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Clinical Pathology > Gynaecological and Breast Pathology > Flashcards

Gynaecological and Breast Pathology Flashcards

1
Q

What are the different types of Intraepithelial Neoplasia?

A

Most of these (below) driven by HPV (human papilloma virus);
• Vulval Intraepithelial Neoplasia- VIN
• Cervical Intraepithelial Neoplasia- CIN
• Cervical Glandular Intraepithelial Neoplasia- CGIN (in glandular epithelium)
• Vaginal Intraepithelail Neoplsia- VaIN
• Anal intraepithelial neoplasia-AIN (affects perianal

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2
Q

What is Dysplasia?

A
  • Dysplasia- subnormal growth of tissue/ organ (abnormal cells not yet gotten ability to invade so can’t spread)
  • Earliest morphological manifestation of neoplasia (multistage process)
  • In-situ disease- non-invasive; shows cytological features of malignancy, but no invasion
  • No invasion= no metastasis= curable (take out the in-situ cancer)
  • Recognising dysplasia gives us chance to treat potential tumour before it arises
  • Elim abnormal cells removes basis cancer will develop- cervical screening programme basis
  • Chromosomal abnormalities
  • Increasing dysplasia, increasing cytological abnormalities
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3
Q

What are Human Papillomaviruses?

A
  • Double stranded DNA viruses
  • 7.9kb circular genome
  • 7 ‘early genes’ (involved in subverting cells replicative apparatus- replicate viral genome & integrate into host)
  • 2 ‘late genes (package virion into struc- intact virions released & attack other cells)
  • > 100 subtypes of HPV based on DNA sequence
  • Diff types of HPV affect diff tissues e.g. HPV that causes skin warts diff to HPV causing genital warts
  • Lifecycle linked to epithelial differentiation
  • Genital HPVs grouped into low & high oncogenic risk of developing neoplasm
  • High risk HPVs also involved in penile intraepithelial neoplasia, squamous cell carcinoma & subgroup of oral cell carcinomas (genital HPV types get into mouth)
  • In most women HPV won’t cause long term harm, will be cleared by immune system
  • Immunosuppression (due to disease/ iatrogenic) can lead to extensive & multifocal intraepithelial neoplasia in lower female genital tract (by uncontrolled HPV infec)
  • Smoking important in cervical cancer aetiology; decreases antigen presenting cells in cervical epithelium & causes local immunosuppression (HPV can cause probs)
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4
Q

What are low risk Human Papillomaviruses?

A
  • BENIGN genital warts & other low-grade cytological abnormalities: 6, 11, 40, 42, 43, 44, 53, 54, 61, 72, 73 & 81
  • Subtypes 6 & 11 linked with genital warts (most common)

‘Low Risk’ HPV 6, 11
• Lower genital tract warts (condylomas= benign squamous neoplasms), low grade ‘IN’s
• Rarley malignant lesions

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5
Q

What are high risk Human Papillomaviruses?

A
  • High-risk subtypes associated with high-grade pre-invasive & invasive disease are 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68
  • 99.7% of cervical cancers contain HPV DNA
  • Types 16, 18 associated with 70% cervical cancers
  • (HPV vaccine deals with 16 & 18 but as these only cause 70% cervical cancers vaccine will never eliminate HPV cervical cancer completely)

High Risk’ HPV 16, 18, (31, 33)
• High grade ‘IN’s & invasive carcinomas

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6
Q

What are available vaccinations for HPV?

A
  • ‘Gardasil’ (Merck) HPV 6, 11, 16, 18
  • ‘Cervarix’ (MSK) HPV 16, 18
  • Uk vaccination began Sept 2008 using Cervarix
  • Age 12-13 with ‘catch-up’ up to 18
  • Switch to Gardasil Sept 2012
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7
Q

What is the Mode of Action of High Risk HPV?

A

• Early genes (expressed early in viral replication) expressed at onset of infec- control viral replication
• In oncogenic viruses, they’re involved in cell transformation
• Late genes- code caspid proteins
• High risk HPVs integrate into host chromosomes (difficult to get rid of)
• Upregulates E6, E7 viral protein (from early gene) expression
o E6 binds to & inactivates p53 (p53 mediates apoptosis in response to DNA damage)- genetic damage accumul
o E7 binds to RB1 gene product (RB1 is tumour suppressor gene, controls G1/S checkpoint in cell cycle)- dysregulation of cell proliferation
• (P53 recognises DNA damage & causes apoptosis to get rid of damaged DNA- E6 gets rid of this)
• (RB1 gene product- stops cell proliferation- E7 stops this)

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8
Q

What is Vulval Intraepithelial Neoplasia?

A
  • Varied clinical appearances of VIN
  • From L to R; warty, white patches, pigmented patches, visualised by painting with toluidine blue
  • Several diff clinical manifestations
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9
Q

What are the two types of Pre-invasive stages of Vulval Intraepithelial Neoplasia?

A

Pre-invasive stage- 2 sorts with diff molecular pathology & pathogenesis;
• Classical/ warty/ baseloid
o Graded VIN 1-3
o Related to high risk HPV infec
o Younger people
• Differentiated VIN
o Not graded
o Not HPV related (diff to above disease)
o In chronic dermatoses (chronic inflamm skin disease) esp, lichen sclerosus
o Older people (70 onwards)
o Sep path to vulval cancer

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10
Q

What is the Behaviour of Vulval Intraepithelial Neoplasia?

A
  • 35-50% recur
  • +ve margins predict recurrence
  • Progression to invasive cancer in 4-7% treated women (reduced risk in treated) & up to 87% of those untreated
  • Invasion more likley in postmenopausal/ immunocompromised
  • Spontaneous regression may occur particularly in young, postpartum women (after had a baby)- e.g. immune modulation in pregnancy
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11
Q

What is Vulval Squamous Cell Carcinoma?

A
  • Most common vulval cancer (90%)
  • Associated with VIN (age <60, assoc lower genital tract neoplasia (CIN), HPV +)
  • Assocaited with inflaamtory dermatoses (age >70, Lichen sclerous, Lichen planus)
  • Symptomatic lichen sclerosis 15% risk of malignancy
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12
Q

What is Vulval Squamous Cell Carcinoma?

