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402 > ID, GUM, HIV > Flashcards

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
Q

what is primary + secondary immunocompromised

A

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

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26
Q

how does immunosuppression affect __
neutrophil
T cell
B cell, immunoglobulin
complement

A

neutropenia or defective neutrophil function - so reduced phagocytic capacity

T-cell = cellular defect
B-cell, immunoglobulin = humeral defect
complement deficiency

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27
Q

how does immunosuppression affect local immune function

A

local immune function reduced, causing lymphoedema

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28
Q

how does immunosuppression present

A

FH
PMH recurrent infections - involving opportunistic pathogens

end organ damage (bronchiectasis)
on immunosuppressive therapy - transplant, leukemia/myeloma

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29
Q

what is neutropenia

A

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

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30
Q

how does neutropenia present

A

rigor
if early - bacterial infection
if prolonged - fungal infection

pt then admitted to haematology ward

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31
Q

where does neutropenia commonly occur

A

mouth or gut
(occurs due to lines or mucositis)

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32
Q

which bacteria cause neutropenia

A

line related - staph aureus, coag negative staph, pseudomonas

mucositis causing - e.coli, enterococci

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33
Q

what fungal infections cause morbidity/mortality

A

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

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34
Q

how are fungal infections treated

A

antifungals = fluconazole, amphotericin

as both candida/yeast + aspergillum/moulds are line related = remove the line

G-CSF given to improve neutrophil count

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35
Q

when is G-CSF used in treatment

A

improve neutrophil numbers

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36
Q

what causes functional asplenia

A

UC, coeliac, sickle cell, SLE, RA

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37
Q

if pt lacks spleen (from splenectomy - trauma, or from functional asplenia), what infections are they vulnerable to

A

pt vulnerable to encapsulated bacteria

strep pneumonia, n.meningitidis, haemophilus influenza

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38
Q

how to prevent post-splenectomy infection

A

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

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39
Q

what organism causes PCP + how is it identified

A

pneumocystis jiroveci (fungus)
occurs in 80% AIDS patients despite antibiotic prophylaxis

silver stain from BAL

40
Q

what are key features of PCP

A

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
Q

how is PCP treated

A

trimethoprim/sulfamethoxazole
dapsone/clindamycin
IV pentamidine
steroids

42
Q

when is PCP prophylaxis given

A

if HIV+ve with CD4 count <200
PCP prophylaxis given with HAART

43
Q

what pathogens cause cell-mediated immunity defect
(AIDS, lymphoma, immunosuppression, organ transplantation)

A

intracellular bacteria (listeria), mycobacteria
fungi (cryptococcus, pneumocystis jiveroci)
virus (EBV, CMV)
protozoa (toxoplasma)

44
Q

what is hypogammaglobulinaemia

A

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
Q

how does hypogammaglobulinaemia present

A

recurrent bacterial infections affecting sinuses and lungs - haemophilus influenza, pneumococci

46
Q

what diseases present with altered levels immunoglobulins

A

hypogammaglobulinaemia (or XLA - x-linked agammaglobulinaemia)

lymphoma
myeloma

47
Q

how is hypogammaglobulinaemia treated

A

IV immunoglobulins

48
Q

what is complement deficiency

A

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
Q

what is the difference between colonisation + infection

A

colonisation = proliferating bacteria that don’t cause host immune response

infection = proliferating bacteria that cause host immune response

50
Q

what is antimicrobial resistance

A

when micro-organism no longer responds to the drugs made to kill them

51
Q

how to interrupt a chain of transmission

A

vaccinating, testing, isolating

hand hygiene

52
Q

what is hospital acquired CDI

A

pt who develops diarrhoea (c.diff infection)
at least 48hr after admission

53
Q

why are post-infection reviews done

A

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
Q

what are RF for multi-drug resistant organisms

A

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
Q

what is the smart + focus approach for antibiotics

A

smart - don’t start abx in the absence of bacterial infection
focus - clinical review after 48-72hr

56
Q

what drug class do vancomycin + gentamicin belong to

A

vancomycin = glycopeptide
gentamicin = aminoglycoside

57
Q

what are risks of giving abx IV

A

line infection, line misplacement
endocarditis
thrombosis

58
Q

what are risks of treating asymptomatic bacteriuria

A

side effects of abx
side effects of resistance

59
Q

how do suspected + confirmed infection outbreaks differ

A

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
Q

what does measles look like

A

morbiliform rash - generalised dusky red macules/papules

61
Q

how does measles present

A

morbiliform rash (generalised red macule/papule)
kolpik spots (small white patches inside buccal membrane)

cough, corozya, conjunctivitis, kolpik spots

fever >39oC + unvaccinated

62
Q

how is measles managed

A

supportive therapy - no specific treatment

inform PHE
if admitted, needs isolation (encephalitis, pneumonitis, otitis media, carditis)

