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Esa 4 > Repro > Flashcards

Repro Flashcards

1
Q

What occurs in the fetal period (breifly)

A

Growth and maturation of structures developed in embryonic period
Early = protein deposition
Late = adipose desposition

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2
Q

LMP vs weeks post fertilisation?

A

LMP = fert +2

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3
Q

When does the CRL increase rapidly?

A

Pre to early fetal

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4
Q

Ante-natal assessment of fetal well being?

A

Mother and fetal movements
Uterine expansion - symphysis fundal height
Ultra sound

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5
Q

Uses of Obstetric ultrasound scan (USS)?

A

Check age in early pregnancy
20 weeks
Fetal abnormalities and growth

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6
Q

Purposes of a 7-13 week scan?

A

Estimate from CRL the EDD and the time of cenception

Check location, number and viability

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7
Q

Uses of the biparietal diameter

A

Used to date pregnancies in T2/3 in combination with other measurements e.g. abdominal circumference and femur length.
Also used for anomaly detection (more AC and FL)

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8
Q

Describe the classification of birth weights

A

3500g normal

4500 maternal diabetes - macrosomia

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9
Q

Stages of lung development?

A

Pseudoglandular 8-16 weeks
Canalicular - 16-26
Terminal sac stage - 26+

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10
Q

Describe the pseudoglandular stage

A

Duct system develops from the bronchopulmonary trunk

Bronchioles

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11
Q

Describe the canalicular stage

A

Respiratory bronchioles bud off from bronchioles formed during the pseudoglandular stage

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12
Q

Describe the terminal sac stage

A

Terminal sacs bud from resp bronchioles.

Differentiation of Type 1 and 2 pneumocytes (surfactant)

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13
Q

What factors aid lung development?

A

Fluid filled

Breathing movements

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14
Q

What are the implications for pre term survival

A

THreshold of viability is the lungs, only possible once lungs have entered the terminal sac stage >24 weeks

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15
Q

What is respiratory distress syndrome?

A

Pre mature infants
insufficient surfactant pproduction
glucocorticoid treatment for mother as this increases surfactant

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16
Q

Definitive fetal HR when?

A

15 weeks

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17
Q

Describe development of urinary system later

A

Kidney function at 10 weeks

Not neccessary for survival but without there is oligohydramnios

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18
Q

Desribe the development of the nervous system

A

Myelination of brain begins at 9 months and finishes after birth
Coordinated voluntary movement develops at 4 month

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19
Q

First movement?

A

8 weeks

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20
Q

What is quickening

A

at 17 weeks, increase in fetal awareness

way of antepartum surveilance

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21
Q

Describe O2 supply to fetus

A

Incre pO2 in mother and low in fetus (4kPa).
Hb 70% sat at 4kPa - more hb than adults
Double bohr effect in both fetal and maternal blood??

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22
Q

Describe CO2 and the fetus

A

Cannot tolerate CO2
Lower maternal CO2
Prog stimulates maternal hyperventilation

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23
Q

Sat of blood and to the brain in fetus

A

Blood shunted to brain- bypass liver via Ductus venosus (70-65% with IVC) - bypass lungs via foramen ovale (directed by crista dividens- part of septum secundum, joins pulmonary flow in LA 65-60%) and ducuts arteriosus
SVC tends to go to RV as is superior to RV

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24
Q

Describe functions and secretions of amniotic fluid

A 
Mechanical protection
Moist environment
Other functions
10ml at 8 weeks
1l at 38 weeks
300ml at 42 weeks.
Constant turnver - early maternal secretion and diffusion with embryo ECF. late - fetal production.
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25
Q

Production of fetal urine

A

100ml a day at 25 weeks to 500ml hypotonic.

Constantly swallows amniotic fluid forming meconium

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26
Q

Fetus and bilirubin

A

Fetus cannot conjugate and thereofore remove bilirubin so crosses the placenta - may get jaundiced as a neonate if conjugation does not establish quickly

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27
Q

Describe rhythms in the fetus

A

Breathing movement and HR.

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28
Q

Function of cytotrophoblast

A

Repairs syncytiotrophoblast

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29
Q

Function of the syncytiotrophoblast

A

Invades maternal epithelium and lacunae to establish utero-placental blood flow.
Allows for diffusion - multi nucleated sheet

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30
Q

what does haemomonochromal mean?