A
  • Associated with VIN
  • Associated with inflammatory dermatoses
  • Eroded plaque or ulcer
  • Can be contralateral depending on if it’s a more central tumour
  • Spreads: locally to involve vagina & distal urethra (affects treatment- surgical complications- need to preserve function)
  • To ipsilateral inguinal lymph nodes (LNs)
  • To contralateral inguinal lymph nodes, deep iliofemoral LNs (25% if inguinal nodes +ve)- can work it’s way up nodes in the body
  • Anything deeper than 1mm- risk of lymph node metastasis higher;
  • Can do lymph node sampling to check (biopsy) e.g. sentinel node biopsy (inject tumour with radioactive tracer- see where 1st lymph node it goes to)
  • Other biopsy methods cause lymphoedema risk
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13
Q

What is the prognosis of Vulval Squamous Cell Carcinoma?

A
  • Gynaecological cancers staged with FIGO system not TMN system
  • Way of practically documenting way tumour spreads (don’t need to know details of the staging)
  • 5 year survival: Stage 1 (95%), Stage 2 (90%), Stage 3 (70%), Stage 4a (20%), Stage 4b (<10%),
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14
Q

What is Malignant vulval melanoma

A

Malignant melanoma (5% of vulval cancers)
• Mean age 50-60
• Local recurrence in 1/3, spread to urethra freq
• Lymph node/ haematogenous spread common
• Depth of invasion (most important prognostic factor) correlates with LN involvement
• Heavily pigmented (not all are- can get amelanotic ones with no pigment)
• Just as aggressive as cutaneous melanomas
• Histopathological exam; diagnosis, prognostic info (guides treatment)

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15
Q

What is Extramammary Paget’s Disease?

A
  • 5% vulval cancers, mean age 80
  • Pruritic/burning/eczematous patch (like Paget’s disease of the nipple- if looks like eczma e.g. of nipple/ vulva- consider Pagets)
  • In-situ adenocarcinoma of squamous mucosa
  • Tend to recur following excision- doesn’t have edge to it, don’t know how wide to make excision
  • Can develop invasive adenocarcinoma
  • Although eczematous eruptions can occur at this site (e.g. allergic contact dermatitis e.g. new washing powder)
  • Paget’s disease should be in differential diagnosis (often looks like eczema) & consider biopsy
  • In the breast Pagets’s due to underlying ductal carcinoma in-situ spreading into the epidermis.
  • In vulva- usually no underlying tumour; can hypothesise glandular malignant cells arise in intraepidermal portion of sweat ducts.
  • Usually no underlying tumour
  • 5% regional malignant disease (local cancer); bladder, cervix, exclude primary rectal cancer, where there is a prominent perianal component
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16
Q

What is Cervical Pathology?

A
  • Transformation zone (TZ)= physiological area of squamous metaplasia
  • TZ vulnerable to oncogenic effects of HPV- is where cervical intraepithelial neoplasia (CIN) happens so cervical cancer starts
  • Transformation zone develops & changes at diff stages in life;
  • Want to sample TZ when taking a cervical cytology sample
  • Post-menopausal state- TZ retracted up canal (might not be able to see it colonoscopically/ sample it cytologically)
  • If CIN there- might not be able to excise it easily completely with a LLETZ.
  • So diagnosing & treating CIN postmenopause can be a prob (as can’t reach up the area to get to the junction for the cytology- will get false –ves in cervical screening programme).
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17
Q

What is Cervical Intraepithelial Neoplasia?

A
  • Pre-invasive stage of cervical SCC
  • Detection of pre-invasive stage is aim of cervical screening programme
  • Graded according to increasing abnormality (can see on cytology)
  • This shows correlation between cytology of cells brushed off epithelium surface, with the underlying dysplastic changes in epithelium.

Look at regression and progression table of the different types

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18
Q

What is the Cervical Screening Programme?

A

• Is a test of CIN (pre-invasive stage) not cancer
• Available test has high sensitivity and specificity & test is not harmful
• Defined pre-invasive stage
• Long enough to allow intervention, simple, successful treatment
• Is NOT a test for cancer
• Regular attendance prevents 90% of cancers (rate would be 50% higher without screening)
• Uses liq based cytology & focused high risk HPV testing
• How screening organised periodically changes (recently with intro of HPV testing)
Why no screening below 25 yrs old?
• Evidence doesn’t support its use
• High HPV carriage rate (in most of them was no harm), incl high risk types (70-80% will be eliminated)- would have worried people it wouldn’t have harmed
• Reactive changes produce confusing cytology
• Unnecessary LLETZ (large loop excision of transition zone- used to treat) procedures can have obstetric consequences

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19
Q

What is Colposcopy & CIN Treatment ?

A
  • Large Loop Excision of the Transformation Zone (LLETZ)
  • Colposcopy- cervix examination with low powered stereoscopic microscope
  • Cervix often painted with acetic acid- highlights potentially abnormal epithelium which can resect (local anaesthetic) with diathermy loop (this histopathologically examined- guide further treatment)
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20
Q

What are the risk factors of Cervical Squamous Cell Carcinoma?

A

• High risk HPV most important causative factor
• Multiple sexual partners
• Male partner with multiple partners
• Young age at first intercourse
• High parity
• Low socioeconomic group
• SMOKING (local immunosupression)
• Immunosuppression (disease related/ induced by drugs)
Looking at ulcerated cervical carcinoma pic- can work out what clinical presentation may be.
Such a lesion will commonly bleed/ cause a discharge.
If tumour presents late, could be signs & symptoms due to local spread, eg into bladder or affecting ureters causing hydronephosis & urinary symptoms.

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21
Q

What is Cervical Adenocarcinoma?

A
  • Presentation/spread same as SCC (squamous cell carcinomas)
  • Related to high risk HPV
  • Precursor is Cervical Glandular Intraepithelial Neoplasia (CGIN)
  • Treated same as CIN/SCC
  • Stage for stage worse prognosis that SCC due to radioresistance
  • Can occur further up canal- more false –ves
  • Not as sensitive to radiotherapy as squamous cell carcinomas
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22
Q

What is Cervical Carcinoma- Staging and prognosis ?

A

Simplified FIGO staging
• I Confined to cervix
• II Invades beyond uterus, not to pelvic side wall
• III Extends to pelvic wall, lower 1/3 vagina, hydronephrosis
• IV Invades bladder or rectum or outside pelvis

Early lesions may not need radical surgery- can be cured by LLETZ (95% 5 yr survival): stage IA1 (73% 5yr survival) has a depth of invasion of <3mm & max lateral dimension of <7mm. Stage IA2 has a depth of invasion of 3-5mm & maximum lateral dimension of <7mm. stage IIA consider chemo and radio, stage 3 and 4 (36/13% 5 year survival- consider palliative chemo/therapy)

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23
Q

What is Metastasis of Cervical Carcinoma?

