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Year 5 😊✌🏼 > Path 5 > Flashcards

Path 5 Flashcards

1
Q

How many children are HIV +ve? (2012) How many of them are in Sub-Saharan Africa?

A

Total 3.3 Million
2.9 Million in SSA

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2
Q

What % of people living wit HIV are children? (2010)

A

1 in 10

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3
Q

How do children get HIV?

A

> 90% due to mother-child transmission

but also:
-child sexual abuse
- exchanging sex for food/shelter

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4
Q

What % of deaths under 5 in S-Africa are due to HIV?

A

~35%

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5
Q

Sx of HIV infection in children

A
  • failure to thrive
  • (chronic bilateral) parotid enlargement
  • (drastic) lymphadenopathy
  • rashes (molloscum, scabies (can even be not itchy b/c immune response is needed for itchiness)/ nappy rash
  • herpes zoster infection
  • hepato-/splenomegaly
  • (severe) oral thrush
  • TB/severe pneumonia/LIP/Pneumocystitis carinii
  • recurrent/persistent diarrhoea
  • clubbing
  • CNS involvement (
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6
Q

LIP

A

lymphoid interstitial pneumonitis

(cannot be distinguished from TB on CXR)

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7
Q

CNS changes in children infected with HIV

A

Basal ganglia calcification
White matter changes
Atrophy

Vasculopathy / Strokes

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8
Q

How can HIV be transmitted from mother to child?

A

in utero
intra partum
breastfeeding

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9
Q

HIV - what is MTCT?

A

mother to child transmission

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10
Q

What is a major risk factor for HIV MTCT?

A

Maternal plasma viral load

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11
Q

What is the pattern of viraemia (with viral load numbers) in HIV infection in humans?

A
  1. rapid rise and initial peak at 10^6 copies/ml
  2. drop and set point at 10^3 - 10^5 copies/ml
  3. rise of copies/ml in late disease
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12
Q

Stats about risk of getting HIV via breast feeding?

A
  • 4% transmission risk for every 6 months of breast-feeding
  • risk of of HIV transmission must be balanced against risk of increased mortality from formula feeding
  • Risk from drinking 1 litre of breast milk = risk from one episode of unprotected sex
  • If IMR is > 40 / 1,000 live births, recommend exclusive breast feeding + ARVs for mother or baby [WHO 2010]

(this is about sub Saharan Africa )

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13
Q

What is IMR?

A

infant mortality rate

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14
Q

Approaches to prevent HIV infection in infants

A
  • prevention of HIV in parents
  • prevention of unintended pregnancies in HIV +ve women
  • prevention of MTCT
  • Care and support for HIV-infected women, their infants and their families
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15
Q

What classes of antiretrovirals are currently used in children with HIV in Africa?

A
  • non-nucleoside reverse transcriptase inhibitors
  • nucleoside analogues
  • nucleotide analogues
  • protease inhibitors
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16
Q

What medication group ends with -gravir?

A

integrase inhibitors

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17
Q

Name examples of integrase inhibitors

A

Raltegravir
Elvitegravir
Dolutegravir

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18
Q

When is Fontana Stain positive?

A

melanoma

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19
Q

What does a positive fontana strain indicate?

A

melanoma

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20
Q

When is Congo red stain positive? What birefringence is seen?

A

amyloidosis

+ apple green birefringence

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21
Q

What stain in +ve in amyloidosis?

A

Congo red + apple green birefringence

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22
Q

What stain is positive in Wilson’s disease?

A

Rhodanine (golden brown against blue counterstain)
+ve for copper

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23
Q

When is Rhodanine stain +ve? What colour does it change to?

A

Wilson’s disease

Golden brown against blue counterstain
(+ve for copper)

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24
Q

Prussian blue stain +ve - diagnosis?

A

Haemochromatosis
(+ve for iron)

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25
Q

Which stains are positive in haemochromatosis?