A

The chorion/ membrane/ placenta is in direct contact with maternal blood

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31
Q

Describe implantation in terms of villi

A

Primary - invaginations of trophoblast
Secondary - invasion of a mesochyme core
Tertiary - invasion of mesenchyme core with fetal blood vessels.
Slowly cyto regresses and syncytio thins

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32
Q

How does the endometrium prepare for an implantation

A

Pre decidual cells

Spiral arterial blood system - high flow, low resistance vascular bed

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33
Q

What is decidualisation

A

Pre decidual cells balance the invasive force of the trophoblast

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34
Q

Describe the development of fetal membranes

A

Initially chorion has villi all around the embryo (week 5).
Week 12 - villi only located at decidua basalis (disk shape chorion) leaving chorion laeve (smooth chorion) the other side. this is because, cytotrophoblast thins so smaller sa needed? Decidua capsularis and parietalis fuse forming composite membrane at week 22

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35
Q

Results if 2 embryoblasts vs 2 primitive streaks

A

2 amnions vs 1, both share a placenta

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36
Q

gross morphology of amnion

A

Maternal aspect - cotyledons

Fetal aspect - umbilical cord. Covered in amnion, chorionic vessels underneath

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37
Q

Major substances that are transported across placenta by mode of travel

A

Simple diffusion- gases, urea, uric acid, water, electrolytes
Facillitated - glucose
Active - aa, iron, vitamins
RME - Igg (Rhesus -prophylactic treatment)

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38
Q

Common tetratogens

A 
Thalidamide
Alcohol
Therapeutic drugs e.g. warfarin
Drugs of abuse
smoking
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39
Q

Infectious agents that can cross placenta

A

Varicella zoster, cytomegalovirus, treponema pallidum, toxoplasma gondii, rubella

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40
Q

Describe the metabolic functions of the placenta

A

Synthesise glycogen, cholesterol and fatty acids

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41
Q

Describe the endocrine functions of the placenta

A 
Produces protein and steroid hormones.
Steroid: Prog and oes
Proteins:
HCG
HCS (somatomammotrophin
HCt thyrotrophin
Hgc Corticotrophin
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42
Q

Clin sig of HCG

A

Pregnancy tests
Only produces by syncytiotrophoblast
Very high HCg - hydratidiform mole (fertilised non viable implantation)
or high in coriocarcinoma

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43
Q

Function of HCs/ HPL (human placental lactogen)

A

Increase glucose available, affects maternal metabolism

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44
Q

How does prog alter maternal metab?

A

Increased appetite

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45
Q

Major causes of complications in pregnancy

A

Placental insufficiency

Pre-eclampsia

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46
Q

Describe placental insufficiency

A

May cause pre eclampsia, stillbirth, olighydramnios or miscarriage.
Not enough blood flow
Often drop in HR later on

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47
Q

Describe pre eclampsia

A

Hypertension and proteinuria - impaired liver and kidney function if severe. When seizures then eclampsia.
Risk factors include hypertension, obesity, DM.
Can be causes by vasoconstriction due to defect in placentation

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48
Q

Describe gestational diabetes

A

Caused by HPL/ hCs increasing insulin resistance and gluconeogenesis (also O&P, prolactin and cortisol)
Decrease in fasting blood glucose normal in preg.
Can lead to macrosomic fetus, stillbirth and increased risk of congenital defects

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49
Q

Describe antenatal screening of mother

A

Risk factors for gestational diabetes
Blood - rhesus, hb, infection e.g. syph and HIV
Urinalysis - protein and kidney function (pre-eclampsia)

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50
Q

Describe CVS changes in pregnancy

A 
From T1:
CO increases 40%
SV increases35%
HR increases 15%
TPR decreases 25-30%
Increase in BVol
BP decreases in T1/2 but returns in T3.
BP may decrease due to prog effect on systemic vascular resistance (SVR) and also compression of uterus on aortocaval but rare that systolic increases,
Endothelium dilates
Vasospasms
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51
Q

Describe urinary effects of prgnancy

A

Increase in RPF and GFR
Filtration capacity intact
Decrease in functional renal reserve.
Urea and creatinine both decrease around 50%
Urinary stasis - pressure - hydroureter
UTI - pyelophritis causing pre term labour

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52
Q

Resp effects of prgancy

A

Decrease functional residual capacity
AP and transverse diameters increase and physiological changes.
Same VC.
Increased tidal vol and minute and alveolar ventilation.
RR unchanged although may increase due to prog and CO2.
Hyperventilation causes alkalosis- compensated by bicarb excretion.

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53
Q

Effects of pregnancy on lipid metabolism

A

Increase in lipolysis from T2 so increase in plasma fa - use instead of glucose. Fas can cross placenta.