A
  • Predictably to pelvic and para-aortic lymph nodes
  • Via blood to lungs, bone etc
  • Local invasion extending out of cervix to baldder, ureters & rectum make primary surgical treatment inappropriate
  • Tumour spreads to lymph nodes- dictates treatment; surgery involves radical hysterectomy with pelvic & paraaortic lymph node dissections, radiotherapy also takes in lymph node fields
  • Haematogenous spread
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24
Q

What is Congenital or Acquired Disorders of the Females Genital Tract?

A

Congenital: Mainly gonadal failure

Acquired” infection/growth disorder/injury/metabolic/immune disorder

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25
Q

What is Endometriosis?

A

Tissue usually inside uterus (endometrium) grows outside uterus e.g. ovaries, abdomen, bladder
• Ectopic endometrium (regurgitation theory/ metaplasia theory/ stem cell theory/ metastasis theory)=bleeding into tissues= fibrosis
• Normal endometrial tissue back tracks & settles in other parts
• Metaplasia theory- certain cells decide to develop into one type instead of another
• Stem cell theory- stem cell precursor e.g. can get endometrial cells in lungs
• 6-10% of women, 30-40yo
• Hx: 25% asymptomatic, dysmenorrhoea (painful menstruation), pelvic pain, subfertility, pain on passing stool, dysuria (painful/difficult dysuria)
• Ix (investigations): laparoscopy (viewing tube in abdomen to see abdominal organs)
• Rx: medical (COCP (combined oral contraceptive pill), GnRH agonists/ antagonists, progesterone antagonists) or surgical (ablation of deposits/ TAH- BSO)
• Links: ectopic pregnancy, ovarian cancer, IBD

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26
Q

What is Endometritis?

A

Inflammation of the endometrium (uterus lining)
• PID, retained gestational tissue, endometrial TB, IUCD infection
• Histology= predominant lymphocytes/ plasma cells
• Caused by forgein bodies chronic retained products, infection
• Pelvic inflamm disease can be associated with chlamydia
• Hx: abdominal/ pelvic pain, pyrexia, discharge, dysuria, abnormal vaginal bleeding
o Acute- systemic infec (e.g. fever), get neutrophil predominant infec
o Chronic- get lymphocyte & plasma cell predominant response & not as much systemic symptoms
• Ix: biochemistry/ microbiology, USS
• Rx: analgesia, abx, remove cause

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27
Q

What is Endometrial Polyps?

A

Mass in inner lining of uterus, can have flat base (sessile) or be attached to uterus by elongated pedicle (pedunculated)
• Sessile/ polypoid E2- dependant uterine overgrowths
• Outgrowth of endometrium into lumen
• May be asynchronous with rest of endometrium
• May be benign but some can harbour pre-malignant changes of endometrial cancer (so usually removed to prevent carcinoma)
• <10% women (40-50s)
• Hx: often asmptomatic, instrumental/ post-menopausal bleeding, menorrhagia, dysmenorrhoea (painful menstruation)
• Ix: USS, hysteroscopy
• Rx: expectant, medical (P4/ GnRH agonists), surgical (curettage)

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28
Q

What is a Leiomyoma?

A

Leiomyoma (Uterine Fibroids)
Benign smooth muscle tumour that rarely becomes cancer
• Smooth muscle of uterus responsible for contracting
• Benign myometrial tumours with E2/P4 dependant growth
• Usually asymptomatic unless very large, usually responsive to oestrogen in terms of proliferation
• 20% women 30-50s
• Risk factors: genetics, nulliparity (woman who’s never borne a child), obesity, PCOS (polycystic ovary syndrome), HTN
• Hx: often asymptomatic, menometorrhagia (heavy bleeding= Fe deficient anaemia), subfertility/ pregnancy probs, pressures sx
• Ix: bimanual examination, USS
• Rx: medical (IUS (interuterine system contraceptive coil)/ NSAIDs/ OCP/ P4/ Fe2+), non-medical (artery embolization, ablation, TAH (total abdominal hysterectomy- uterus & cervix removal))
• Prognosis: menopausal regression, LOW malignancy risk

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29
Q

What is Endometrial Hyperplasia?

A

Abnormal endometrium prolif (more than that occurs for menstruation)- endometrial carcinoma risk factor
• Excessive endometrial proliferation (↑E2, ↓P2)
• Endometrium overgrowth- high levels/ unopposed oestrogen (oestrogen has antagonistic effect in menstruation, progesterone stops prolif in menstruation)
• Risk factors: obesity, exogenous E2, PCOS (polycystic ovary syndrome), E2- producing tumours, tamoxifen (usually blocks oestrogen signal but in endometrium opposite), HNPCC (PTEN mutations- predispose you to develop colorectal & endometrial cancer)
• Obesity- causes peripheral oestrogen increase- favours metaplasia, polycystic kidney disease (favours this too)
• Cytotopic atypia- pre-malignant lesion
• Types;
o Simple non-atypical, simple atypical
o Complex non-atypical, complex atypical
• Hx: presents as abnormal bleeding- IMB/PCB/PMB (post menopausal bleeding)
• Ix (diagnose by): USS (endometrium thickening), hysteroscopy +/- biopsy (of endometrium- see if atypia or not)
• Rx: medical (IUS, P4- progesterone antagonises effect of oestrogen), surgical (TAH)

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30
Q

What is Malignant Progression of Hyperplasia?

A
  • Endometrial hyperplasia= endometrioid carcinoma is progression from simple hyperplasia through complex to atypical hyperplasia & invasive carcinoma
  • Simple hyperplasia (relatively common), endometriod carcinoma less freq
  • Chances of progression through full spectrum increases further down spectrum woman is
  • Caused by excess oestrogens from variety of possible sources
  • 1st stage- simple hyperplasia with overgrowth of whole endometrium (thick endometrium on USS)
  • In complex hyperplasia- more glandular epithelium &epithelium can be folded in complex architectural patterns
  • Atypical hyperplasia (intraepithelial neoplasia) onset- cells show architectural changes of neoplasia with increased nuclear cytoplasmic ratio (bigger nuclei & less cytoplasm), irregular shapes, increased numbers of mitoses (some abnormal)
  • Non-atypical hyperplasia hard to diagnose
  • Increase in nuclear cytoplasmic ratio
  • Stroma strands disappear when cancer

Normal to non-atypical hyperplasia (resembles normal proliferative endometrium) to atypical hyperplasia EIN Endometrial intraepithelial neoplasia (presence of cytological abnormality) to endometrial adenocarcinoma (invasion into myometrium)

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31
Q

What is Endometrial Adenocarcinoma?

