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ID, GUM, HIV Flashcards

1
Q

what is the commonest cause of death for travellers in tropics

A

cardiovascular disease

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2
Q

what disease is most common in returning travellers from:
sub-saharan africa
SE asia + caribbean
SC asia

A

sub-saharan africa = malaria, rickettsial disease

SE asia + caribbean = dengue

SC asia = enteric fever

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3
Q

where are these diseases from:
malaria
dengue
enteric fever
rickettsial disease

A

malaria = sub-saharan africa
dengue = SC asia + caribbean
enteric fever = SC asia
rickettsial disease = sub-saharan africa

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4
Q

what key qs to ask in travel history

A

where - rural, urban
when - incubation period for pathogen, acute/chronic
what did you do - food, sex, tattoo/piercing, drugs
prophylaxis - antimalarials, vaccines

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5
Q

what diseases have __ incubation periods
short <10 days
medium 11-21 days
long 21+ days

A

short <10days: malaria (p.falciparum), enteric bacteria, dengue, pneumonia

medium 11-21 days: malaria (p.falciparum), typhoid, strongyloides

long 21+ days: malaria, viral hepatitis, amoebic liver disease

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6
Q

what diseases have low platelet count

A

dengue
enteric fever
HIV seroconversion
malaria
sepsis

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7
Q

when is CRP high + around 70

A

high = pyogenic infection, malaria

around 70 = viral infection

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8
Q

what causes malaria

A

protozoan parasite = plasmodium

p.falcifarum spread by bites of female anopheles mosquitoes (sub-Sahara)

p.falcifarum most common globally
p.vivax most common outside Africa

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9
Q

how do complicated + uncomplicated malaria differ

A

complicated = parasitaemia >10%
OR parasitaemia <2% + clinical signs

uncomplicated = parasitaemia <2% + no schizont + no clinical signs

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10
Q

what EIR (entomological inoculation rate) is stable + unstable

A

stable = EIR >10/yr
unstable = EIR <5/yr

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11
Q

how often do fever spikes occur in active malaria

A

every 48hr - fever spike corresponds with schizont rupture causing haemolytic anaemia

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12
Q

how does malaria present

A

recent travel to endemic country

pallor + jaundice = haemolytic anaemia
hepatomegaly

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13
Q

what is protective against malaria

A

HbS sickle cell trait - common in africa

Duffy group + ve protective to p.vivax infection (common outside Africa)

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14
Q

how is malaria diagnosed

A

giema stain on blood film = RBC lyse appearing blue/purple

peripheral blood film = identify parasitaemia (how many schizonts to determine parasite stage)

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15
Q

for uncomplicated malaria, how does it present + what are lab findings

A

uncomplicated = parasitaemia <2%, no schizont, no clinical signs

examination: fever, splenomegaly
no rash, no pharyngitis, no lymphadenopathy

investigations: thrombocytopenia, normal WCC - but lymphopenia (+ anaemia)

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16
Q

what are signs of complicated malaria

A

parasitaemia >10%
shock BP<90/60

DIC, spontaneous bleeding

impaired consciousness, seizures, hypoglycaemia
pulmonary oedema, ARDS
renal impairment, acidemia pH<7.3

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17
Q

what is enteric fever

A

typhoid + paratyphoid fevers
caused by salmonella typhi + paratyphi (types A,B,C)

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18
Q

what are key features of enteric fever

A

transmitted faeco-orally - from food or contaminated water
incubation period 5-21 days (as intracellular pathogen)

endemic to Indian subcontinent (S asia, africa, S america)

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19
Q

what is pathophysiology of enteric fever

A

after ingesting contaminated food/water, st.typhi penetrates intestinal mucosa
then replicates + enters bloodstream