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54
Q

Effects of pregnancy on thyroid

A

More T3/4, hCG stims, TSH decreases

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55
Q

Effects of pregnancy on GI

A

Anatomical - appendix in RUQ

Physiological - decrease in SM tone by prog so risk of biliary stasis, pancreatitis and delayed emptying,

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56
Q

Immune system effects of pregnancy

A

Fetus is an allograft so non specfic suppression of local immune response at materno-fetal interface needed. Transfer of antibodies can transfer haemolytic diseases and graves/ hashimotos.

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57
Q

Haematological consequences of pregnancy

A

Pro thrombotic, fibrin at implantation site. Increase fibrinogen and clottin factors. Reduced fibrinolysis
stasis and venodilation
Thromboembolic disease (cant have warfarin)
Anaemic - dilutional and due to Fe and folate deficiency
haemoglobinopathies

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58
Q

List the phases of coitus

A

Excitement
Plateau
Orgasmic
Resolution (+/- refractory phase)

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59
Q

Describe the events of the female sexual response

A 
Blood engorgement and erection: clitoris, vaginal mucosa, breast and nipples
glandular activity
Sexual excitement 
\+/- orgasm
No physiological refractory period
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60
Q

Describe the main components of semen and their origins

A

60% seminal vesicles- fructose, clotting factors (semeogelin), alkaline to neutralise urethra and vagina, prostaglandins.
25% prostate - slightly acidic, citrate, acid phosphatase, proteolytic enzymes, (reliquify in 10-20 mins)
Bulbourethral glands - alkaline, lubricate urethra and penis,
2-4ml total.
20-200 x106 sperm per ml,

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61
Q

Describe stimulants and efferents involved in erection of the penis

A

Stimulants - psychogenic and tactile -penis and perineum via spinal reflex
Efferents - peudendal (somatic), pelvic (PNS)

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62
Q

Describe physiological

A

Central arteries of corpora cavernosa dilate due to inhibition of SNS, activation of PNS and non-adrenergic/ cholinergic autonomic nerves to arteries to release NO.
PNS - M3 (endothelial) - Ca - NO - diffuse into SM - vasodilate

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63
Q

What does viagra do?

A

Inhibits cGMP breakdown (cGMP inhibits MLCK)

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64
Q

What causes erectile dysfunction

A

Psychological - inhibition of spinal reflexes
Tears in fibrous tissue of corpora cavernosa
Alcohol, antihypertensives and diabetes blocking NO
Vascular

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65
Q

Describe mechanisms of ejaculation

A

Leakage of ejaculate into prostatic urethra (VD peristalsis). secretions of bulbourethral glands - EMISSION

SNS (L1-2)- spinal and cerebral reflex:
Contraction of glands and ducts.
Rhythmic contraction of bulbo/ischiospongiosus, hip and anal muscles
Bladder internal sphincter contracts.

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66
Q

Describe capacitation of sperm

A

Further maturation of sperm in female reproductive tract 6-8 hours.
Membrane changes allowing fusion with oocyte.
Tail from beat to whip like action

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67
Q

Describe the acrosome reaction process

A

Sperm moves through granulosa and head proteins bind to ZP3 on zona pellucida. Acrosome reaction, hydrolysis enzymes digest path through ZP, one sperm penetrates.
Cortical reaction blocks polysperm

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68
Q

What happens when sperm is in cytoplasm?

A

Meiosis 2
Fusion of pronuclei
Mitosis.

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69
Q

Why does sperm wait in uterine tube for 3 days?

A

Waiting for rise in prog to cause SM relaxation

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70
Q

What aids sperm transplant?

A

Loss of mucous plug in cervic (only with prog).

Oestrogen makes it abundant clear non viscous mucous

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71
Q

List the phases of coitus

A

Excitement
Plateau
Orgasmic
Resolution (+/- refractory phase)

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72
Q

What is wrong with coitus interruptus?