A

Cancer that begins in the uterus- carcinoma from glandular tissue (adenocarcinoma)
• Most common cancer of female genital tract (9,200 new cases/ 2,500 deaths per yr UK)
• Hx: PMB (post menstrual bleeding)/ IMB, pain if late
• Ix: USS (endometrium growth), biopsy, hysteroscopy
• Staging: FIGO (1-4)
• Rx: medical (pordesterone- P4), surgery (TAH-BSO- remove ovaries & uterus & tubes), adjuvant therapy (chmo-/radiotherapy)
• Prognosis: stage 1= 90% 5yr survival, stage 2-3= <50%
• Early diagnosis- reduce mortality rate
• Remove oestrogen – help control their development- type 1 (endometroid)
• Type 2 (serous)- not oestrogen sensitive

Type 1: 75% of cases, pre or post menopausal, PTEN/Kras mutations, E2 positive, Grades 1,2 and 3
Type 2: 25% of cases, post menopausal, p53 mutations, E2 negative, Grades 3

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32
Q

What is Polycystic Ovary Syndrome?

A

Oestrogen & progesterone out of balance which leads to growth of ovarian cysts (benign masses on ovaries)
• Endocrine disorder- need 2 out of 3 triad; hyperandrogenism (lots of androgens- hairy, acne, abnormally long cycle length, no ovulation so no progesterone produc, constatnt oestrogen env increases canacer risk), menstrual abnormalities, polycystic ovaries
• Hypothalamic pituitary ovarian axis; hypothalamus makes gonadotrophin releasing hormone, release into hyperpophaseal portal system= gonadotropin RH causes FSH & LH (causes ovulation) release, causes oestrogen release which feedsback to hypothalamus
• Changes in relationship between FSH & LH- pulsatility gnRH released affected
• No feedback mechanism by oestrogen (????)
• Main hormone high in PCOS is LH (released by GnRH), oestrogen has +ve feedback on LH which would then cause more testosterone to be made (clomiphene drug blocks this oestrogen feedback)
• 6-10% women (20-30% have polycystic ovaries)
• Ix: USS, fasting biochemical screen (↓ FSH, ↑LH, ↑ testosterone, ↑DHEAS), OGTT (oral glucose tolerance test)
• Dx: Rotterdam criteria 2/3 of polycystic ovaries, hyperandrogenism (hirsuitism/ biochemical), irregular periods (>35 days)
• Rx: lifestyle (weight loss, exercise- get regression of disorder & reduces risk of type 2 diabetes), medical (metformin, OCP (oral contracp pill), clomiphene- blocks oestrogen feedback system on hypothalamus so upregulation of FSH & LH produc so can resume normal), surgical (ovarian drilling- puncture ovary)
• Links: infertility, endometrial hyperplasia/ adenocarcinoma
• Associated with: metabolic syndrome; obesity, insulin resistance (predisposes you to develop type 2 diabetes)

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33
Q

What is Hypogonadism?

A

Gonadal Failure (Hypogonadism)
Deficiency in secretory activity of ovaries/ testes
• Hypergonadotrophic hypogonadism (primary failure of gonads- don’t get appropriate development of kidneys)
o Congenital causes: Turner syndrome (XO), Klinifelters (XXY)
o Acquired causes: infection, surgery, chemo-radiotherapy, toxins/ drugs
• Pituitary & hypothal working but no –ve feedback from ovaries, get high levels of gonadotrophin but ovaries not functioning
• Hypogonadotrophic hypogonadism (hypothalamic/ pituitary failure= 2nd failure)- Sheen syndrome, pituitary tumours, brain injury PCOS
• Presentation: amenorrhoea/ absent menarche; delayed puberty, ↓ sex hormone levels +/- ↑ LH & FSH levels
• Ix: hormonal profiling (work out what’s missing & replace it), karyotyping (see if congenital cause)
• Rx: difficult- address cause: HRT
• Hypopohaseal portal system
• Woman leeds in during birth= hypovolaemia= pituitary vulnerable (limited vasculature)= pituitary ischaemic & dies so ovaries functional but pituitray’s not
• Prolactinomas- cells make more prolactin, crush other pituitary cells
• Brian injuries- hard impact, jolt of brian shears off pituitary stalk so hypothal can’t communicate with pituitary

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34
Q

What is the Origin of Ovarian Neoplasms?

A
  • 3 key areas in ovary that can result in tumours
  • Serous carcinomas, 2 types; high & low grade (don’t behave in same way) , sometimes tumours affect tubes but no primary tumours
  • High grade carcinomas- originate in tube; cancer cells develop from epithelial cells of fallopian tube, then move & settle on ovary
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35
Q

What are Epithelial ovarian Tumours?

A 
•	Most common group of ovarian neoplasms (90%) 
•	3 major histological types; 
o	Serous (tubal) 
o	Mucinous (endocervical)- give out mucin 
o	Endometrioid (endometrium)- not where they come from just morphological appearance 
•	Each type contains benign/ borderline/ malignant variants 
•	Benign tumours subclassified based on components; cystic (cystadenomas- filled with fluid), fibrous (adenofibromas), cystic &amp; fibrous (cystadenofibromas- fibrous &amp; cystic) 
•	Malignant epithelial tumours= cystadenocarcinomas 
•	Hard to tell if benign or not
36
Q

What is Serous Cystadenocarcinoma?

A
  • Inside of a cyst cavity- malignant epithelium, can be benign
  • This tumour characterised by complex, branching, papillae & glands incorporating slit-like spaces
  • Destructive stromal invasion identified most conspicuously within the confluent solid growth pattern exhibited within the ovarian cortex
37
Q

What are Germ Cell Tumours? What are the 2 types?

A

Neoplasm from germ cells (germ cells normally in ovary & testis)
• 15-20% of all ovarian tumours
• Cystic struc on ovaries
• Germinomatous
o Dysgerminomas (differentiation- oogonia, malignant, chemosensitive)
• Non-germinomatous
o Teratomas (differentiation towards multiple germ layers); most mature (benign; 1% malignant transformation), malignant in males, benign in females
o Yolk sac tumours (differentiation towards extraembryonic yolk sac, malignant, chemosensitive)
o Choriocarcinomas (differentiation- placenta, malignant, often unresponsive to chemo)

38
Q

What are Sex Chord Stromal Tumours?