A

Prussian blue and Perl’s stain

(both are +ve for iron)

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26
Q

Perl’s stain +ve - diagnosis? What makes it +ve?

A

haemochromatosis

iron

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27
Q

Cytokeratin stain +ve - what is it?

A

positive for epithelial cells -> carcinoma

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28
Q

CD45 stain +ve - what is it?

A

+ve for lymphoid cells / lymphocytes

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29
Q

Ziehl Neelsen Stain +ve - diagnosis?
What colour change can be seen?

A

+ve for acid fast bacilli - TB

red against a blue background

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29
Q

Rhodamine-Auramine stain +ve - diagnosis and colour

A

TB

colour: bright yellow

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30
Q

What stains are +ve in TB

A

Ziehl Neelsen and Rhodamine-Auramine

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31
Q

What stain is positive in pneumocystitis jirovecii? What can be seen?

A

Gomori’s methanamine silver stain

flying saucer shaped cysts

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32
Q

Gomori’s methanamine silver stain with flying saucer shaped cysts - diganosis?

A

Pneumocystis jirovecii

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33
Q

What type of pathogen is Pneumocystis jirovecii?

A

fungus

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34
Q

What stain to test for cryptosporidium parvum?

A

Modified Kinyoung acid fast stain

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35
Q

Modified Kinyoung acid fast stain - diagnosis?

A

Cryptosporidium parvum

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36
Q

When is India ink stain +ve ? What can be seen?

A

Cryptococcus neoformans
(yeast cells surrounded by halos)

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37
Q

What stain is +ve in Cryptococcus neoformans and what can be seen?

A

India ink stain

(yeast cells surrounded by halos)

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38
Q

when is Giemsa stain +ve?

A

Chlamydia psittaci (cytoplasmic inclusions seen)

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39
Q

Which stain is +ve in Chlamydia psittaci and what can be seen?

A

Giemsa stain

(cytoplasmic inclusions seen)

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40
Q

Fite stain +ve - diagnosis?

A

Mycobacterium leprae

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41
Q

What stain is +ve in mycobacterium leprae?

A
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42
Q

What are the symptoms of Zika virus?

A

1 in 5 infected people have symptoms

  • fever
  • rash
  • joint pain
  • headache
  • conjunctivitis
  • muscle pain

Sx last for several days to a week

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43
Q

How can you get Zika virus?

A
  • mosquito bite
  • mother to child transmission in pregnancy
  • sex
  • blood transfusion
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44
Q

HOW does Zika virus cause damage in pregnancy?

A
  • crosses the placenta
  • targets neuronal progenitor cells (neuronal growth, proliferation, migration is disrupted)
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45
Q

What problems does Zika virus cause to the baby in pregnancy?

A
  • microcephaly
  • craniofacial disproportion
  • skull abnormalities
  • damage to the brain
  • seizures
  • problems with hearing (?SN hearing loss)
  • problems with vision
  • problems with feeding (issues swallowing)
  • problems with moving limbs and body
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46
Q

Advice for women regarding Zika and pregnancy

A
  • All travellers – bite avoidance
  • Pregnant women – avoid travel to areas with current transmission
  • Avoid conception for 2 – 6 months after travel (prolonged viral shedding in semen)
  • Testing only if symptomatic or abnormalities identified on antenatal USS
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47
Q

Is a flare-up of genital herpes in pregnancy dangerous?

A

No

you have antibodies that protect you and the baby

only primary infections are worrying

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48
Q

What are the risks of primary HSV infection in pregnancy to the baby?

A
  • miscarriage
  • congenital abnormalities (ventriculomegaly, CNS abnormalities)
  • preterm birth
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49
Q

What cancer does EBV infection predispose you to?

A

Burkitt’s lymphoma

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50
Q

What kind of virus is CMV?

A

enveloped
dsDNA genome

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51
Q

In which cells does CMV remain latent?

A

Lies latent in monocytes
and dendritic cells

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52
Q

which cells does EBV remain latent in?