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20
Q

how does enteric fever present

A

fever
abdo pain, diarrhoea/constipation

exam: rose spots, hepatosplenomegaly

non-specific: myalgia, headache, lethargy, anorexia

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21
Q

what resevoir is used for enteric fever

A

human intestinal tract

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22
Q

what lab results indicate enteric fever

A

lymphopenia (+ thrombocytopenia)

confirm diagnosis with bone marrow aspirate + culture

definitive diagnosis = culture
blood, stool, urine, rose spots, bone marrow

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23
Q

how is enteric fever managed

A

report to public health

IV ceftriazone for 10-14 days

supportive treatment - fluids, antipyretic, antiemetic

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24
Q

if untreated, what complication occur from enteric fever

A

wk3-4:
intestinal perforation/haemorrhage, cholecystitis

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25
what is primary + secondary immunocompromised
primary = congenital (rare) secondary - common iatrogenic (cytotoxic, radiation, long-term steroids) physiological (elderly, pregnancy, neonates, diabetes) autoimmune (SLE, RA) acquired - HIV splenectomy - trauma, functional asplenia toxicity - alcohol
26
how does immunosuppression affect __ neutrophil T cell B cell, immunoglobulin complement
neutropenia or defective neutrophil function - so reduced phagocytic capacity T-cell = cellular defect B-cell, immunoglobulin = humeral defect complement deficiency
27
how does immunosuppression affect local immune function
local immune function reduced, causing lymphoedema
28
how does immunosuppression present
FH PMH recurrent infections - involving opportunistic pathogens end organ damage (bronchiectasis) on immunosuppressive therapy - transplant, leukemia/myeloma
29
what is neutropenia
neutrophil count <0.5-1 10^9/l most severe if <0.1 for prolonged time common after chemotherapy most common form of immunosuppression seen in hospitals
30
how does neutropenia present
rigor if early - bacterial infection if prolonged - fungal infection pt then admitted to haematology ward
31
where does neutropenia commonly occur
mouth or gut (occurs due to lines or mucositis)
32
which bacteria cause neutropenia
line related - staph aureus, coag negative staph, pseudomonas mucositis causing - e.coli, enterococci
33
what fungal infections cause morbidity/mortality
candida/yeast - line related, can be cultured from blood aspergillus/molds - difficult to diagnose so needs bronchoscopy after prolonged neutropenia, presents as fungal balls in lungs
34
how are fungal infections treated
antifungals = fluconazole, amphotericin as both candida/yeast + aspergillum/moulds are line related = remove the line G-CSF given to improve neutrophil count
35
when is G-CSF used in treatment
improve neutrophil numbers
36
what causes functional asplenia
UC, coeliac, sickle cell, SLE, RA
37
if pt lacks spleen (from splenectomy - trauma, or from functional asplenia), what infections are they vulnerable to
pt vulnerable to encapsulated bacteria strep pneumonia, n.meningitidis, haemophilus influenza
38
how to prevent post-splenectomy infection
annual influenza vaccine immunisation - prior to surgery (pneumovax - for strep pneumonia haemophilus influenza B + meningitis C - for haemophilus influenza meningitis B, then meningitis ACWY a month later - for n.meningitidis) lifelong penicillin prophylaxis if high-risk (discontinue after 2yr if low-risk) home supply of amoxycillin
39
what organism causes PCP + how is it identified
pneumocystis jiroveci (fungus) occurs in 80% AIDS patients despite antibiotic prophylaxis silver stain from BAL
40
what are key features of PCP
fungus - unicellular eukaryote found globally causes infections in pt with underlying T cell disorders AIDS, CLL, lymphoproliferative disorders, post stem cell transplant, prolonged corticosteroid therapy
41
how is PCP treated
trimethoprim/sulfamethoxazole dapsone/clindamycin IV pentamidine steroids
42
when is PCP prophylaxis given
if HIV+ve with CD4 count <200 PCP prophylaxis given with HAART
43
what pathogens cause cell-mediated immunity defect (AIDS, lymphoma, immunosuppression, organ transplantation)
intracellular bacteria (listeria), mycobacteria fungi (cryptococcus, pneumocystis jiveroci) virus (EBV, CMV) protozoa (toxoplasma)
44
what is hypogammaglobulinaemia
