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12- REPRO > Pathology > Flashcards

Pathology Flashcards

1
Q

Histology of the ectocervix and endocervix

A

Ectocervix: lined by stratified, non keratinizing squamous epithelium

Endocervix: lined by columnar, mucous secreting epithelium

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2
Q

Squamo columnar junction

A

Squamo-columnar junction: the point at which the squamous and columnar epithelium meet
• At birth and in childhood, the squamo columnar junction cannot be seen
• Exposed columnar epithelium = ectropion
• Columnar cells re-epithelialise into squamous epithelium as it is more resistant to the acidic vaginal environment

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3
Q

What is the transformation zone?

A

Transformation zone: portion of columnar epithelium that is replaced by squamous epithelium (this is where pre-malignant lesions and carcinomas develop)

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4
Q

What is chronic cervicitis?

A
  • Squamous metaplasia at transformation zone obstructs cervical crypt opening leading to cyst formation and stromal inflammation (acute and chronic)
  • Clinically the cervix appears red, inflamed and irregular with wide transformation zone
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5
Q

Infective cervicitis: candidiasis

A
  • Common, caused by overgrowth of commensal organism
  • Generally causes a vulvovaginitis with pruritis, bruning and white discharge
  • Treated with topical/oral antifungals
  • Organisms seen on cervical pap smear
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6
Q

Infective cervicitis: Trichomonas

A
  • Trichomonas vaginalis infection is transmitted by sexual contact
  • Patients may be asymptomatic or have yellow, frothy vaginal discharge, vulvovaginal discomfort, dysuria and dyspareunia

• Large flagellated ovoid protozoan that can be identified on Pap smear

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7
Q

Acute complications and other sequela of PID

A

Acute complications include
• Peritonitis and bacteremia
• Endocarditis, meningitis, and supparative arthritis
Other sequelae
• Infertility, tubal obstruction
• Increased risk of ectopic pregnancy
• Intestinal obstruction due to adhesions between the bowel and pelvic organs

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8
Q

HSV changes seen on a pap smear

A

Swollen nuclei with mulitnucleation, ground glass chromatin with prominent nuclear membranes, nuclear inclusions

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9
Q

What proportion of females chow clinical symptoms of HSV-2? and what are they?

A

Clinical symptoms only seen in 1/3

o Red papules vesicles painful ulcers

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10
Q

Human papilloma virus

A
  • Sexually transmitted infection
  • Most patients are asymptomatic
  • Double stranded DNA virus
  • Over 40 genotypes can infect the genital tract
  • Divided into low and high oncogenic risk categories
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11
Q

Lesions caused by HPV

A

Condyloma acuminatum

Koilocytosis

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12
Q

How does HPV cause pre-malignant changes?

A
  • Integration of HPV into cell DNA allows for an overexpression of E6 and E7 viral genes which encode proteins
  • Both E6 and E7 enhance degredation of p53, therefore interrupting cell death pathways
  • E7 binds to p21 and prevents its function as a cell cycle inhibitor
  • E7 inactivates the retinoblastoma gene (Rb) blocking its proliferation-inhibitory function
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13
Q

Classification of low and High grade squamous intraepithelial lesions

A

Low : HPV infection, CIN I

High: CIN II + III

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14
Q

Proportion of HPV/CIN I that progress to high grade lesion

A

10%

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15
Q

Proportion of CIN II/III that progress to carcinoma

A

10%

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16
Q

Risk factors for cervical cancer

A

o HPV exposure – Age at first intercourse, multiple sexual partners

o Viral oncogenicity – Persistent infection with high risk HPV subtypes

o Inefficiency of immune response – Immunosuppression, HIV infection

o Other risk factors – Smoking, coexisting infections (HSV, Chlamydia), dietary deficiencies, OCP and hormonal changes

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17
Q

Clinical presentation of cervical cancer

A

¥ Most asymptomatic

¥ Abnormal pap smear

¥ Abnormal bleeding

o Post-coital, intermenstrual
¥ Pain

¥ Haematuria

¥ Weight loss

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18
Q

Histological subtypes of cervical cancer

A

Squamous cell carcinoma most common – about 80%
¥ Precursor lesion is CIN III
¥ Characterized by nests and infiltrative tongues of malignant squamous cells invading the stroma

Adenocarcinoma
¥ About 15%
¥ Precursor lesion is adenocarcinoma in situ

Adenosquamous and NET
¥ Remaining 5%
¥ More aggressive and have a worse prognosis

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19
Q

PAP SMEAR

A

¥ Cells from transformation zone obtained via spatula or brush

¥ Smeared onto slide and stained using Papanicolaou method

¥ Liquid based medium

¥ Screened by scientist

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20
Q

HPV vaccine

A

¥ Became available in 2006

¥ Designed to reduce incidence of cervical cancer caused by HPV 16 and 18 and condylomas caused by HPV 6 and 11

¥ Available in Australia Gardasil – quadrivalent Cervarix – bivalent

¥ Most effective when given to young people before they become sexually active

¥ Girls and boys aged 12–13 can receive the HPV vaccine for free under the National Immunisation Program at their school

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21
Q

Congenital abnormalities of the testis and epididymis

A 
Cryptorchordism 
Anorchidism 
Polyorchidism (>2 testes)
Adrenal cortical testes
Splenic-gonadal fusion
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22
Q

What is cryptochordism

A
  • One or both testes fail to descend into scrotum
  • May be found in inguinal canal, upper scrotum or abdomen
  • Increased risk of germ cell tumours (3 -5x)
  • Risk of torsion and infarction
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23
Q