A

B-cells
epithelial cells
NK cells
T-cells

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53
Q

What are the features of congenital varicella syndrome?

A

neurological abnormalities
ocular abnormalities (e.g. microphtalmia)
limb abnormalities
GI abnormalities
low birth weight
skin scarring

54
Q

What are the risks to mum in VZV infection in preganncy

A
  • 10-20% pregnant women are susceptible to VZV
  • 10-20% pregnant women with varicella will have varicella pneumonia
  • encephalitis (Rare, but 5-10% cases are fatal)
  • pregnant women are 5x more likely to develop varicella pneumonitis compared to the general population
55
Q

What is the risk of baby developing congenital varicella syndrome at different points in the pregnancy

A

0.4% if maternal infection weeks 0-12
2% if weeks 12-20

studies have not shown cases after 28w

56
Q

management of varicella zoster exposure in pregnancy

A

if immunity status is unknown, CHECK FOR ANTIBODIES FIRST

If no antibodies
<20 w give VZIG asap

> 20 w give oral antivirals (acyclovir or valacyclovir) for days 7-14 post exposure

57
Q

management of chickenpox in pregnancy

A
  • seek specialist advice
  • ≥ 20 weeks and she presents within 24 hours of onset of the rash - give oral acyclovir
  • if < 20 weeks the aciclovir should be ‘considered with caution’

RCOG guidelines

58
Q

How long should PTSD sx be present for to make the diagnosis?

A

4w

or 1 month

59
Q

Causes of microcytic anaemia

A
  • iron deficiency
  • anaemia of chronic disease
  • sideroblastic anaemia
  • beta thalassemia
60
Q

What is sideroblastic anaemia?

A

Ineffective erythropoiesis → the body produces enough iron but is unable to effectively put it in RBCs. Iron loading (bone marrow) causes haemosiderosis (endocrine, liver and cardiac damage due to iron deposition)

60
Q

How are lithium levels monitored?

A

once weekly in the beginning

once settled: every 3 months.

Lithium levels should be measured 12h after taking the medication

61
Q

CHESS organisms

A

-> cause bloody diarrhoea

C - campylobacter
H - Hemorrhagic E. coli (O157:H7)
E - Entamoeba histolytica
S - salmonella
S - shigella

62
Q

What are the different types of HSV infection in neonates?

A

SEM (skin, eye, mouth disease)
- 45% cases
- initially benign, high risk of progression to CNS
- must be treated (acyclovir)
- usually first 14 days, up to 16w

CNS (+/- SEM)
- 30% cases
- weeks 203 of life (up to 6)
- Sx: seizures, lethargy, irritability, poor feeding, fevers - need CSF

Disseminated
- presents like sepsis
- often in 1st week of life
- multi organ involvement (liver, lungs, CNS, heart, GIT, renal tract, BM)

63
Q

How do you manage HSV in pregnancy?

A

aciclovir (can be used in any trimester)

if primary HSV in 3rd TM recommend C/S

64
Q

What is in-utero HSV infection?

A

very rare but severe

baby gets HSV in utero from mother with primary infection

Risks:
Primary infection only
Miscarriage
Congenital abnormalities ( ventriculomegaly, CNS abnormalities)
Preterm birth
IUGR

65
Q

Risks of varicella in pregnancy to the baby

A

Congenital Varicella syndrome
- skin scarring
- neurological abnormalities
- ocular abnormalities
- low birth weight
- limb abnormalities
- GI abnormalities

66
Q

Risks of varicella in pregnancy to the mum

A
  • 10-20% pregnant women susceptible
  • 5x higher risk of VZV pneumonia than gen pop (10-20% pregnant women with VZV will get this)
  • VZV encephalitis is rare but severe

if presenting with exposure/sx -> check immunity status and measure antibodies

67
Q

Management of VZV exposure and infection in pregnancy

A

Exposure: if hx of infection or 2 vaccinations -> sufficient evidence of immunity; otherwise measure VZV IgG in blood; if VZV IgG <100 mIU/ml offer PEP

PEP: aciclovir or valaciclovir

Infection: treat with aciclovir

68
Q

How high is the risk of transmitting VZV to baby in pregnancy?