A

Group of tumours from the stromal component of ovary & testis
• Rare; arise from ovarian stroma, which was derived from sex cord of embryonic gonad
• Primordial germ cells- give rise to sperm, oocytes
• Can generate cells from the opposite sex;
o Thecoma/ fibrothecoma/ fibroma
 Benign, thecomas & fibrothecomas make E2 (also rarely androgens), fibromas hormonally inactive
 Comprised of spindle cells (plump spindle cells with lipid droplets = thecoma appearance)
Meig’s syndrome = occurs usually with ovarian tumour, develop a right sided hydrothorax & ascites (EXAM Q!!!)- remove tumour & hydrothorax & ascites resolves
o Granulosa cell tumours
 Low grade malignant, produces E2
o Sertoli-Leydig cell tumours
 Produces androgens; 10-25% malignant
 Vary in composition- in testis shouldn’t be in ovaries
 But if are- give out testosterone

39
Q

What is Thecoma? What syndrome id it associated with?

A

Sex Chord Stromal Tumours
 Benign, thecomas & fibrothecomas make E2 (also rarely androgens), fibromas hormonally inactive
 Comprised of spindle cells (plump spindle cells with lipid droplets = thecoma appearance)
Meig’s syndrome = occurs usually with ovarian tumour, develop a right sided hydrothorax & ascites (EXAM Q!!!)- remove tumour & hydrothorax & ascites resolves

40
Q

What is Ovarian Cancer?

A
  • 2nd commonest gynae cancer (>7,100 women >4,300 deaths/yr UK, 80% >50’s, 80-90% epithelial
  • Over ½ women end up dying, is post menaupausal disease
  • Peripheral fat- makes oestrogen
  • Malignant germ cell tumours- affect younger women
  • Cyst carcinomsa- affect older women
  • Risk factors: FH, ↑ age, PMH breast cancer, smoking, E2- only HRT, Lynch II syndrome, obesity, nulliparity
  • Protective factors: OCP, breastfeeding, hysterectomy
  • Hx: non-specific symptoms; pain, bloating (as developing ascites), weight loss, PV bleeding, urinary frequency, anorexia
  • FIGO staging: 1-4
  • Rx: stage <1C (hasn’t breached capsule of ovary so can remove tumour) epithelial tumours TAh/BSO, omentectomy, appendectomy, lymphadenectomy & adjuvant chemo (chemo only sensitive in GCTs)
  • Prognosis: overall 5 yrs 43% survival
41
Q

What is Ovarian Metastatic Tumours? (2 types)

A

Müllerian tumours (most common in ovarian tract, other spread to ovaries e.g. in GI (exam Q!!!)): uterus, fallopian tube, pelvic peritoneum, contralateral ovary
• Non-Müllerian tumours:
o Lymphatic/ haematogenous spread:
 GI tract: Large bowel, stomach (Krukenberg tumour), pancreatobiliary
 Breast
 Melanoma- spreads to ovaries
 Less commonly, kidney and lung
o Direct extension (2 adjacent organs- nibbles it’s way to outside of organ & to the next): bladder, rectal
• Any organ with rich vascular supply- vascular deposits
• Can tell if metastatic- look under microscope
• Do immunohistochem- look for specific markers to see where originate

42
Q

What is Endometrial hyperplasia?

A

oestrogenic stimulation of endometrial proliferation; continuous stimulation may lead to atypical hyperplasia and carcinoma

43
Q

What is Leiomyomata?

A

benign smooth muscle tumours of the myometrium

44
Q

What are Ovarian neoplasms?

A

90% epithelial and based on cell type; benign cystadenoma = borderline = malignant cystadenocarcinoma progression; germ cell tumours; sex cord stromal tumours; metastatic tumours

45
Q

What is the Breast Screening Programme?

A
  • Designed to detect breast cancer at its earliest stages
  • Invite women between ages 50-70
  • Age extension 47-73
  • Mammography main tool
46
Q

What is Breast Multidisciplinary Meeting?

A
  • Surgeons, oncologists, radiologists, research nurses, breast care nurses, students, pathologists
  • Radiology, histopathology, clinical impression- need to agree
  • Ensures the triple diagnosis
  • No further action return to breast screening
47
Q

What is Fibrocystic Change?

A
  • Benign condition in which breasts feel lumpy
  • At least 50% of women of childbearing age
  • Some studies indicate lifetime prevalence of fibrocystic change may be as high as 70% to 90%
  • Except for patients with a strong family history of breast cancer where risk is 2 fold- non-proliferative lesions have no increased risk (otherwise no risk you can change in clinic)
  • Diff distinct morphological appearances
  • Can mimic malignancy e.g. bits of calcification
  • Some people have marked fibrocystic change (lumps in breast)- need to check for reassurance that it’s not anything else
  • Hard to interpret
  • Association with florid fibrous change & breast cancer; more estrodiol exposed to more likely to get fibrocystic change & more likely to get breast cancer
48
Q

What is Fibrocystic Disease?

A
  • Constellation of diff benign changes seen in breast including apocrine change, usual type ductal hyperplasia & sclerosing adenois
  • Can form a lump, can be associated with calcium, can mimic cancer- common incidental finding
  • Can cause discomfort related to menstrual cycle
  • Shares same risk factors as breast cancer
49
Q

What is Fibroadenoma?

A
  • Common- form lumps (usually found as a lump- scare people)
  • Usually occur in women- ages 10 & 40 yrs
  • Most common breast mass in adolescent & young adult population
  • Incidence decreases after 40 years
  • Very round on x-ray, or may need ultrasound to find it in young people
  • These are NOT fixed/ tethered & doesn’t cause skin dimpling (if normal tissue pulled down as tether)
  • Usually not removed
  • Cancers grow into adjacent tissue & become tethered, so if mobile may not be cancer
50
Q

What is the Epidemiology of Breast Cancer?

A
  • Rates vary around 5 fold around the world, but increasing in regions that had low rates
  • Risk factors linked to oestrogens
  • Risk increased by early menarche, late menopause, & obesity in postmenopausal women (higher oestrogen level)
  • Prospective studies shown- high endogenous oestradiol concs associated with an increased risk
  • Childbearing reduces risk, with greater protection & breastfeeding (dominant breast most protected)
  • Slight peak of risk during preg
  • Oral contraceptives & hormonal therapy for menopause cause a small increase in breast cancer risk- diminishes once use stops
  • Alcohol increases risk (taking folate may reduce this risk)
  • Mutations in certain (tumour suppressor e.g. BRCA1) genes greatly increases breast cancer risk (permits sccumul of mutations)- but these account for minority of cases
51
Q

What is DCIS?

A
  • DCIS- stage of cancer BEFORE it invades & is a factor of time (if leave it loing enough will become invasive)
  • Pure DCIS can’t produce a metastasis
  • Has the potential to progress to invasion if left
52
Q

What should a Path Report Tell You about Malignancy ?