Predisposing factors for testicular torsion and infarction

A
  • Absence of scrotal ligament
  • Shortened attachment of peritoneal ligaments incomplete descent
  • Atrophy
  • Needs Rx within 6-8 hrs of onset to prevent loss of testis
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24
Q

Hydrocele

A
  • Commonest intrascrotal swelling
  • accumulation of serous fluid within tunica vaginalis of testis
  • smooth, pear-shaped swelling
  • tense but usually fluctuant
  • transilluminable
  • testis not palpable due to surrounding fluid
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25
Q

Types of testicular hydrocele

A

Congenital
• Appears first few weeks of life
• Due to patent processus vaginalis

Secondary
• may be associated with underlying lesion of testis or epididymis:
• inflammatory; mumps, gonococcal
• neoplastic

Acute Inflammatory hydrocele – accumulates rapidly, often painful

Chronic hydrocele – stretching of tunica, dragging sensation

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26
Q

What is varicocele

A
  • abnormal dilatation and tortuosity of veins of pampiniform plexus in spermatic cord
  • due to insufficiency of venous valves
  • 90% left sided, 10% bilateral
  • associated with infertility
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27
Q

Common causes of viral and bacterial epididymis-orchitis?

A 
Viral epididymo-orchitis
•	mumps, Coxsackie B
•	bilateral involvement  infertility
Bacterial epididymo-orchitis
•	young – C. trachomatis, N. gonorrhea
•	older – E. coli from UTI
•	haematolymphatic seeding – Klebsiella spp., Streptococci, Staphylococci, Salmonella, Actinomyces
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28
Q

Neoplasms of the testis

A
  • Germ cell tumours (GCT)
  • Sex-cord stromal tumours (SCST)
  • Mixed GCT-SCST
  • Primary tumours not specific to testis (lymphoma, leukaemia)
  • Metastatic tumours - e.g melanoma, prostate Ca
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29
Q

Classic and spermatocytic seminole

A

Classic type:
• most common GCT (approx 50% of all cases)
• mean age at diagnosis is 40 years
• may present with painless mass; 15% normal O/E
• 30% have mets at presentation but only 3% have Sx from these mets
• PLAP(placental alkaline phosphatase) and CD117 (c-kit) POS
• serum AFP normal; 10-20% have β-HCG

Spermatocytic type
•	2% of GCT and occurs only in testis
•	average age 65 years, present with a mass
•	very rarely metastasise
•	PLAP negative
•	usually cured with orchidectomy
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30
Q

Types of NSGCT

A 
Embryonal carcinoma
Yolk sac tumour
Teratoma
Choriocarcinoma
Mixed germ cell tumours
Intratubular germ cell neoplasia, unclassified (IGCNU)
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31
Q

Seminoma treatment

A
  • Stage 1 and non-bulky stage 2 radical orchidectomy and radiation to ipsilateral paraaortic and pelvic LN (some S1 Rx with rad orchid alone); 95% cure rate for S1 and 90% for S2 tumours
  • bulky S2 and advanced disease orchidectomy, radiation and chemotherapy; survival rate of 80%
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32
Q

NSGCT treatment

A
  • Stage 1 radical orchidectomy and retroperitoneal lymph node dissection (90-95% cure rate; 5-10% relapse) OR radical orchidectomy and surveillance (60-70% cure rate; 30-40% relapse)
  • Stage 2 non-bulky orchidectomy, LND and chemo (90% cure rate)
  • Stage 2 bulky orchidectomy, chemo and resection of residual masses (cure rate 70-80%)
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33
Q

Leydig cell tumour

A
  • Tumour of interstitial cells
  • 1 – 3% of testicular tumours
  • May be assoc with androgen or oestrogen prodn
  • Present in adulthood with testicular lump
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34
Q

Penile congenital lesions (4)

A

Hypospadias
epispadias
phimosis
paraphimosis

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35
Q

Hypospadias

A
  • commonest congenital abnormality of male urethra
  • due to failure of fusion of urethral folds over the urogenital sinus
  • commonest site is a meatus on the inferior (ventral) aspect of the glans
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36
Q

Epispadias

A
  • much less common
  • urethra opens onto dorsum of penis, usually at the base of the shaft near the pubis
  • results in urinary incontinence and infections
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37
Q

Commonest medical inclination for male circumcision

A

Phimosis - prepuce unable to be retracted

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38
Q

Balanitis xerotica obliterans (BXO)

A
  • thickened white plaques and fissures on glans and prepuce
  • non-retractile prepuce or discharge
  • children and elderly
  • treated with circumcision
  • histology similar to lichen sclerosus of vulval skin
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39
Q

Itching followed by appearance of closely grouped vesicles surrounded by erythema

A

Genital herpes - HSV2 more common

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40
Q

Genital warts

A
  • commonest urogenital lesion
  • infection with HPV (DNA papovavirus) types 6 and 11 (cf cutaneous warts types 1, 2 and 4)
  • epidermis shows papillomatous hyperplasia
  • cytoplasmic vacuolation
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41
Q

Primary, secondary and tertiary syphilis

A

primary
• Secondary stage: condyloma lata, generalised lymphadenitis
• Tertiary stage: gumma, often in testis

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42
Q

Polycystic ovarian disease

A

¥ Aka Stein-Leventhal Syndrome
¥ Numerous cystically dilated follicles, assoc with;
¥ Oligomenorrhea
¥ Obesity
¥ Hirsuitism
¥ Virilism
¥ Infertility
¥ Genetic and environmental causes; severity related to insulin resistance/obesity/‘metabolic syndrome’
¥ Rx: diet, lifestyle, diabetic meds (metformin), ovulation induction, ?wedge excision/‘drilling’ of ovary