A

0.4% if maternal infection weeks 0-12

2% if weeks 12-20

20+ weeks: ?????????

69
Q

What antibody is checked for VZV immunity and what is the cut off level?

A

VZV IgG

<100 mIU/ml -> offer PEP

70
Q

What % women are susceptible to CMV? How many of them will become infected with CMV in pregnancy? How many of them will transmit it to baby?

A

50 % susceptible
1% of them will develop infection in pregnancy
40% babies will get it

71
Q

what % babies exposed to CMV in pregnancy will develop sx?

A

5% have clinical issues at birth, e.g. hepatosplenomegaly, petechia, most of them will have neurodevelopment disabilities later in life e.g. SN hearing loss, CP, epilepsy, cognitive impairment

5% develop issues later in later, mainly SN hearing loss

90 % normal at birth and normal development

72
Q

When are the greatest risks with rubella infection in pregnancy

A

1st TM

73
Q

What are the risks with rubella infection at different times in pregnancy?

A

before 8 weeks -> 20% spont abortion
before 10 weeks 90% incidence of fetal defects
after 18-18 weeks -> hearing defects and retinopathy
after 20 weeks risk is much lower

74
Q

How is rubella spread to baby in pregnancy?

A

via the placenta

75
Q

congenital rubella syndrome

A

Early manifestations:
- Bone lesions
- Microcephaly
- Cataracts
- Retinopathy
- Meningoencephalitis
- congenital cardiac disease (PDA, PS)
- Purpura
- Hepatosplenomegaly
Late onset manifestations
- Hearing loss
- Intellectual disability
- Panencephalitis
- DM
- Thyroid dysfunction

76
Q

Rubella viraemia post birth - problem?

A

yes, it continues to damage the infant

77
Q

How do rubella and measles rashes spread?

A

rubella: starts on face, spreads to trunk

measles: starts at hairline/behind ears, spreads cephalocaudally over 3 days `

78
Q

What type of virus is rubella?

A

Togavirus

79
Q

What type of virus is measles

A

Paramyxovirus – RNA virus

80
Q

How Is measles transmitted?

A

respiratory (isolate!)

conjunctiva

81
Q

How is rubella transmitted?

A

respiratory (isolate!)

82
Q

Fetal risks with Rubella

A

Congenital rubella syndrome

Early manifestations:
- Bone lesions
- Microcephaly
- Cataracts
- Retinopathy
- Meningoencephalitis
- Congenital heart disease(PDA, PS)
- Purpura
- Hepatosplenomegaly

Late onset manifestations
- Hearing loss
- Intellectual disability
- Panencephalitis
- DM
- Thyroid dysfunction

83
Q

Maternal sx and risks with measles infection

A

Measles sx:
- Prodrome 2-4 days
- Conjunctivitis
- Koplick spots
- Rash

Complications for mother:
- Secondary bacterial infection
- Otitis media / pneumonia / GI
- encephalitis

84
Q

Fetal risks of maternal measles infeciton

A
  • foetal loss,
  • preterm delivery
  • no congentila abnormalities
  • SSPE (subacute sclerosing panencephalitis – fatal, progressive disease of the CNS, occurs 7-10 years after natural infection
85
Q

What is SSPE?

A

subacute sclerosing panencephalitis

fatal, progressive disease of the CNS

occurs 7-10 years after natural infection with measles

possible complication of measles in pregnancy

86
Q

Parvovirus transmission

A

respiratory and blood products

87
Q

what proportion of adults have parvovirus antibodies?