A
  • In situ or invasive
  • Type
  • Grade
  • Size
  • Vacular invasion.
  • Nodal status
  • Relationship to margins
  • ER, PR and HER2 status (receptors)
53
Q

What are the Main Recognised Types of Breast Carcinoma?

A 
Morphology; 
•	Ductal - 75%
•	Lobular - 12%
•	Tubular/cribriform - 3%
•	Medullary - 3%
•	Mucoid - 2%
•	Metaplastic - 1%
•	Others - 4%
54
Q

What the grades and [prognosis of breast cancer?

A

Grade
• Score based on how pleomorphic, mitosis etc
• Grade 1 to 3
• Grade 1 tumours do better than grade 3 tumours
Vascular Invasion & Relationship to Margins
• +ve lymph nodes- more likely to give chemo
• If –ve lymphnodes but cancer in lymphatics- can give chemo anywhere
• If down on skin/ near pec muscle- more likely to give radiotherapy
Key Prognostic Factors
For treatment plan;
• Tumour grade
• Tumour size
• Nodal status
Nottingham Prognostic Index
• Grade + nodal status (0: score 1, 1-3: score 2 & 4 or more: score 3) + 0.2 x tumour size)
• 3.4 or less- good 80% + 16 yr survival
• 3.4 or less- good 80% + 16 year survival
• 3.41- 5.4- moderate 46%
• 5.41+ - poor 10%
Prediction versus Prognosis
• The future- ER, PR & HER2 status (receptrors)
• Moving towards more using biological therapies that picks out specific markers

55
Q

What is a Phyllodes Tumour?

A
  • Hard lump of tissue in supportive tissue (stroma) of breast
  • Usually benign (but can sometime be malignant)
  • Grouped into 3 types; benign, borderline malignant, malignant
  • More common in women with fibroadenomas, pre-menopausal women between 40-50
  • Noticed as a quick growing lump in breast
  • Tests; mammogram, USS, fine needle aspiration, core biopsy
  • Treatment; surgery- remove tumour
56
Q

What are the effects of infections on pregnancy?

A

• Pregnancy doesn’t alter resistance to infec
• But some infecs during preg more severe & can also affect foetus
• Infecs may cause;
o Miscarriage
o Congenital abnormalities
o Fetal hydrops (abnormal fluid accumul in 2 or more fetal compartments- can lead to spontaneous abortion)
o Fetal death
o Preterm delivery (can have neurodevelopmental disabilities)
o Preterm rupture on membranes
• Maternal antibodies cross placenta & give passive immunity to fetus
• Council women about key infecs & how to avoid getting them

57
Q

What is the NHS Infectious Diseases in Pregnancy Screening Programme ?

A

NHS Infectious Diseases in Pregnancy Screening Programme (minimum 95% uptake of screening in pregnancy for all conditions) – pick up infecs as early as possible to provide management by MDT (obstetrician, paediatrician, infectious disease consultant etc)
• Guidelines if mum +ve for HIV or syphilis
• If mum hep B +ve baby should be offered vaccine/ immunonoglobulin within 24hrs of birth so baby doesn’t get active hep B- whether they get immunoglobulin dpends on how infective mum is
• Get vaccine immediately then in 1, 2 & 12 months of age, then get a blood test to see if baby has hep B

58
Q

What Neonatal Infections can be Acquired During Passage Through Birth Canal?

A
  • Group B Streptococcus (most common cause of neonatal sepsis)
  • Herpes simplex virus (HSV)- transmitted in utero/ passage in birth canal
  • Gonorrhoea
  • Human immunodeficiency virus *
  • Hepatitis B virus *
    • = can be transmitted in any stage of preg & post-delivery
59
Q

What is the NICE CG62: Antenatal Care for Uncomplicated Pregnancies?

A
  • Antenatal- before birth, during pregnancy
  • Women should be offered routine screening for asymptomatic bacteriuria by midstream urine culture early in preg
  • Identification &treatment of asymptomatic bacteriuria reduces pyelonephritis risk in mum
  • Mid stream urine culture in 1st antenatal, if organism then repeat urine test, if same organism treatment
  • Most caused by E.coli
60
Q

What is Asymptomatic Bacteriuria (ASB) in Pregnancy?

A
  • Asymptomatic bacteruria usually before symptomatic UTI in pregnancy
  • 5% prevalence
  • Untreated, at least 30%women with ASB develop acute pyelonephritis
  • ASB screening cost effective approach to prevent pyelonephritis- reduces risk of pre-term delivery & low birth weight (where they would be particularly susceptible to infecs)
61
Q

What is Group B Streptococci Screening?

A

• Until it’s clear that antenatal GBS carriage screening does more good than harm &benefits are cost effective, the National Screening Committee doesn’t recommend routine screening in UK
• Prevention of early onset neonatal Group B Streptococcal Disease RCOG Green-top Guideline No.36- intrapartum antibiotic prophylaxis (IAP) for GBS offered to;
o Women with previous baby with neonatal GBS disease
o Women with GBS in current preg
o Women pyrexial in labour should be offered broad-spectrum antibiotics including antibiotic for prevention of neonatal EOGBS disease e.g. IV clomoxiclav
• But as part of screening for asymptomatic bacteriuira offer intrapartum prophylaxis at the time of labour as higher risk of neonatal sepsis

62
Q

What is a Urinary Tract Infection (UTI) During Pregnancy?

A
  • ‘Bacteriuria’ screening indicated in pregnancy
  • Asymptomatic bacteriuria= no UTI symptoms & 2 samples containing >105 same organism
  • Bacteriuria can develop intro symptomatic UTI if untreated
  • Continuing bacteriuria associated with premature delivery & increased perinatal mortality
63
Q

What is Antimicrobial Prescribing in Pregnancy & Puerperium?

A
  • Puerperium- 6 wks after childbirth where mum’s reproductive organs return to original pre-preg condition (normal physiological state)
  • Antimicrobials- grouped according to microoganisms they act against e.g. antibiotics against bacteria, antifungals against fungi
  • Must consider potential to cause harm to embryo/foetus/neonate
  • All antimicrobials cross the placenta to some extent &virtually all appear in breast milk if given in therapeutic amounts to breast feeding women
  • Some antimicrobials considered ‘safe’ in pregnancy: penicillins, cephalosporins
  • Some antimicrobials unsafe in pregnancy; chloramphenicol, tetracycline, fluoroquinolones e.g. ciprofloxacin), trimethoprim-sulphamethoxazole (adverse consequences on newborn)
64
Q

What are Intra-amniotic Infections?