CVID - common variable immune deficiency X-linked disease (so affects men more - X linked agammaglobulinaemia) mutation on X-chr affects btk gene (codes tyrosine kinase), mutating B-cell maturation
45
how does hypogammaglobulinaemia present
recurrent bacterial infections affecting sinuses and lungs - haemophilus influenza, pneumococci
46
what diseases present with altered levels immunoglobulins
hypogammaglobulinaemia (or XLA - x-linked agammaglobulinaemia) lymphoma myeloma
47
how is hypogammaglobulinaemia treated
IV immunoglobulins
48
what is complement deficiency
rare genetic disorder when child unable to form MAC responsible for killing capsulated organisms so presents as recurrent infections of same pathogen (eg pt had meningococcal meningitis + meningococcal septic arthritis from the same pathogen n.meningitidis)
49
what is the difference between colonisation + infection
colonisation = proliferating bacteria that don't cause host immune response infection = proliferating bacteria that cause host immune response
50
what is antimicrobial resistance
when micro-organism no longer responds to the drugs made to kill them
51
how to interrupt a chain of transmission
vaccinating, testing, isolating hand hygiene
52
what is hospital acquired CDI
pt who develops diarrhoea (c.diff infection) at least 48hr after admission
53
why are post-infection reviews done
to identify the cause of the infection (see whether it was avoidable or unavoidable) and come up with ways to prevent it spreading again
54
what are RF for multi-drug resistant organisms
antibiotic use urinary catheter, prosthetic materials (central line, drains, endotracheal tube) prolonged hospital stay age 60+ yr (care-home resident), immunocompromised travel, occupational exposure
55
what is the smart + focus approach for antibiotics
smart - don't start abx in the absence of bacterial infection focus - clinical review after 48-72hr
56
what drug class do vancomycin + gentamicin belong to
vancomycin = glycopeptide gentamicin = aminoglycoside
57
what are risks of giving abx IV
line infection, line misplacement endocarditis thrombosis
58
what are risks of treating asymptomatic bacteriuria
side effects of abx side effects of resistance
59
how do suspected + confirmed infection outbreaks differ
suspected = 2+ cases occurring in ward/bay in hospital without lab confirmation confirmed = 2+ cases occurring in ward/bay in hospital with lab confirmation
60
what does measles look like
morbiliform rash - generalised dusky red macules/papules
61
how does measles present
morbiliform rash (generalised red macule/papule) kolpik spots (small white patches inside buccal membrane) cough, corozya, conjunctivitis, kolpik spots fever >39oC + unvaccinated
62
how is measles managed
supportive therapy - no specific treatment inform PHE if admitted, needs isolation (encephalitis, pneumonitis, otitis media, carditis)
63
what is parvovirus 18 (erythrovirus)
only parvovirus to infect humans flu-like illness causes transient anaemia (if immunocompromised, becomes chronic)
64
how does provirus b19 (erythrovirus) present
rash + arthralgia slapped cheek appearance (erythema infectosum)
65
what happens if pregnant with provirus b19 (erythrovirus)
spontaneous abortion in 2nd trimester
66
how do coxsackie A16 virus (type of enterovirus) present
called 'hand, foot and mouth disease' starts with URTI - tired, sore throat, dry cough, fever then few days later, mouth ulcers (esp on tongue) + blistering red spots (pustular lesions) across body diagnosed based on appearance of rash + close contacts with similar symptoms (as highly contagious disease)
67
how is cosackie A16 virus managed
supportive management - fluids, analgesia (paracetamol) rash/illness resolve spontaneously within 10 days highly contagious disease (wash hands, don't share bedding) to avoid transmission
68
what is erythema nodosum
red lumps/knots across both shins (unlike cellulitis which is just 1) due to inflammed subcutaneous fat (panniculitis) on shins - hypersensitivity reaction
69
what are RF for erythema nodosum
young females during winter-spring recent strep pyogenes throat infection
70
what causes erythema nodosum
erythema nodosum is a hypersensitivity reaction due to other diseases: mainly - strep pyogenes throat infections other causes: [gastroenteritis, mycoplasma pneumonia, TB, pregnancy COCP, NSAID IBD, sarcoidosis, lymphoma, leukaemia] main chronic causes - IBD, sarcoidosis
71
how does erythema nodosum present
red, inflammed subcutaneous fat across both shins raised, painful/tender nodules
72