A

30-60%

88
Q

Parvovirus dx

A

Virus detection (PCR)
Serology

89
Q

Rubella dx

A

Virus detection (PCR)
Serology

90
Q

CMV dx

A

PCR of urine/saliva/amniotic fluid/tissue
Serology

91
Q

HSV dx

A

viral detection - lesion swab for PCR
serology

92
Q

Sx of parvovirus in pregnancy

A
  • Mostly asymptomatic
  • Erythema infectiosum/ slapped cheek/5ths disease
  • Polyarthropathy
  • Transient aplastic crisis
93
Q

When are you infectious with parvovirus?

A

6d post exposure - 1 week (infectious before sx commence)

94
Q

Risks to fetus in parvovirus infection in pregnancy

A

Before 20 weeks
* Transmission 33%
* 9% risk of infection
* 3% hydrops fetalis if infection)
* 1% fetal anomalies
* 7% fetal loss

Refer to FMU, may require intrauterine transfusion

No documented risks after 20 weeks

95
Q

What is hydrops fetalis?

A

Fetal hydrops
Cytotoxic to fetal red blood precursor cells
-> anaemia
-> accumulation of fluid in soft tissues and serous cavities.
-> can rapidly cause fetal death

96
Q

Which enterovirus poses the main risk in pregnancy? How?

A

Coxsackie

Perinatal newborn infection can occur in last week of pregnancy
Neonates are at risk of myocarditis, fulminant hepatitis, encephalitis , bleeding and MOF.

97
Q

questions to ask pregnanct woman presenting with rash

A
  • Gestation
  • Date of onset, clinical features, type and distribution of rash, associated features
  • Past relevant history of infection
  • Past relevant history of antibody testing
  • Past immunisation history (and dates/places)
  • unwell contacts
  • Travel history
98
Q

advice for women traveling to zika endemic areas

A
  • avoid conception for 2-6 months after travel (prolonged viral shedding in semen)
  • avoid travel to endemic areas in pregnancy
99
Q

What % of babies born to people with Zika while pregnant will develop the typical abnormalities

A

5%

100
Q

What organisms cause PID secondary to abortion?

A

staph, strep, coliform bacteria, clostridium perfringens

usually start form the uterus and spread by lymphatics and blood vessels upwards, deep tissue layer involvement

101
Q

What does CIN stand for?

A

cervical intraepithelial neoplasia

102
Q

RFs for cervical cancer

A

Human Papilloma Virus -present in 95%
Many sexual partners
Sexually active early
Smoking
Immunosuppressive disorders

103
Q

Cervix: what is the SCJ?

A

squamocolumnar junction

between the columnar epithelium and the transformation zone

104
Q

Why has the incidence of cervical cancer declined?

A

Papanicolaou-test screening (Pap smear) and human papillomavirus (HPV) vaccination

105
Q

What does Pap smear stand for?

A

Papanicolaou-test screening

105
Q

What is CIN grading dependent on?

A

degree of atypia on cytology

106
Q

Sx of cervical cancer

A

Patients are usually asymptomatic in the early stages and develop symptoms later in the course of the disease.

Early symptoms
Abnormal vaginal bleeding: irregular vaginal bleeding, heavy, irregular menstrual bleeding, postcoital spotting
Abnormal vaginal discharge: blood-stained or purulent malodorous discharge (not necessarily accompanied by pruritus)
Dyspareunia
Pelvic pain

Late symptoms: hydronephrosis, lymphedema, fistula formation
Cervical examination: ulceration, induration, or an exophytic tumor

107
Q

What are the types of cervical cancer you can get, how common are they and what virus are they associated with

A

Squamous cell carcinoma - 80% - HPV 16

Adenocarcinoma - 20% - HPV 18

Small Cell Carcinoma - 2% - neuroendocrine tumour

108
Q

What stages of HPV infection are there

A

latent/non-productive: HPV continues to reside in the basal cell, infectious visions are NOT produced, viral DNA replication is coupled to epithelial cell replication. complete viral particles are not produced. no cellular effects seen. infection can only be identified with molecular methods.
-> leads to immune response and regression

productive: viral DNA replication occurs independent of host chromosomal DNA synthesis. Large number of viral DNA are produced and result in infectious visions. characteristic histological and cytological features are seen.
-> can lead to malignant cells.

