyl-tRNA

66
Q

what is the mechanism of resistance of tetracyclines ?

A

increased efflux of the bacteria by plasmid-encoded transport pumps, ribosomal protection

67
Q

what are some indications for tetracyclines?

A

acne vulgaris
Lyme disease
Chlamydia
Mycoplasma pneumoniae

68
Q

what are the notable adverse effects of tetracyclines?

A

discolouration of teeth: therefore should not be used in children < 12 years of age
photosensitivity
angioedema
black hairy tongue

69
Q

what is botulism?

A

Clostridium botulinum
gram positive anaerobic bacillus
7 serotypes A-G
produces botulinum toxin, a neurotoxin which irreversibly blocks the release of acetylcholine
may result from eating contaminated food (e.g. tinned) or intravenous drug use
neurotoxin often affects bulbar muscles and autonomic nervous system

70
Q

what are the features of Botulism?

A

patient usually fully conscious with no sensory disturbance
flaccid paralysis
diplopia
ataxia
bulbar palsy

71
Q

what is the treatment used for botulism?

A

botulism antitoxin and supportive care
antitoxin is only effective if given early - once toxin has bound its actions cannot be reversed

72
Q

what is Leprosy?

A

Leprosy is a granulomatous disease primarily affecting the peripheral nerves and skin. It is caused by Mycobacterium leprae.

73
Q

what are the features of leprosy?

A

patches of hypopigmented skin typically affecting the buttocks, face, and extensor surfaces of limbs
sensory loss

74
Q

what are the types of leprosy?

A

Low degree of cell mediated immunity → lepromatous leprosy (‘multibacillary’)
extensive skin involvement
symmetrical nerve involvement

High degree of cell mediated immunity → tuberculoid leprosy (‘paucibacillary’)
limited skin disease
asymmetric nerve involvement → hypesthesia
hair loss

75
Q

how is leprosy managed?

A

WHO-recommended triple therapy: rifampicin, dapsone and clofazimine

76
Q

what is anthrax?

A

Anthrax is caused by Bacillus anthracis, a Gram positive rod. It is spread by infected carcasses. It is also known as Woolsorters’ disease. Bacillus anthracis produces a tripartite protein toxin
protective antigen
oedema factor: a bacterial adenylate cyclase which increases cAMP
lethal factor: toxic to macrophages

77
Q

how is anthrax managed?

A

the current Health Protection Agency advice for the initial management of cutaneous anthrax is ciprofloxacin

further treatment is based on microbiological investigations and expert advice

77
Q

what are the features of anthrax?

A

causes painless black eschar (cutaneous ‘malignant pustule’, but no pus)
typically painless and non-tender
may cause marked oedema
anthrax can cause gastrointestinal bleeding

78
Q

How is syphilis diagnosed?

A

non-treponemal tests
not specific for syphilis, therefore may result in false positives (see below)
based upon the reactivity of serum from infected patients to a cardiolipin-cholesterol-lecithin antigen
assesses the quantity of antibodies being produced
becomes negative after treatment
examples include: rapid plasma reagin (RPR) and Venereal Disease Research Laboratory (VDRL)

treponemal-specific tests
generally more complex and expensive but specific for syphilis
qualitative only and are reported as ‘reactive’ or ‘non-reactive’
examples include: TP-EIA (T. pallidum enzyme immunoassay), TPHA (T. pallidum HaemAgglutination test)
the TP-EIA test has become increasingly popular in recent years

79
Q

what does a negative non-trepnoemal test + positive treponema test indicate?

A

successfully treated syphilis

80
Q

what does a Positive non-treponemal test + negative treponemal test indicate?

A

consistent with a false-positive syphilis result e.g. due to pregnancy or SLE (see list above)

81
Q

What is the incubation period of Syphillis?

A

9-90 days

82
Q

What are the primary features of Syphillis?

A

chancre - painless ulcer at the site of sexual contact
local non-tender lymphadenopathy
often not seen in women (the lesion may be on the cervix)

83
Q

What are the secondary features of syphilis?

A

systemic symptoms: fevers, lymphadenopathy
rash on trunk, palms and soles
buccal ‘snail track’ ulcers (30%)
condylomata lata (painless, warty lesions on the genitalia )

84
Q

What are tertiary features of Syphilis?

A

gummas (granulomatous lesions of the skin and bones)
ascending aortic aneurysms
general paralysis of the insane
tabes dorsalis
Argyll-Robertson pupil

85
Q

What are the features of congenital syphilis?

A

blunted upper incisor teeth (Hutchinson’s teeth), ‘mulberry’ molars
rhagades (linear scars at the angle of the mouth)
keratitis
saber shins
saddle nose
deafness

86
Q

What are gram positive and gram negative bacteria?