how is erythema nodosum diagnosed
clinical presentation investigations done to identify underlying cause (as EN is hypersensitivity reaction): bacterial throat swab - for strep throat infection faecal calprolectin - for IBD FBC, CRP/ESR, ASOT (Antistreptolysin O titer), glandular fever screen CXR - TB, sarcoidosis, lymphoma
73
how is erythema nodosum managed
investigate/treat underlying cause EN managed conservatively - rest, analgesia (+ steroids for inflammation) fully resolves within 6wk
74
what is erythema multiforme
erythematous rash caused by hypersensitivity reaction usually from - viral infection (herpes simplex virus, EBV), mycoplasma pneumonia, medications (NSAID, anticonvulsant) [malignancy, CVD]
75
how does erythema multiform present
widespread, itchy, erythematous rash - forms target lesions (darkest red ring in centre, surrounded by other rings) sore mouth = stomatitis
76
how is erythema multiform diagnosed
clinical diagnosis based on appearance of rash identify underlying cause recent cold sore = HSV if no clear underlying cause - do CXR = mycoplasma pneumonia
77
how is erythema multiform managed
mild, so resolves spontaneously within 1-4wks without treatment if severe = IV fluid, analgesia, steroids
78
how does rubella present
unvaccinated forehead rash spreading down to chest swollen LN - posterior articular + sub-occipital fever, headache, polyarthralgia
79
what causes dermatomally distributed rash with midline demaracation
shingles = herpes zoster
80
what is shingles
painful, unilateral vesicular rash spread across 1 dermatome occurs due to reactivation of VZV from dorsal root ganglion (if pt immunosuppressed)
81
how does shingles present
painful, unilateral, erythematous vesicular rash spread across 1 dermatome - usually lumbar/thoracic pain, fever, malaise hyperasthesia across area of rash - v.sensitive to touch/pain/pressure/temp (neurological condition)
82
how do chickenpox + shingles differ
chickenpox = generalised vesicular rash shingles = dermatomal vesicular rash
83
what is chickenpox
highly contagious generalised vesicular rash (not contagious when lesions scab over) caused by VZV spread via aerosols, droplets, contact transmission initially presents with fever, itch, general malaise then rash on trunk/face, spreading across body
84
how does chickenpox present
rash on trunk/face, spreading across body density reduces as it spreads out widespread, erythematous, raised vesicular lesions papules -> vesicles -> crusted (no longer contagious)
85
which areas are + aren't affected by chickenpox
rash starts on trunk/face then spreads across affects mouth not palms/soles
86
when do children become infectious with chickenpox
2 days before rash develops stop being infectious when lesions scab/crust over
87
how does ringworm present
painless, annular scaly lesions well-demarcated slowly enlarging
88
what is ringworm
fungal skin infection due to trichophyton fungus spread via contact (humans, animals, soil) on body = tinea corpis on head = tinea capitis (well demarcated hair loss, itchy/dry/erythematous scalp) on foot (athletes foot) = tinea pedis (flaky/cracked skin patches between toes, occurs when feet sweaty/damp for long periods) on nail = onchyomycosis (thick/discoloured nails)
89
how is ringworm diagnosed
clinical diagnosis can scrape off scales for M+C to confirm diagnosis (by identifying organism)
90
how is ringworm managed
anti-fungal cream - clotrimazole, miconazole oral anti-fungal - fluconazole, itracanazole shampoo for tinea capitis - ketoconazole
91
what is atypical lymphocytosis (seen on blood film)
large, misshapen lymphocytes with multiple nuclei
92
how do aminopenicillins affect EBV
aminopenicillins can worsen EBV rash, so need to be avoided
93
what is cellulitis
cut/abrasion disrupts skin barrier, so bacteria/pathogens enter acute bacterial skin infection (staph aureus, B-haemolytic strep) affects dermis + subcutaneous tissue occurs anywhere in body
94
how does cellulitis present
pain, redness, swelling anywhere on body - but usually LL fever, malaise
95
how is cellulitis diagnosed
clinical diagnosis only investigate if pt systemically unwell: skin swab - open wound, blood glucose - if diabetic x-ray - assess for osteomyelitis
96
how is cellulitis managed
if mild = oral abx (penicillin = strep, flucloxacillin = staph if pen-allergic = erythromycin/clarithromycin) if more severe - needs hospital admission, IV abx if group-A B-haemolytic strep = clindamycin

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