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43
Q

Classification of epithelial surface tumours of the ovary

A 
¥	Serous
¥	Mucinous
¥	Endometrioid
¥	Clear cell
¥	Transitional/Brenner
  • benign, borderline or malignant
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44
Q

Serous tumours

A

¥ 20-50% of ovarian tumours
¥ Ciliated, fallopian tube-like epithelium
¥ Derived from epithelial inclusion cysts, or;
¥ Implanted epithelium from the distal fallopian tube epithelium.
¥ 70% benign = ‘serous cystadenoma’
¥ 10% borderline = ‘serous borderline tumour’
¥ 20% malignant = ‘serous (cyst)adenocarinoma’

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45
Q

Mucinous tumours

A

¥ ~25% of ovarian tumours
¥ Intestinal-like (in 85%) or endocervical-like (in 15%) mucinous epithelium
¥ 80% benign = ‘mucinous cystadenoma’
¥ 10% borderline = ‘mucinous borderline tumour’
¥ 10% malignant = mucinous (cyst)adenocarcinoma
¥ Can become very large: >30 cm; >4kg

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46
Q

Endometrioid tumours

A

¥ ~20% of ovarian tumours
¥ Often arise within endometriosis
¥ Majority of endometrioid tumours are carcinomas

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47
Q

Stromal tumours

A

Neoplasms derived from ovarian stromal cells including fibroblasts, thecal cells, granulosa cells…

Classification
¥	Fibro-thecoma*
¥	Granulosa cell tumour* (adult and juvenile types)
¥	Sertoli-leydig tumours
¥	Steroid tumours NOS
¥	Sex cord tumours with annular tubules
¥	Sclerosing stromal tumours
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48
Q

Germ cell tumours in ovaries and most common type

A

¥ 30% of ovarian tumours - teratoma

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49
Q

Pathological findings in pre-eclampsia and eclampsia

A

¥ Placental infarcts
¥ Retroplacental haematomas
¥ Increased villous ischemia (syncitial knots, villous hypomaturation)
¥ Fibrinoid necrosis of maternal vessel walls

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50
Q

Pathogenesis of pre eclampsia and eclampsia

A

¥ Abnormal formation of placental blood supply placental ischaemia release of vasoconstrictors, inflammatory mediators and prothrombotic substances vasoconstriction, endothelial injury and activation of coagulation damage to kidneys, liver, brain…

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51
Q

Classification of human placenta

A

Haemochorial - placenta where the chorion comes in direct contact with maternal blood
Discoid shaped

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52
Q

Implantation of the blastocyst

A

Commences around day 5-7, post fertilisation, completed by day 12
** blastocyst penetrates the endometrium completely

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53
Q

Nutrition for the blastocyst

A

Histiotrophic nutrition from endometrial glands until wk 10 when maternal blood supply is established (haemotrophic nutrition)

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54
Q

Function of the chorion, amnion, allantois and yolk sac

A
  • The Chorion (trophoblast) will become the placenta.
  • The Amnion will enclose the amniotic cavity/fluid
  • The Allantois becomes the umbilical cord
  • The Yolk Sac provides blood cells until the baby can make its own. This will eventually dissolve away.
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55
Q

Main structural and functional units of the placenta

A

Chorionic villi

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56
Q

Blood supply to the embryo

A

The villous structure provides a tremendous absorptive surface to facilitate exchange between the maternal and fetal circulation. The maternal blood arrives from the spiral arteries and circulates through the intervillous space. Fetal blood moves in the core of the chorionic villi within the villous vessels; thus, fetal and maternal blood is never mixed in this system.

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57
Q

Cells lining the placental villi

A

syncytiocytotrophoblasts

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58
Q

Stages of chorionic villi development

A

Primary: The chorionic villi are at first small (anchoring) and non-vascular (intermediate villi) - 13–15 days (cells: trophoblast only)

Secondary: The villi increase in size and ramify, while the mesoderm grows into them (intermediate and stem villi development) - 16–21 days (cells: trophoblast and mesoderm)

Tertiary: Branches of the umbilical vessels grow into the mesoderm, and in this way the chorionic villi are vascularized (stem villi and numerous terminal villi) – from day 21 on (cells: trophoblast, mesoderm, and blood vessels)

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59
Q

Blood supply to the placenta

A

• 2 arteries
• 1 vein
The placenta returns oxygenated (oxygen-rich) blood to the fetus via a single vessel, the umbilical vein. This process is an exception to the usual pattern (arteries carry oxygenated blood, veins carry deoxygenated blood). Some oxygenated blood from the umbilical vein passes through the fetal liver, but most of it enters the fetus’ inferior vena cava through the ductus venosus

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60
Q

Trophoblasts and types

A 
•	The defining cell type of the placenta is the TROPHOBLAST
•	Trophoblasts are epithelial cells of FETAL origin which exhibit unique properties. Four main types:
o	Cytotrophoblasts (CTB)
o	Extravillous trophoblasts (interstitial EVTs)
o	Endovascular trophoblasts (endovascular EVTs)
o	Syncytiotrophoblast (STB)
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61
Q

What makes up amniotic fluid in early and late pregnancy

A

¥ In early pregnancy amniotic fluid is initially derived from maternal blood
¥ In late pregnancy, after fetal renal development, amniotic fluid is made up primarily of fetal urine and fetal lung fluid.