A

• Affects 1-2% term pregnancies
• Affects 20-25% pregnancies with pre-term labour (strong associated with intra-amniotic infecs & pre-term labour)
• Major cause of perinatal morbidity &mortality
• ‘Chorioamnionitis’- inflammation of umbilical cord, amniotic membranes or placenta
• Risk factors
o Most common after prolonged rupture of membranes
o Amniocentesis, cordiocentesis, cervical cerclage multiple vaginal examinations, bacterial vaginosis (in some cases)
o Pathogenesis
o Ḅacteria in vagina cause infec by ascending through cervix
o Haematogenous (via blood) infection is rare e.g. Listeria monocytogenes
• Mother presents; fever, purulent amniotic fluid
• Causative organisms;
o Group B streptococcus (most common cause)
o Enterococci
o Escherichia coli (2nd most common cause)
o Management
o Antimicrobials & delivery of foetus
o Should administer antimicrobials at time of diagnosis (not after delivery)- to prevent transmission to new-born

65
Q

What is Puerperal Endometritis?

A

• Womb infec (of endometrium) during puerperium affects 5% pregnancies
• Puerperal sepsis- major cause of maternal death
• Risk factors; C-section, prolonged labour, prolonged rupture of membranes, multiple vaginal examinations
• Clinical features;
o Fever (38.5°C in first 24h post delivery or >38° for 4 hrs, 24h+ after delivery)
o Uterine tenderness
o Purulent, foul-smelling lochia
o Increased white cell count
o General malaise, abdominal pain
• Causative organisms (frequently mixed);
o Escherichia coli
o Beta-haemolytic streptococci (group a & b streptococcus)
o Anaerobes
o Diagnosis
o Role of transvaginal endometrial swabs controversial
o Treatment
o Broad-spectrum IV antimicrobials (at time of delivery)- continued until patient has been apyrexial for 48hrs
• With group a strep- give antibiotics at time of birth, then prophylactic antibiotics to new born baby 10 days after birth
• Maternal & neonatal infecs REMEMBER- e.coli & group b streptococcus

66
Q

What is the leading cause of neonatal death?

A

Sepsis & meningitis

67
Q

What is Early Onset Sepsis?

A
  • Early-onset sepsis (usually within 72 hrs)- major cause of mortality & morbidity in newborn babies
  • High mortality, particularly in premature & low birth weight babies
  • Death: 1 in 4 babies who develop it, even when given antibiotics
  • 90% will present within 48hrs of birth
  • Can still develop sepsis even if given antimicrobials
  • Organisms from maternal genital tract
  • Typical to have multisystem involvement/ pneumonia
  • Higher mortality, particularly those infections evident within 1st 24hrs
  • GBS (46%), E coli (20%, other strep (26%)
68
Q

What is Late Onset Sepsis?

A
  • Mostly in babies after 7 days of life
  • Coagulase –ve staphylococci- mostly low weight babies dependant on vascular access & ventilator support
  • Diff organisms that cause early & late neonatal sepsis- so treatment for each completely diff
69
Q

What are Childhood Infections ?

A

• Strep pneumoniae- leading cause of childhood infecs & deaths from infec
• Common symptoms reported in early education settings;
o Respiratory (66%)- most present with Sob, tachypnoea etc
o Fever (14%)
o Gastroenteritis (9%)
o Earache (6%)
o Rash (5%)

70
Q

What is a sore throat aetiology?

A
  • Sore throat- any of various inflammations of the tonsils, pharynx or larynx characterised by pain in swallowing
  • Viral 70-80%- don’t need antibiotics
  • Group A beta-haemolytic Streptococcus (20-30%)- need to give penicillin B to child
71
Q

What is Otitis Media? What are its causes and features and treatment?

A
  • One of the most common presentations
  • Midlle ear effusion
  • Unusual irritability
  • Difficulty sleeping
  • Tugging/pulling at 1/ both ears
  • Fever (need otoscope ear examination)
  • Fluid draining from ear
  • Loss of balance
  • Unresponsiveness to quiet sounds/ other signs of hearing difficulty
  • Prescribe oral antibiotics

Strep pneumonia (35%), H.influenzae(23%)

72
Q

What are common Lower Respiratory Tract Infections (LRTIs) in Children?

A

• 30-40 cases/ 1000 children per yr in UK (GP sees 1-2 cases per yr)
• Prevalence;
o Every yr pneumonia contributes to 750,000-1.2million neonatal deaths worldwide
o Includes pneumonia, acute bronchitis & bronchiolitis
o Respiratory viruses remain leading cause of lower resp tract infec in children under 5 yrs
• H.influenzae infec rare amongst UK children due to immunisation
• RSV- resp syncytial virus (especially in children under 2 yrs old) (63%)
• Distinguish if viral or bacterial infec

73
Q

What is Bronchiolitis?

A

• Bronchiolitis- a seasonal viral illness characterised by feve, nasal discharge, whezzy cough. On examination- fine inspiratory crackles and/or high-pitched expiratory wheeze
• Acute bronchiolitis- one of commonest admissions in winter period
• Causes;
o Respiratory syncytial virus (RSV)- leading casue
o Metapneumovirus
o Adenovirus
o Para-influenza virus
o Influenza
o Rhinovirus
• Rapidly progressive illness- can deteriorate very quickly
• Risk assess child early & make diagnosis
• Can present with apnoea (as inflamm of airways) but may not be present with any other symptoms (this also a symptom of meningitis)

74
Q

What are the common pathogens for pneumonia?

A 
•	Newborn
o	Group B streptococci 
o	Gram –ve bacilli 
o	Listeria monocytogenes
o	Herpes simplex 
o	Cytomegalovirus 
o	Rubella

• 1-3 Months
o Chlamydia trachomatis
o Respiratory syncytial virus
o Other resp viruses

•	3-12mnths 
o	Respiratory syncytial virus 
o	Other respiratory viruses 
o	Streptococcus pneumoniae 
o	Haemophilius influenza 
o	Chlamydia trachomatis
o	Mycoplasma pneumoniae
•	Under 5 year old viruses leading cause of resp illness 
•	2-5 years
o	Respiratory viruses 
o	Streptococcus pneumoniea
o	Neamophilus influenza 
o	Mycoplasma pneumoniae 
o	Chlamydia pneumoniae 
•	5-18 years 
o	Mycoplasma pneumoniae 
o	Streptococcus pneumoniae 
o	Chlamydia pneumoniae 
o	Haemophilus influenza 
o	Influenza virus A &amp; B 
o	Adenovirus 
o	Other respiratory viruses
75
Q

What are the clinical features of pneumonia?