A

Gram-positive cocci = staphylococci + streptococci (including enterococci)
Gram-negative cocci = Neisseria meningitidis + Neisseria gonorrhoeae, also Moraxella catarrhalis

Therefore, only a small list of Gram-positive rods (bacilli) need to be memorised to categorise all bacteria - mnemonic = ABCD L
Actinomyces
Bacillus anthracis (anthrax)
Clostridium
Diphtheria: Corynebacterium diphtheriae
Listeria monocytogenes

Remaining organisms are Gram-negative rods, e.g.:
Escherichia coli
Haemophilus influenzae
Pseudomonas aeruginosa
Salmonella sp.
Shigella sp.
Campylobacter jejuni

87
Q

what is the incubation period of measles

A

10-14 days

88
Q

What is Measels?

A

an RNA paramyxovirus

89
Q

What are the features of Measles?

A

prodromal phase
irritable
conjunctivitis
fever

Koplik spots
typically develop before the rash
white spots (‘grain of salt’) on the buccal mucosa

rash
starts behind ears then to the whole body
discrete maculopapular rash becoming blotchy & confluent
desquamation that typically spares the palms and soles may occur after a week

diarrhoea occurs in around 10% of patients

90
Q

Which cause of pneumonia is associated with cold sores?

A

Streptococcus pneumoniae commonly causes reactivation of the herpes simplex virus resulting in ‘cold sores’

91
Q

which type of pneumonia is classically seen in alcoholics?

A

Klebsiella

92
Q

what are thread worms?

A

small, white parasitic nematodes that primarily inhabit the human gastrointestinal tract

93
Q

what is cutaneous larva migrans?

A

Cutaneous larva migrans is a dermatological condition prevalent in tropical and subtropical regions, largely attributable to cutaneous penetration and subsequent migration of nematode larvae, primarily from the Ancylostoma genus (e.g. Ancyclostoma braziliense). Typically, the transmission vectors are faecal-contaminated soil or sand, posing significant risks to individuals with a history of barefoot beach visits or direct soil contact.

94
Q

what is enteric fever?

A

Typhoid/parathyphoid
Typhoid and paratyphoid are caused by Salmonella typhi and Salmonella paratyphi (types A, B & C) respectively. They are often termed enteric fevers, producing systemic symptoms such as headache, fever, arthralgia.

transmitted via the faecal-oral route

95
Q

what are the features of Enteric fever?

A

initially systemic upset as above
relative bradycardia
abdominal pain, distension
constipation: although Salmonella is a recognised cause of diarrhoea, constipation is more common in typhoid
rose spots: present on the trunk in 40% of patients, and are more common in paratyphoid

96
Q

what are the complications of enteric fever?

A

osteomyelitis (especially in sickle cell disease where Salmonella is one of the most common pathogens)
GI bleed/perforation
meningitis
cholecystitis
chronic carriage (1%, more likely if adult females)

97
Q

what are characteristic features of streptococcus pneumonia?

A

rapid onset
high fever
pleuritic chest pain
herpes labialis (cold sores)

98
Q

what would be seen on a bacterial CSF analysis?

A

appearance - cloudy
Glucose - low
Protein - high
white cells - 10-5000 polymorphs

99
Q

what would you see in a viral CSF analysis ?

A

appearance - clear/cloudy
Glucose - 60-80% of plasma glucose
Protein - normal or raised
White cells 15-1000 lymphocytes

100
Q

What would you see in TB CSF analysis?

A

Appearance - slight cloudy, fibrin web
glucose - low (<1/2 plasma)
protein - high (>1g/l)
White cells - 30 -300 lymphocytes

101
Q

What would you see in fungal CSF analysis ?

A

appearance - cloudy
Glucose - low
Protein - high
White cells - 20 -200 lymphocytes

102
Q

Which type of viral meningitis may have characteristically low glucose CSF level

A

mumps meningitis

103
Q

What is Toxoplasmosis ?

A

Toxoplasma gondii is an obligate intracellular protozoan that infects the body via the gastrointestinal tract, lung or broken skin. It’s oocysts release trophozoites which migrate widely around the body including to the eye, brain and muscle. The usual animal reservoir is the cat, although other animals such as rats carry the disease.

104
Q

What are the symptoms of toxoplasmosis?

A

In immunocompetent patients - most are asymptomatic, some may have a self limiting infection - clinical features resembling infectious mononucleosis. Other less common manifestations include meningoencephalitis and myocarditis.