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62
Q

Substrates transferred from maternal to fatal placenta

A 
¥	Oxygen, carbon dioxide, carbon monoxide
¥	Water, glucose, vitamins, elements
¥	Amino acids, lactate, oxalate
¥	Cholesterol and its esters
¥	Long chain fatty acids
¥	Short chain fatty acids
¥	Steroid and thyroid hormones
¥	Electrolytes (e.g. cationic metal ions)
¥	Maternal IgG (Fc)
¥	Apolipoproteins and carrier proteins
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63
Q

Placental transport substrates - fetal to maternal

A

¥ carbon dioxide, carbon monoxide
¥ waste products - urea, uric acid, bilirubin
¥ Xenobiotics and toxins
¥ Steroid conjugates / metabolites

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64
Q

Blood flow factors that can limit fetal oxygenation, nutrition, and metabolism are:

A

(1) altered maternal perfusion
(2) altered fetoplacental perfusion
(3) reduced placental permeability
(4) increased placental metabolic needs

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65
Q

Placental immunological aspects

A

¥ Trophoblasts secrete factors which promote formation of Tregs and macrophages with a unique phenotype in decidua
¥ EVTs express ‘non-classical’ MHC I (e.g. HLA-G) as they invade the endometrium to induce uNK cell tolerance

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66
Q

Factors effecting fetal growth

A

Maternal factors:
Placental factors
Fetal factors

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67
Q

Growth factors identified in fetal tissues

A 
Growth promoting
¥	Insulin-like growth factors (IGF-I & IGF-II)
¥	Epidermal growth factor (EGF)
¥	Transforming growth factor-a (TGF-a)
¥	Platelet-derived growth factor (PDGF)
¥	Fibroblast growth factor (FGF)
¥	Nerve growth factor (NGF)
¥	Haematopoietic growth factors
Growth inhibitory
¥	Transforming growth factor-b (TGF-b)
¥	Inhibin/activin family
¥	Mullerian inhibitory substance
¥	Binding proteins
68
Q

How are nutrients supplied to fetal tissues?

A

o Transported across the placenta from maternal circulation
o Synthesised in the placenta & released into the fetal circulation
o Produced endogenously by the fetal tissues by mobilisation of stored reserves or de novo synthesis

69
Q

Placental oxygen transport

A
  • Oxygen: crosses the placenta by simple diffusion down a concentration gradient from maternal to fetal blood. Transfer falls only if placental blood flow is reduced >50%.
  • Transplacental oxygen gradient depends on the placental vascular architecture, placental oxygen consumption & oxygen affinity of the fetal blood.
  • Uteroplacental tissues use 50% of the oxygen delivered to them and have a rate of oxygen consumption 4-6 x greater than the fetus.
70
Q

Placental glucose transfer

A
  • Glucose is taken up & transported across the placenta by facilitated diffusion.
  • This process requires glucose transporters and a glucose concentration gradient from the maternal to the fetal circulation
  • The main determinant of the transplacental glucose concentration gradient is the maternal glucose level
  • Rate of placental glucose transfer increases in the second half of pregnancy as nutrient demands of the fetus rise.
71
Q

Increased capacity for glucose transfer is due to:

A
  • Structural remodelling of the placenta increasing the surface area and reduces the diffusion distance for transfer
  • Increase in transplacental glucose concentration gradient with advancing gestation. Fetal glucose levels are lower at term than earlier in gestation.
  • Redistribution of uterine glucose uptake between the fetus and uteroplacental tissues with a proportionate increase in glucose delivery to the fetus.
  • GLUT 1 is the major placental glucose transporter in humans but does not appear to alter with increasing gestation (unlike other animal species)
72
Q

Pre-labour

A

Myometrial excitement
• Irregular uterine contractions (Braxton Hicks Contractions)
Descent of the fetal head
• Fetal head enters the pelvis
Cervical ripening
• Cervix becomes soft - collagen concentrations are reduced & replaced by water content.
Show

Loss of the blood-tinged mucoid plug within the cervix

73
Q

Onset of labour

A

regular painful contractions associated with effacement and dilatation of the cervix

74
Q

Cervical effacement and dilatation

A

Cervical effacement refers to the gradual inclusion of the cervix into the lower uterine segment.
Cervical dilatation is the opening of the cervix from closed to full dilatation

75
Q

1st stage of labour

A

• Time of onset of labour to full dilatation of the cervix (10cm)

Latent labour – time between the onset of labour to 4cm dilatation

Active labour – describes the time from 4cm to 10cm dilatation (full dilatation)

Progress in first stage of labour

Latent phase: no time frame
Active phase: 1cm/hour

Average duration
• 12-14 hours in nullipara and 8 hours in multipara

76
Q

2nd stage of labour

A

• Full dilatation of the cervix until expulsion of the fetus from the birth canal.3 (delivery of the baby)
Average duration: 1-2 hours in nullipara and <1hour in multipara

77
Q

Third stage of labour

A

•

Begins after delivery of the fetus and ends expulsion of the placenta and membranes
Average duration:
• No more than 3o minutes
• Often 5 minutes depending on management employed

78
Q

Monitoring the progress of labour

A

Abdominal palpations
• Confirm lie is longitudinal, fetal presentation is cephalic, position of fetal back. attitude of good flexion & position occipital lateral or anterior.