A

Sperm in pre ejaculate

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73
Q

Describe abnormal sperm production

A

Testicular disease
Obstruction -surgery or infection
Hypo/ pit dysfunc
Semen analysis - >2ml, >20 mil per mil, motility >50, morphology >50

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74
Q

Describe vasectomy

A

Bilaterally divided

Measure sperm before using

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75
Q

Describe ways of preventing sperm reaching the cervix from the vagina

A

Condoms - STDs
Diaphragm - diagonally - holds in acidic environment of vagina, needs correct fitting, does not completely occlude
Cap - Fits across cervix, physical barrier
Useful with spermicide

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76
Q

Ways of preventing ovulation and other effects

A

Combined OCP - prevent LH surge, inhibit follicular development via neg feedback
Depot prog - 3 monthly injections, neg feedback
Oral prog - low dose only - may inhibit ovulation, main action is to affect cervical mucus
Implant - same as oral.
All affect cervical mucus and affect receptivity of endometrium

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77
Q

Methods of female sterilisation

A

Tubes - rings, ligation and clips.

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78
Q

Describe post coital contraception

A

Combines O/P high dose or prog. Disrupt ovulation, block implantation and impair luteal functioning

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79
Q

Describe intra-uterine device

A

Post-coital contraception up to 5 days after.
Inert, copper or prog impregnanted.
Copper - endometrial enxymes, sperm transport and implantation

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80
Q

Define infertility and the types

A

Failure to conceive within 1 year of trying (15%) primary or secondary (previous pregnancy)

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81
Q

Causes of infertility

A

20-30% ARE UNEXPLAINED
Anovulation 15-20
Tubule occlusion 15-40
Abnormal/ absent sperm production 2-25

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82
Q

Causes of anovulation

A

Pituitary tumour, extremes of reproductive life, ovarian failure, weight loss, stress, exercise, hyperprolactinaemia (hypo), radiotherapy, chemotherapy, menopause.
Can be pit, hypo or ovary.

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83
Q

Describe polycystic ovarian syndrome

A

Not sure if pit or ovary.
Excess androgens and increased LH/ FSH
Multiple small ovarian cysts
Insulin resistance
Anovulation with possible amenorrhoea or oligomenorrhoea.
Diagnose voa serum prog and hormones - differentiate from Menopause, ovarian failure and hypo/ pit failure

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84
Q

Induction of ovulation how?

A

Anti oestrogen to inhibit neg feedback, plsalise GnRH agonist and Gonadotrophs (FSH)

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85
Q

Describe tubule occlusion

A

Cause - sterilisation, endometriosis or scarring from infection
Diagnosed laparoscopically, dye insufflation or hysterosalpingogram
Treatment - surgical reanastomosis and assisted conception

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86
Q

Describe the scrotum, its innervation, lymphatic drainage and blood supply

A

Develop from labioscrotal folds.
Anterior - lumbar plexus (anterior scrotal nerve)
Posterior - sacral plexus (posterior scrotal nerve)
Lymph - superficial inguinal nodes
Arteries - anterior (femoral) and posterior (internal pudendal) scrotal arteries
Vein - anterior and posterior scrotal veins

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87
Q

Common pathology of testes and scrotum

A

Hydrocoele - serous fluid in tunica vaginalis
Haematocoele - blood in tunica vaginalis (translumination to differentiate)
Varicocoele - varcosities of panpiniform plexus
Spermatocoele e.g. epididymal cyst
Epididymitis - inflam
Indirect hernia if processus vaginalis reopens
Testicular torsion - necrosis of testes - absent gubernaculum

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88
Q

Anatomy of the epidydimis

A

Head, body, tail, connects via efferent ductules and rete testis

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89
Q

Route of the spermatic cord

A

From deep inguinal ring to posterior boarder of the testis. Through the superficial ring and inguinal canal.

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90
Q

Contents of the spermatic cord

A

3x3ish
Arteries: To vas, cremasteric and testicular
Nerves: Genital branch of genitofemoral (to cremastor), testicular (symp) and ilioinguinal (outside of cord)
Other: Lymph, vas and processus vaginalis, pampiniform plexus

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91
Q

Describe the coverings of the spermatic cord

A

External spermatic fascia (external oblique) Cremasteric muscle and fascia (internal oblique and transversalis), Internal spermatic fascia (transversalis)

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92
Q

Describe the course of the vas

A 
Ascends in spermatic cord
travels around pelvic side wall
Passes between bladder and ureter
Forms dilated ampulla 
Opens into ejaculatory duct
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93
Q

describe the anatomy of the seminal vesicles

A

Between bladder and rectum.
Diverticulum of vas.
Duct of SV combines with vas to form ejaculatory duct

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94
Q

Describe the anatomical relationships of the prostate

A

Base - neck of bladder
Apex - urethral sphincter and deep perineal muscles
Anterior - urethral sphincter?
Posterior - ampulla of rectum

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95
Q

Describe the lobes and zones of the postate

A

lateral, anterior, posterior and median lobes.