63
Q

what is parvovirus 18 (erythrovirus)

A

only parvovirus to infect humans

flu-like illness

causes transient anaemia (if immunocompromised, becomes chronic)

64
Q

how does provirus b19 (erythrovirus) present

A

rash + arthralgia
slapped cheek appearance (erythema infectosum)

65
Q

what happens if pregnant with provirus b19 (erythrovirus)

A

spontaneous abortion in 2nd trimester

66
Q

how do coxsackie A16 virus (type of enterovirus) present

A

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
Q

how is cosackie A16 virus managed

A

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
Q

what is erythema nodosum

A

red lumps/knots across both shins (unlike cellulitis which is just 1)

due to inflammed subcutaneous fat (panniculitis) on shins - hypersensitivity reaction

69
Q

what are RF for erythema nodosum

A

young females
during winter-spring

recent strep pyogenes throat infection

70
Q

what causes erythema nodosum

A

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
Q

how does erythema nodosum present

A

red, inflammed subcutaneous fat
across both shins

raised, painful/tender nodules

72
Q

how is erythema nodosum diagnosed

A

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
Q

how is erythema nodosum managed

A

investigate/treat underlying cause

EN managed conservatively - rest, analgesia (+ steroids for inflammation)
fully resolves within 6wk

74
Q

what is erythema multiforme

A

erythematous rash caused by hypersensitivity reaction

usually from - viral infection (herpes simplex virus, EBV), mycoplasma pneumonia, medications (NSAID, anticonvulsant)
[malignancy, CVD]

75
Q

how does erythema multiform present

A

widespread, itchy, erythematous rash - forms target lesions
(darkest red ring in centre, surrounded by other rings)

sore mouth = stomatitis

76
Q

how is erythema multiform diagnosed

A

clinical diagnosis based on appearance of rash

identify underlying cause
recent cold sore = HSV

if no clear underlying cause - do CXR = mycoplasma pneumonia

77
Q

how is erythema multiform managed

A

mild, so resolves spontaneously within 1-4wks without treatment

if severe = IV fluid, analgesia, steroids

78
Q

how does rubella present

A

unvaccinated

forehead rash spreading down to chest
swollen LN - posterior articular + sub-occipital

fever, headache, polyarthralgia

79
Q

what causes dermatomally distributed rash with midline demaracation

A

shingles = herpes zoster

80
Q

what is shingles

A

painful, unilateral vesicular rash
spread across 1 dermatome

occurs due to reactivation of VZV from dorsal root ganglion (if pt immunosuppressed)

81
Q

how does shingles present

A

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
Q

how do chickenpox + shingles differ

A

chickenpox = generalised vesicular rash
shingles = dermatomal vesicular rash

83
Q

what is chickenpox

A

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
Q

how does chickenpox present

A

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
Q

which areas are + aren’t affected by chickenpox

A

rash starts on trunk/face
then spreads across

affects mouth
not palms/soles

86
Q

when do children become infectious with chickenpox

A

2 days before rash develops

stop being infectious when lesions scab/crust over

87
Q

how does ringworm present

A

painless, annular scaly lesions
well-demarcated
slowly enlarging

88
Q

what is ringworm

A

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
Q

how is ringworm diagnosed

A

clinical diagnosis
can scrape off scales for M+C to confirm diagnosis (by identifying organism)

90
Q

how is ringworm managed

A

anti-fungal cream - clotrimazole, miconazole
oral anti-fungal - fluconazole, itracanazole

shampoo for tinea capitis - ketoconazole

91
Q

what is atypical lymphocytosis (seen on blood film)

A

large, misshapen lymphocytes with multiple nuclei

92
Q

how do aminopenicillins affect EBV

A

aminopenicillins can worsen EBV rash, so need to be avoided

93
Q

what is cellulitis

A

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
Q

how does cellulitis present

A

pain, redness, swelling
anywhere on body - but usually LL

fever, malaise

95
Q

how is cellulitis diagnosed

A

clinical diagnosis

only investigate if pt systemically unwell:
skin swab - open wound, blood glucose - if diabetic
x-ray - assess for osteomyelitis

96
Q

how is cellulitis managed

A

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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