Vaginal examinations –
• Progressive effacement & dilatation of cervix
~1cm an hour in the ‘active’ phase of labour
• Progressive descent of presenting part
• Assess flexion & position

Palpation of contractions
• frequency, length & strength

Maternal well-being
•	Vital signs 
•	Input &amp; output – hydration
voiding - non-distended bladder 
•	Pain management – support choices, advise when necessary 
•	Continuous supportive environment
79
Q

Cardinal movements in labour

A
  1. Before Engagement
  2. Engagement, flexion, descent
  3. Further descent, internal rotation
  4. Complete rotation, beginning extension
  5. Complete extension
  6. Restitution / external rotation
  7. Delivery of anterior shoulder
  8. Delivery of posterior shoulder
80
Q

3rd stage of labour

A

The third stage begins immediately after delivery of the baby & involves separation & expulsion
of the placenta & membranes
& control of haemorrhage from the placental site.

81
Q

Structure of the female breast

A
  • Breast development along ‘milk line’
  • 6-10 major ducts at the nipple (open via lactiferous sinuses)
  • Successive branching gives rise to the terminal duct lobular unit, TDLU (bunch of grapes)
  • A normal TDLU has a dual lining: inner layer of (luminal) epithelial cells and an outer layer of myoepithelial cells
  • Each ductal system overlaps with adjacent
  • Each TDLU is surrounded by a cuff of loose intralobular stroma
  • Interlobular stroma a variable combination of more dense fibrous and adipose tissue
82
Q

Where do most in situ and malignant breast disease occur?

A

TDLU - terminal duct lobular unit

83
Q

Breast duct

A

dual epithelial lining = true epithelial lining and layer of myoepithelial cells

84
Q

TLDU undergoes changes in pregnancy:

A

Breast enlargement
Hyperplasia
Hypertrophy

85
Q

Clinical presentations of breast disease

A

• Breast presentations are common in clinical practice (e.g. 16% of women over a 10 year period)
• Breast biopsies make up about 5% of the work of a surgical pathology laboratory
• Breast disease presents in 2 major ways:
1. screen detected abnormalities
2. symptomatic presentations

86
Q

Breast screening

A
  • 85,000 screening mammograms per annum
  • 5% recalled for assessment
  • 76% cleared after examination/further views/US
  • overall malignancy: 10% of assessments (0.6% of screens)
87
Q

Major abnormalities seen in mammography

A
  • densities
  • distortions
  • calcification
88
Q

Major clinical presentations/symptoms of breast disease

A

o pain
o lumpiness

o discrete mass (lump)

o nipple discharge

o skin changes (tethering, peau d’orange, ulceration etc)

o other (including distant manifestations)

89
Q

Acute mastitis

A

• Almost always occurs early in lactation

• Usually due to infection by Staphylococcus (rarely
Strep) which enter through cracks in the nipple

The histology is of typical acute inflammation: predominantly neutrophilic inflammation +/- necrosis and abscess formation

90
Q

Subareolar abscess

A
  • Presents as erythematous sub-areolar mass
  • 90% are smokers
  • Squamous metaplasia of lactiferous ducts (SMOLD) resulting in obstruction, dilation and rupture with granulomatous reaction. Infection may supervene.
91
Q

Mammary duct ectasia

A
  • Most commonly seen in postmenopausal parous women
  • Dilated ducts filled with debris
  • Periductal fibrosis and inflammation
  • Can mimic carcinoma clinically and on mammography
92
Q

Fat necrosis in the breast

A
  • Palpable mass, skin retraction or calcifications.
  • History of prior trauma in many cases

• Typical macro and micro appearance

93
Q

Nipple discharge and other nipple related symptoms

A

• Galactorrhoea - hormonal, drug related

• Serous/bloody discharge - cysts, intraduct papilloma,
DCIS

• Excoriation, crusting, itching – eczema, Paget disease, other malignancy

94
Q

Histological changes seen in non-proliferative breast change

A

cysts, metaplasia, fibrosis, adenosis

– OVERALL = FIBROCYSTIC CHANGE

95
Q

Benign proliferative breast change

A
  • Very common
  • Histological Changes include AKA non-proliferative changes: cysts, metaplasia, fibrosis, adenosis
  • Macroscopically apparent in 20%
  • Microscopically in 59%
  • Described clinically as fibrocystic change
  • No significant increased risk of breast carcinoma
96
Q

Benign proliferative breast disease pathologies

A
  • Moderate/florid epithelial hyperplasia
  • Sclerosing adenosis
  • Complex sclerosing lesion/radial scar
  • Papilloma
97
Q

Most common benign tumour in females

A

Fibroadenoma

98
Q

Features of fibroadenoma

A
  • Most common in younger women
  • Often multiple/bilateral
  • A ‘biphasic’ neoplasm (glands and stroma)
  • There is a more aggressive “counterpart”- Phyllodes tumour - behaviour ranges from local recurrence to frankly malignant (It is the stromal component which shows atypia)
  • Glandular and epithelial and stromal proliferation
99
Q

Gynaecomastia

A

Breast enlargement in males
- thought to be androgen/estrogen imbalance
Occurs in: puberty, cirrhosis, drug use, elderly

100
Q

How many women develop breast cancer

A

1 in 10

101
Q

Major risk factors for breast cancer

A
  • Gender (> 99% occur in women)
  • Age (77% over 50)
  • Previous breast carcinoma and other benign proliferative breast disease
  • Oestrogen exposure:
  • Family Hx/Genetics
  • Breast density
  • Radiation
102
Q

Hereditary breast cancer

A
  • 5-10% inherited, often present at younger age, bilateral
  • About 3% of all breast cancers can be attributed to mutations in one of BRCA1/BRCA2 tumour suppressor genes. Many different mutations.
  • Highly penetrant, autosomal dominant pattern
  • Incidence BC 50-85%
103
Q

BRCA1/2 association with cancer

A
  • 50-85% of those with mutation will develop breast cancer
  • they are tumour suppressor genes
    BRCA1 - associated with ovarian cancer too
    BRCA2 - also associated with male breast cancer
104
Q