HIV/immunocompramised patients - Cerebral toxoplasmosis accounts for around 50% of cerebral lesions in patients with HIV
constitutional symptoms, headache, confusion, drowsiness

Immunosuppressed patients may also develop a chorioretinitis secondary to toxoplasmosis.

105
Q

How is toxoplasmosis investigated?

A

serology is the investigation of choice

cerebral toxoplasmosis - CT shows ingle or multiple ring-enhancing lesions, mass effect may be seen

106
Q

How is toxoplasmosis managed?

A

No treatment is usually required unless the patient has a severe infection or is immunosuppressed.

cerebral toxoplasmosis - pyrimethamine plus sulphadiazine for at least 6 weeks

107
Q

what are the effects of congenital toxoplasmosis?

A

neurological damage
cerebral calcification
hydrocephalus
chorioretinitis

ophthalmic damage
retinopathy
cataracts

108
Q

What are exotoxins and endotoxins?

A

Exotoxins are secreted by bacteria where as endotoxins are only released following lysis of the cell. Exotoxins are generally released by Gram positive bacteria with the notable exceptions of Vibrio cholerae and some strains of E. coli

109
Q

How are exotoxins classified?

A

pyrogenic toxins
enterotoxins
neurotoxins
tissue invasive toxins
miscellaneous toxins

110
Q

What is the action of pyrogenic toxins?

A

Pyrogenic toxins stimulate the release of endogenous cytokines resulting in fever, rash etc. They are superantigens which bridge the MHC class II protein on antigen-presenting cells with the T cell receptor on the surface of T cells resulting in massive cytokine release.

111
Q

Which bacteria release Pyrogenic toxins?

A

Staphylococcus aureus
Toxic shock syndrome (TSST-1 superantigen) toxin
Results in high fever, hypotension, exfoliative rash

Streptococcus pyogenes
Streptococcal pyrogenic exotoxin A & C
Results in scarlet fever

112
Q

What is the action of enterotoxins ?

A

Enterotoxins act on the gastrointestinal tract causing one of two patterns of illness:
diarrhoeal illness
vomiting illness (‘food poisoning’)

113
Q

Which organisms release enterotoxins?

A

Vibrio cholerae
Cholera toxin
Causes activation of adenylate cyclase (via Gs) leading to increases in cAMP levels, which in turn leads to increased chloride secretion and reduced sodium absorption

Shigella dysenteriae
Shiga toxin
Inactivates 60S ribosome → epithelial cell death

Escherichia coli
1. Heat labile toxin
Activates adenylate cyclase (via Gs), increasing cAMP → watery diarrhoea
2. Heat stabile toxin
Activates guanylate cyclase, increasing cGMP → watery diarrhoea

Staphylococcus aureus
Staphylococcus aureus enterotoxin
Vomiting and diarrhoeal illness lasting < 24 hours

Bacillus cereus
Cereulide
Potent cytotoxin that destroys mitochondria. Causes a vomiting illness which may present within 4 hours of ingestion

114
Q

What is the action of Neurotoxins?

A

Neurotoxins act on the nerves (tetanus) or the neuromuscular junction (botulism) causing paralysis.

115
Q

What organisms release neurotoxins?

A

Clostridium tetani
Tetanospasmin
Blocks the release of the inhibitory neurotransmitters GABA and glycine resulting in continuous motor neuron activity → continuous muscle contraction → lockjaw and respiratory paralysis

Clostridium botulinum
Botulinum toxin
Blocks acetylcholine (ACh) release leading to flaccid paralysis

116
Q

What organisms release tissue invasive toxins?

A

Clostridium perfringens
α-toxin, a lecithinase
Causes gas gangrene (myonecrosis) and haemolysis

Staphylococcus aureus
Exfoliatin
Staphylococcal scalded skin syndrome

117
Q

What toxin does Corynebacterium diphtheriae release ?

A

Diphtheria toxin
ADP ribosylates elogation factor (EF-2), resulting in inhibition, causing a ‘diphtheric membrane’ on tonsils caused by necrotic mucosal cells. Systemic distribution may produce necrosis of myocardial, neural and renal tissue

118
Q

What toxin does pseudomonas aeruginosa release?

A

Exotoxin A
ADP ribosylates elogation factor (EF-2), resulting in inhibition, causing a ‘diphtheric membrane’ on tonsils caused by necrotic mucosal cells. Systemic distribution may produce necrosis of myocardial, neural and renal tissue

119
Q

What exotoxin doe Bacillus anthraces release?

A

Oedema factor (EF) Forms a calmodulin-dependent adenylate cyclase which increases cAMP, impairing the function of neutrophils/macrophages → reduced phagocytosis

120
Q

What endotoxin does bodetella pertussis release ?