A

o Presentation: acute febrile illness, possibly preceded by typical viral URTI
o Symptoms;
 Breathlessness (poor feeding)
 Irritability
 Sleeplessness
 Cough, chest or abdominal pain in older patients
 Audible wheezing rare in LRTI but can occur
 Younger children rarely cough, may be present with grunting tachypnoea & chest retractions

76
Q

What is Pertussis?

A

Pertussis (Whooping Cough)
• Usually affect children before vaccine available, recent resurgence noted
• Clinical illness in 3 stages
• Highly communicable acute resp infec caused by B. pertussis
• Person-to-person transmission through aerosolised resp droplets
• Humans- sole reservoir
• Diagnosis: culture organism (e.g. nose/ throat swab) & PCR in early stages (in 1st couple of wks of infec)
• Serology test if illness >3wks (find out form patient when symptoms started)
• Immunised; adults in older years immunity waning
• Women- booster vaccine to protect newborns getting pertussis

77
Q

What are the stages of Pertussis?

A
  1. CATARRHAL PHASE
    o Cold-like symptoms (coryza, conjunctival irritation, occasionally a slight cough)
    o 7-10 days
  2. PAROXYSMAL PHASE
    o Coughing sounds start
    o Long duration (2-6 wks), no fever
    o Series of rapid, forced expirations, followed by gasping inhalation (typical whooping sound)
    o Post-tissue vomiting common
    o Very young infants may present with apnea/ cyanosis in absence of cough
  3. CONVALESCENT PHASE
    o May take up to 6 wks of symptoms to subside
78
Q

What is Meningitis in Children?

A
  • Newborn & infants: non-specific clinical presentation (symptoms) at early age
  • Fever
  • Irritability
  • Lethargy
  • Poor feeding
  • High pitched cry, bulging AF
  • Convulsions, opisthotonus
79
Q

What is the aetiology of Meningitis in Children?

A

• Neonates: Group B streptococcus, Escherichia coli, Listeria monocytogenes
• >1month- 5 years: Streptococcus pneumoniae, Neisseria meningitides
• Viral meningitis;
o Most common infec of CNS especially in <1 yr
o Enterovirus (commonest meningitis in 50% of children <3mnths), HSV, influenza, EBV, adenovirus, CMV
o Mononuclear lymphocytes in CSF (lumbar puncture- if it was bacterial would see polymorphic response)
o Symptomatic treatment CP

80
Q

What are the features of UTIs in children?

A

• Up to 7% girls & 2% boys- symptomatic culture-proven UTI before 6 yrs old
• Of febrile neonates (have fever) up to 7% have UTIs
• Most UTIs in children from ascending bacteria
• E.coli (60-80%), Proteus, Klebsiella, Enterococcus & Staphylococcus saprophyticus
• Overall UTI prevalence in febrile infants 5%- varies widely by race & sex
• Caucasian children 2 to 4 fold higher UTI prevalence compared to African-American children
• Females- 2 to 4 fold higher UTI prevalence than circumcise males
Symptoms
• Classic UTI symptoms in older children; dysuria, frequency, urgency, small-volume voids, lower abdo pain
• Infants with UTIs have non-specific symptoms; fever, irritability, vomiting, poor appetite
• So recommend urine culture if child presents with fever & can’t find another cause

81
Q

What is Meningococcemia?

A
  • Mortality 5-10% (90% if DIC)
  • Morbidity 10% (deafness, neurological probs, amputations)
  • Peak incidence <4yrs
  • Immunisation programme includes Men C
  • 60% bacterial meningitis in UK due to meninigococcus B
  • Fever, non-specific malaise, lethargy, vomiting, meningism, resp distress, irritability, seizures
  • Maculopapular rach common in early disease
  • Petechial rash seen in 50-60% children
82
Q

What is Impetigo?

A
  • Staphylococcus aureus/ streptococcus pyogenes
  • Classically ruptured vesicles with honey- coloured crusting
  • May be bullous
  • More common in pre-existing skin disease e.g. eczema
  • Very contagious, rapid spread
  • Commonly infec starts around face/ mouth
  • Topical antibiotics or oral flucloxacillin (antibiotics if not responding to normal treatment) or can be self-limiting
  • Advice re nursery/ school
83
Q

What is Scarlet Fever?

A
  • Gp A beta-haemolytic Sterptococcus
  • 2-4 days post-Streptococcal pharyngitis (sore throat)
  • Fever, headache, sore throat, unwell
  • Flushed face with circumoral pallor (white area around mouth)
  • Rash may extend to whole body
  • Rough ‘sandpaper’ skin
  • Desquamation (skin peeling) after 5/7, particularly soles & palms
  • School age children
  • White strawberry tongue
  • Diagnosis: throat swab, ASO titres
  • Treat: penicillin B for 10 days (need antibiotics)
84
Q

What is Measles?

A
  • Acute viral infection
  • Fever, coryza, conjunctivitis, maculopapular rash & koplik spots
  • Rash starts at hairline= trunk & extremities, lasts about 6 days
  • Transmitted person-to-person by direct contact with infectious droplets/ less commonly by airborne spread
  • Peak incidence of infec usually during late winter & spring
  • Incubation period: 10-12 days
  • Communicable 4 days before to 4 days after rash onset
  • Measles is a PUBLIC HEALTH EMERGENCY- rapidly transmitted to other susceptible individuals
85
Q

What is Rubella?

A

Rubella (German measles)
• Mild febrile viral illness compared to measles
• Children usually few/ no clinical symptoms
• Rash pink maculopapular, starts on face then spreads downward & lasts 2-5 days (3-day measles)
• Transmitted- contact with infected nasopharyngeal secretions
• Incubation perios: 16-18 days
• Communicable period: 5 days before to 5-7 days after rash onset
• Infection can be detrimental to developing foetus
• If mum gets rubella during preg= eye probs, deafness, brain damage, heart abnormalities in baby

86
Q

What is Chicken Pox?

A

Chicken Pox (varicella)
• Contagious disease caused by member of herpes virus family
• Chickenpox- relatively harmless disease
• Symptoms; fever, runny nose, sore throat, itchy skin rash which can appear anywhere on body
• Rash & disease usually disappear after 1 or 2 wks
• Disease confers permanent life-long immunity- child won’t contract it again
• Complications (e.g. pneumonia) in adults who didn’t have chickenpox as a child, or youngsters with already weakened immune systems or preg women that get chicken pox

Clinical Pathology (11 decks)

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