Benign lesions and cancer risk

A

•

Most benign breast changes are not associated with increased risk of cancer
• Some epithelial proliferative conditions increase the risk of invasive carcinoma

105
Q

Atypical proliferative lesions

A
  1. Atypical ductal hyperplasia

2. Atypical lobular hyperplasia

106
Q

Simple classification of primary breast carcinoma

A

In situ carcinoma (confined within duct or lobule)
• Ductal (DCIS)

• Lobular (LCIS)
Invasive carcinoma (spread beyond duct or lobule) potentially metastatic
• Invasive ductal carcinoma (IDC)

  • Invasive lobular carcinoma (ILC)
  • Others
107
Q

DCIS

A
  • a neoplastic epithelial proliferation which has not penetrated the basement membrane
  • for practical purposes, DCIS (like LCIS) is entirely curable because it has no metastatic potential
  • Increased risk of subsequent carcinoma 10x classified according to:

o growth pattern (solid, solid with comedonecrosis, cribriform, micropapillary etc)

o nuclear grade

• more commonly detected in a screened population – often associated calcifications

108
Q

Pagets disease of the nipple

A

• Presents as reddened, weeping “eczematous” nipple

• Almost always associated with underlying high grade
DCIS (+/- IDC)

• Prognosis depends upon the features of the underlying invasive tumour (if present)

109
Q

DCIS risks and management

A

Risk of recurrence affected by:
• Nuclear grade

• Size of lesion

• Margins of excision
Rx: mastectomy or conservative excision (WLE) +/-

  • adjuvant radiotherapy
  • hormonal therapy
110
Q

Risk of LCIS cancer

A
  • Risk of invasive Ca is around 1% p.a. (around 10x general population)
  • Risk is bilateral

• Risk is higher at site of LCIS and more often
carcinoma is invasive lobular type

• Both LCIS and adjacent ILC show similar genetic features

111
Q

Clinical presentation of invasive breast cancer

A
  • Lump – breast or axilla
  • Distortion
  • Nipple abnormalities
  • Skin abnormalities
  • Mammographic abnormalities
112
Q

Diagnosis of invasive breast cancer

A
  • Clinical examination – breast, axilla, general

* Cytology or histology: FNAC, core biopsy or tissue sample

113
Q

How do invasive carcinomas of the breast spread and where do they metastasise to?

A

o local invasion through chest wall, skin
o lymphatic spread especially axillary, internal mammillary nodes
o blood borne metastasis: liver brain bone lung adrenal ovary etc

114
Q

Inflammatory breast carcinoma

A
  • This is not a ‘special’ type of carcinoma but rather a clinical description
  • Skin changes – red, thickened, ‘peau d’orange’ appearance

• Appearance due to permeation of dermal lymphatics by tumour
and resultant oedema

The prognosis is poor

115
Q

Most important prognostic features in breast cancer

A
  • Histological type (in situ vs invasive and histomorphology)
  • Stage –TNM (Tumour size etc, Nodes, Metastasis)
  • Histological grade (1, 2, 3)
116
Q

Routinely assessed prognostic factors in breast cancer

A
  1. hormone receptor status - ER + PR

2. HER2 status

117
Q

HER2 and breast cancer

A

• HER2 is an oncogene

• Gene amplification or receptor overexpression
activates HER2 receptors and stimulates cell growth

  • Occurs in about 10-15% of BC, up to 30% of metastatic carcinomas
  • Associated with poor prognosis
  • Amplification is an indication that anti HER2 therapy may be useful
118
Q

normal menstrual cycle

A

Proliferative phase
secretory phase - 14 days following menstruation
menstrual phase - stromal breakdown following involution of the corpus luteum

119
Q

Abnormalities in cycle development which result in dysfunctional uterine bleeding

A

o anovulatory cycles

o inadequate luteal phase

o irregular or delayed shedding

120
Q

Anovulatory cycles

A

• commonest cause DUB

  • typically occurs near menarche/menopause
  • follicles develop with oestrogen production
  • no ovulation – no prog from corpus luteum
  • endometrium proliferates and then when follicles regress - withdrawal bleeding
  • histology: proliferative endometrium with stromal breakdown
  • if prolonged – disordered proliferative - variably spaced and shaped glands with cystic dilatation
  • can eventually lead to hyperplasia/cancer
121
Q

Inadeqaute luteal phase

A

• ovulation occurs but inadequate prog secretion by corpus luteum
• either fails to develop or premature regression
• histology: secretory changes but less well developed with glands lacking tortuosity, discordant stromal breakdown
can be a cause of infertility/spontaneous abortion

122
Q

Effects of exogenous hormones: oestrogen and progestins

A

Oestrogen:
• proliferative changes + stromal breakdown as endometrium cannot support continued growth

  • disordered proliferative
  • eventual hyperplasia/carcinoma

Progestins:
• variable effect

  • short term: secretory glandular changes and stromal decidualisation
  • long term: downregulation of ER/PR receptors with eventual atrophy
  • high dose therapy can cause superficial necrosis
123
Q

Effect of oral contraceptive pill on uterus

A

• simple tubular glands in vascular decidualised stroma +/- stromal breakdown

124
Q

Endometrial polyps

A
  • common, particularly perimenopausal, less frequent after 60yrs
  • increased in tamoxifen treatment
  • biphasic growth of benign glands + stroma
  • usually non-functional (no cyclical change)
  • abnormal PV bleeding