109
Q

How does HPV transform cells?

A

encodes proteins E6 and E7

these bind to and inavtivate two tumour suppressor genes:
- p53 (E6)
- Retinoblastoma (Rb) gene protein (E7)

both interfere with apoptosis and increase unscheduled cellular proliferation both of which contribute to oncogenesis.

110
Q

How does HPV transform cells?

A

encodes proteins E6 (mainly HPV and E7 mainly HPV (

these bind to and inavtivate two tumour suppressor genes:
- p53 (E6)
- Retinoblastoma (Rb) gene protein (E7)

both interfere with apoptosis and increase unscheduled cellular proliferation both of which contribute to oncogenesis.

111
Q

What happens usually with HPV infection? What can happen?

A

Mostly:
nothing happens, body eliminates the infection.
HPV becomes undetectable in 2 y
relatively few develop symptoms

Persisten infection with high risk HPV types is associated with pre-cancerous and cancerous cervical changes.

112
Q

Sensitivity of cervical cytology

A

50-95%

113
Q

specificity of cervical cytology

A

90%

114
Q

How is HPV tested for on cytology?

A

molecular genetic approaches.

HPV DNA test (nucleic acid solution hybridisation assay with signal amplification that uses long synthetic RNA probes complementary to low risk HPV types 6, 11, 42, 43 and 44 as well as high risk types 16, 18, 31, 33, 35, 39, 45, 51, 56, 58, 59, 68)

115
Q

Which mutation affects >50% endeometriod cancers of the uterus?

A

PTEN

115
Q

Which mutation affects >50% endeometriod cancers of the uterus?

A

PTEN

116
Q

What is the commonest uterine tumour?

A

leiomyoma

117
Q

p53, P13KCA, Her-2 amplification in endometrial biopsy - which cancer type?

A

endometrial serous carcinoma

118
Q

Which mutations present in 90% endometrial serous carcinoma?

A

p53

119
Q

Which mutations are seen in clear cell carcinoma?

A

PTEN
CTNNB1
Her-2 amplification

120
Q

What are the risk factors for ovarian torsion?

A

ovarian mass (e.g. cyst or cancer)
ovary >5cm

121
Q

Ultrasound findings in ovarian torsion

A
  • whirlpool sign
  • one ovary is larger than the other (due to oedema and blood pooling)
  • decreased or absent blood flow
122
Q

Mx of ovarian torsion

A
  • urgent surgical detorsion (to avoid ischaemia and loss of the ovary and tube)
  • unilateral sapling oophorectomy if ovary cannot be saved
123
Q

Emergency adnexal masses

A
  • ovarian torsion
  • ruptured ovarian cyst
  • tubo ovarian abscess
  • ectopic pregnancy
124
Q

ruptured ovarian cyst sx

A

sudden onset pain
either spontaneous or e.g. during sex or exercise

125
Q

Mx of ruptured ovarian cyst

A

Minor bleeding
-> hameodynamic status and Hb not affected
-> treat with NSAIDs
-> sx should resolve in a few days.

Major bleeding
- present with peritoneal irritation e.g. guarding, tenderness
- USS shows blood in cavity
- admit and give IV fluids
- surgery may be needed to stop bleeding and remove the cyst

126
Q

Sx of tuboovarian abcess

A
  • acute lower abdo pain
  • fever
  • chills
  • vaginal discharge
  • mass is tender and painful
  • high WCC
  • USS shows complex mass that obliterates normal architecture.
127
Q

Mx of tube-ovarian abscess

A
  • admit urgently
  • abx
  • may need surgery
128
Q

Mx of tube-ovarian abscess

A
  • admit urgently
  • abx
  • may need surgery
129
Q

USS findings in simple ovarian cysts

A

<10 cm
thin, regular walls
ulilocular
filled with anechoic fluid (homogenous)

-> benign

Year 5 😊✌🏼 (53 decks)

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