A

Pertussis exotoxin Inhibits Gi leading to increases in cAMP levels, impairing the function of neutrophils/macrophages → reduced phagocytosis

121
Q

what are endotoxins?

A

Endotoxins are lipopolysaccharides that are released from Gram-negative bacteria such as Neisseria meningitidis.

122
Q

What are the most common causes of meningitis in 0-3 months?

A

Group B Streptococcus (most common cause in neonates)
E. coli
Listeria monocytogenes

123
Q

What are the most common causes of meningitis in 3months - 6 years?

A

Neisseria meningitidis
Streptococcus pneumoniae
Haemophilus influenzae

124
Q

What is the most common cause of meningitis in 6 years to 60 ?

A

Neisseria meningitidis
Streptococcus pneumoniae

125
Q

What is the most common causes of meningitis > 60 years >?

A

Streptococcus pneumoniae
Neisseria meningitidis
Listeria monocytogenes

126
Q

most common cause meningitis in the immunosupressed?

A

Listeria monocytogenes

127
Q

what kind of bacteria is Neiseria meningitis?

A

gram negative diplococci.

128
Q

What kind of bacteria is S.pmeumonia?

A

gram positive diplococci/chain

129
Q

What kind of bacteria is E.coli?

A

gram negative bacilli

130
Q

what kind of bacteria if H.influenzae?

A

gram negative coccobacailli

131
Q

what kind of bacteria in L.monocytogenes?

A

gram positive rod

132
Q

Which anti-fungal is commonly used to treat nail fungal infections?

A

Terbinafine

133
Q

What is yellow fever?

A

A type of viral hemorrhagic fever
Zoonotic infection - spread by aedes mosquitos
Incubation period 2-14 days

134
Q

what are examples of hemorrhagic fever?

A

yellow fever
Dengue fever
Lassa fever
Ebola

135
Q

what are the features of yellow fever?

A

may cause mild flu-like illness lasting less than one week
classic description involves sudden onset of high fever, rigors, nausea & vomiting. Bradycardia may develop. A brief remission is followed by jaundice, haematemesis, oliguria
if severe jaundice, haematemesis may occur
Councilman bodies (inclusion bodies) may be seen in the hepatocytes

136
Q

what is considered severe falciparum malaria?

A

High parasitaemia (>2%)
Hypoglycaemia
Severe anaemia
Renal failure
Pulmonary oedema
Metabolic acidosis
Abnormal bleeding
Multiple convulsions
Seizures
Shock

137
Q

how do you manage severe falciparum?

A

Severe falciparum, malaria IV artesunate
Non-severe falciparum malaria oral artesunate combination therapy (ACT)
Non-falciparum malaria oral ACT or chloroquine if not resistant

138
Q

what are the general features of falciparum malaria?

A

Fever - the hallmark of malaria, typically cyclical
Sweating and riggers
GI - vomiting, abdo pain, diarrhoea, mild jaundice
Cough and mild tachypnoea
body aches
Neurological - headache, dizziness
Tachycardia
thrombocytopenia, mild anaemia

139
Q

What IV abx do you give for meningitis?

A

3 months - 50 years: BNF recommends cefotaxime (or ceftriaxone)
> 50 years: BNF recommends cefotaxime (or ceftriaxone) + amoxicillin (or ampicillin) for adults

139
Q

When should LP be delayed in suspected meningitis?

A

Lumbar puncture should be delayed in the following circumstances
signs of severe sepsis or a rapidly evolving rash
severe respiratory/cardiac compromise
significant bleeding risk
signs of raised intracranial pressure
focal neurological signs
papilloedema
continuous or uncontrolled seizures
GCS ≤ 12

If LP can not be done with in the first hour then IV abx should be given after blood cultures have been taken

140
Q

what are the stereotypical features of legionella?

A

flu-like symptoms and a dry cough, relative bradycardia and confusion. Blood tests may show hyponatraemia

pleural effusion seen in around 30% of patients

141
Q

what are the causes of pelvic inflammatory disease?

A

Chlamydia trachomatis: the most common cause
Neisseria gonorrhoeae
Mycoplasma genitalium
Mycoplasma hominis

142
Q

how is PID managed?

A

1st line - IM ceftriaxone followed by 14 days of oral doxy and oral metronidazole
2nd line - oral ofloxacin and oral metronidazole

143
Q

what are the complications of PID?

A

perihepatitis (Fitz-Hugh Curtis Syndrome)
occurs in around 10% of cases
it is characterised by right upper quadrant pain and may be confused with cholecystitis

infertility - the risk may be as high as 10-20% after a single episode

chronic pelvic pain

ectopic pregnancy

MRCP (18 decks)

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