• may be involved by neoplastic processes

125
Q

Endometritis

A
  • may be acute or chronic
  • often non specific
  • specific forms: Neisseria gonorrheae/Chlam (STD), TB, post-partum/abort, pyometra, IUCD
  • variable symptoms, may lead to PID (abdo pain, fever, raised WCC), infertility
  • often unable to date endometrium
126
Q

Adenomyosis

A

• common, benign, non-neoplastic

  • deep extension of endometrial glands and stroma into myometrium (?1mpf)
  • associated with muscle hypertrophy
  • typically occurs late reproductive yearscan cause abnormal uterine bleeding/pain
  • may cause recurrence of symptoms after endometrial ablation therapy
127
Q

Staging of endometrial carcinomas

A

Stage 1 - confined to uterus (subdivided according to depth of myometrial invasion)

Stage 2- extension to cervix

Stage 3- invasion of serosa, adnexae or positive peritoneal cytology

Stage 4- bladder/bowel invasion or distant metastasis

128
Q

Most common gynaecological malignancy

A

endometrial cancer

129
Q

Type 1 endometrial carcinoma

A
  • oestrogen driven, arising in hyperplasia
  • Endometrioid subtype

• perimenopausal and post menopausal women (younger than type 2 )
• Molecular changes:
PTEN, beta catenin, MMR gene mutations, K-ras
• p53 mutations rare

• generally good prognosis - low grade/early stage

130
Q

Hereditary endometrial carcinoma

A
  • tend to develop disease 15yrs earlier
  • most have Lynch syndrome (HNPCC): endometrial Ca as common as CRC, 70% lifetime risk
  • mutations in DNA mismatch repair genes producing MSI
  • MSH 2/6 mutations more common
  • generally seen type 1 endometrial carcinoma  BRCA patients- increased risk?
131
Q

Risk factors for type 1 endometrial cancer - causes of hyper-estrogenism

A
  • obesity
  • anovulation (PCOS)
  • hormonal therapy (HRT, tamoxifen)
  • oestrogen secreting ovarian tumours
  • relative progestogen deficiency
132
Q

Endometrial hyperplasia

A
  • precursor lesion to type 1 carcinoma
  • oestrogen induced
  • typically perimenopausal (anovulatory cycles)
  • also younger women (PCO) or postmenopausal (excess endogenous or exogenous oestrogen)
  • may present with abnormal bleeding
  • macroscopically thickened endometrium
133
Q

Histology of simple hyperplasia without apia

A
  • increased gland to stromal ratio
  • variable sized and shaped glands, often dilated

cytologically resembles normal proliferative

134
Q

Atypical hyperplasia

A
  • usually complex
  • very crowded glands with complex infoldings
  • nuclear enlargement, rounding, nucleoli
135
Q

Treatment of hyperplasia

A
  1. surgery

2. progestins

136
Q

Type 2 endometrial cancer

A

• 10-15%

  • no assoc with raised oestrogen/hyperplasia
  • older patients (post-menopausal)
  • often high grade serous or clear cell types
  • p53 mutations common
  • often extrauterine spread
  • generally poor prognosis
137
Q

Precursor leasions in type 2 endometrial carcinoma

A
  • endometrial intra-epithelial carcinoma (EIC)/serous carcinoma in situ
  • similar molecular pathology to invasive serous carcinoma
  • non-invasive replacement of endometrial surface or glandular epithelium by one or more layers of malignant serous cells
138
Q

Types of mesenchymal tours of the uterus

A

Smooth muscle tumours
• leiomyoma - benign
• leiomyosarcoma - malignant
Endometrial stromal tumours

139
Q

Leiomyosarcoma

A
  • Malignant smooth muscle tumour

<1-2% of all uterine SMT
• rapid growth, especially post menopausal
• macro: often single, large, variegated, hemorrhage, necrosis
• micro: high cellularity, cellular atypia, infiltrative, mitotic activity, tumour necrosis
• aggressive (<50% 5YS)
• not responsive to therapy

140
Q

Endometrial stromal tumours classification

A
  • endometrial stromal nodule – circumscribed
  • endometrial stromal sarcoma (low grade)
  • Endometrial stromal sarcoma (high grade)

undifferentiated stromal sarcoma – no resemblance to endometrial stroma

141
Q

Low grade endometrial stromal sarcoma

A
  • most common, low grade malignancy
  • composed of cells resembling endometrial stroma

• infiltrative growth

  • treatment: surgery, high dose progestins
  • indolent growth, late recurrence, can metastasize
142
Q

Carcinosarcomas

A
  • malignant mixed mullerian tumours (MMMT)
  • epithelial malignancy with a malignant mesenchymal component
  • shares some molecular findings and risk factors with type 1 endometrioid carcinoma
  • often polypoid mass
  • epithelial component often serous
  • homologous or heterologous stroma (eg chondrosarcoma/rhabdomyosarcoma)
  • poor prognosis
143
Q

Prostate anatomy and function

A
  • Pear shaped retroperitoneal glandular and fibromuscular organ encircling neck of bladder and urethra
  • Weighs up to 20g in normal adult
  • Depends on androgenic hormones from testis for differentiation, growth and survival
  • Castration leads to atrophy caused by widespread apoptosis
144
Q

Lobes and zones of the prostate

A

• Traditionally five lobes (Lowsley): anterior, posterior, middle, two lateral
• Some consider 4 zones – peripheral, central transitional, periurethral
• Simplest physiological and pathological division is into:
inner (periurethral) zone: site of origin of nodular hyperplasia and (rare) large duct carcinoma
outer (cortical) zone: site of predilection for usual adenocarcinoma of prostate

145
Q

3 Common conditions of the prostate

A
  1. Benign prostatic hyperplasia – most common
  2. Neoplasms of the prostate
  3. Inflammatory conditions – prostatitis – acute, chronic, bacterial, abacterial, granulomatous
146
Q

Causes of bacterial prostatitis

A

• E coli and other Gram negative organisms

147
Q

Acute and chronic bacterial prostatitis

A
  • Acute - acute febrile illness, painful prostate+++

* Chronic- pelvic pain, history of recurrent urinary tract infection. May be asymptomatic

148
Q

Histology of bacterial prostatitis

A

• Histologically – inflammatory infiltrate includes neutrophils even in chronic prostatitis

149
Q

Abacterial prostatitis

A
  • More common than bacterial
  • Not associated with UTI
  • Leucocytes in secretions but negative culture
  • Some are STD-associated (Chlamydia trachomatis, Ureaplasma urealyticum, Mycoplasma hominis, Trichomonas vaginalis)
  • Can be refractory and difficult to treat
150
Q

Granulomatous prostatitis

A
  • May be non-specific: seen following duct rupture
  • Some specific infections – tuberculosis, fungal infections etc
  • Most often seen following BCG (attenuated mycobacterial strain instilled into the bladder for treatment of superficial bladder cancer
151
Q

Incidence of benign prostatic hyperplasia

A

Histologically 20% of men aged 40
70% of men aged 60
90% of men aged 80
But less than 50% are symptomatic

152
Q

Pathogenesis of BPH

A
  • dependent on action of androgenic hormones
  • dihydrotestosterone (DHT) derived from testosterone (enzyme Type 2 -reductase, located in stromal cells)
  • DHT accumulates in prostate, binds to receptors and promotes transcription of growth factors (esp FGF which stimulates stromal and, indirectly, epithelial growth, and TGF-β which stimulates stromal but inhibits epithelial growth)
  • increased epithelial cell numbers probably due to reduced apoptosis
  • relative increase in oestrogens (oestradiol) in elderly may sensitise prostate to DHT- by inducing androgen receptor (esp in inner zone)
153
Q

Macroscopic morphology of BPH

A
  • Firm rubbery enlargement up to 200g (N=20g)
  • Begins in inner part of gland (transition zone)
  • Nodules encroach on lateral walls of urethra
  • Multinodular proliferation surrounded by compressed prostatic tissue (pseudocapsule)
  • Nodules vary in appearance according to composition, May be cystic
154
Q

Microscopic morphology of BPH

A
  • Hyperplasia may be glandular, muscular, fibrous or mixed
  • Glandular proliferation - aggregates of small- large, often cystically dilated glands, lined by 2 cell layers
  • Cysts contain secretions ± corpora amylacea
  • Often squamous metaplasia, secondary inflammation, infarction
155
Q

Clinical manifestations of BPH

A
  • early symptoms relate to urinary obstruction due to increased size and muscular contraction
  • “prostatism”- poor urinary stream, dribbling, frequency, difficulty in ‘starting and stopping’, nocturia, dysuria etc
  • rectal examination- enlarged, nodular, soft, boggy gland
  • may be acute urinary retention requiring catheterisation
  • late manifestations related to urinary retention, infection, recurrent urinary infections
156
Q

End stage BPH

A
  • bladder hypertrophy
  • ureteric obstruction
  • hydronephrosis
  • chronic pyelonephritis
157
Q

Treatment of BPH

A
  • Controlled volume, timing and type of fluid intake
  • -blockers to decrease prostatic muscle tone
  • Inhibitors of 5- reductase to shrink prostate size
  • Surgery (TURP)
  • Alternative procedures – ultrasound, laser therapy, radiofrequency ablation etc
158
Q

Commonest cancer in males and the prevalence

A

Carcinoma of the prostate and 1 in 6-7 lifetime risk

159
Q

Nearly all prostate neoplasms are:

A

Adenocarcinomas

160
Q

Risk factors/aetiology of prostate cancer

A
  • age

race (polymorphisms in AR gene etc)
• endogenous hormones: DHT required
• family history
• “? premalignant” conditions- atypical acinar hyperplasia, duct-acinar dysplasia, prostatic intraepithelial neoplasia
• carcinoma in situ (usually high grade +/- invasion)
l environmental factors- ? cadmium, methyl cholanthrene,
• viruses, dietary factors etc
• various acquired genetic abnormalities and epigenetic phenomena recognised

161
Q

Familial prostate cancer

A
  • 3-5% of cases
  • autosomal dominant inheritance
  • various genes identified – BRCA2, HOXB13
  • early onset, often < 50 years
  • often multifocal disease
  • 40 ‘risk associated’ loci identified which account for approximately 25% of familial risk
162
Q

> 75% of prostate cancer arises in which zone?

A

Outer zone/ peripheral

163
Q

TNM staging of prostatic cancer

A

T1 - incidental, unsuspected clinically (T1a/b according to volume and grade)
T2 - palpable, confined to prostate
T3a/b - extracapsular extension
(a/b according to seminal vesicle invasion)
T4 – direct invasion of pelvic organs

N0/N1 according to presence or absence of lymph node metastasis. Lymph node metastasis: ’incurable’

M0-1

164
Q

Clinical course of prostate cancer

A

Stage T1 and T2: better than 90% 15 year survival (but still 30-50% of T1b progress)
Stage T4: 10-40% 10 year survival

165
Q

Treatment of prostate cancer

A

nil, surgery (if node negative), radiation, hormonal manipulation (oestrogens, anti-LHRH) ? gene therapy

12- REPRO (7 decks)

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