Zones - Central peripheral

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96
Q

Describe BHP

A

Middle lobule, nocturia, dysuria, urgency

Obstruction of internal urethral orifice

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97
Q

Describe prostatic malignancies

A

Peripheral zone. mets to internal iliac or sacral nodes. venous to internal vertebral plexus - to vertebrae or brain

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98
Q

Treatment of pelvic floor dysfunction

A

Pelvic floor exercises
Incontinence surgery e.g. vaginal tapes, slings - overactive bladder disease and voiding difficulty.
Prolapse surgery - replace organs, restore CT, maintain function - recurrence, incontinence and dyspareunia

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99
Q

Descirbe the muscles of the superficial perineal space

A

Ischiocevernosus - Increase pressure on venous system to help maintain erection.
Bulbospongiosus - expell last drops of urine and helps maintain erection,
Lavator ani
External anal sphinctor
Superficial transverse perineal muscle.
Cremasteric muscle - regulation of balls temp

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100
Q

What is the most inferior part of the peritoneum and how is it accessed in a female?

A

Pouch of douglass/ rectouterine pouch. Posterior vaginal fornix
Culdocentesis

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101
Q

Describe the broad ligament and the round ligamnet

A

Broad ligament - double fold of peritoneum.
Round ligament - from uterine horns to labia major.- keeps anteflexion along with cardinal lgament (base of broad ligament). also lymph to superficial inguinal nodes along it

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102
Q

Where is the deep perineal pouch?

A

Between pervic diaphragm and perineal membrane. Sometimes referred to as superior and inferior fascia of pelvic diagphragm

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103
Q

contents of the deep perineal pouch

A

Membranous (males)/ proximal (female) urethra
Inferior part of external urethral sphincter
Anterior extension of ischio-anal fat pad.
Male - deep transverse perineal muscles, bulbourethral glands

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104
Q

Location of the superficial perineal pouch

A

Between perineal fascia around muscles and perineal membrane bounded laterally by ischiopubic rami.

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105
Q

Contents of the superficial perineal pouch

A 
Superficial transverse perineal muscles.
Bulbospongiosus and Ischiocavernosus. 
Urethra (bulbous in males)
Deep perineal branches of the internal pudendal vessels and nerves.
Females:
Vagina, clitorus
Males: Crus and bulb of penis)
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106
Q

Functions of the perineal body. What is it?

A

Anchors perineal muscles, rectum and aids pelvic support.

A connective tissue mass in the centre of the perineum (muscle fibres too which converge from everything).

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107
Q

When can the perineal body become damaged and what would be the consequences?

A

During child birth

Weakness in pelvic floor leading to prolapse of vagina and uterus. Urinary incontinence

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108
Q

How can childbirth damage the pelvic floor

A

Stretch pudendal nerves - neuropraxia and muscle weakness.
Damage to muscles - weakness
Stretch/ repture of ligaments and supports of muscles

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109
Q

What other factors lead to pelvic floor dysfunction

A

Age, menopause (atrophy from oestrogen withdrawral), obesity, chronic cough, connective tissue disorders

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110
Q

Describe blood supply to the ovaries

A

Ovarian artery from AA

Right and left into IVC and left renal vein respectively

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111
Q

Describe the ligaments of the ovary

A

Suspensory ligament - fold in the peritoneum (terminal part of broad ligament and the ligament of the ovary

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112
Q

Describe the position of the uterus

A

Anteverted (at vagina) and anteflexed (cervix). May be retroflexed/ verted meaning its more likely to prolapse/ child brith complications e.g. constipation

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113
Q

Parts of the uterine tube

A

Abdominal ostium, infundibulum (funnel), ampulla, isthmus (thin)

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114
Q

Parts of the cervix

A

internal and external os with endocervical canal inbetween

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115
Q

Ligaments of the cervix

A

Transverse cervical ligaments (cardinal) - thickening at base of broad ligament. stabalises laterally.
Uterosacral ligament - posterior (2 of them) opposes anterior pull of round ligament assisting mantainence of anteversion

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116
Q

Blood supply to cervix

A

Uterine and internal pudendal (both anterial division of internal iliac)

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117
Q

Lymphatic drainage of internal female organs

A

Ovary - paraortic
Fundus - aortic and inguinal
Body - external iliac
Cervic - external and internal iliac and sacral

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118
Q

Describe the female external genitalia

A

Labia majora - encloses pudendal cleft
Labia minora - encloses vestibule
Vestibule - orifaces of vagina, urethra and greater and lesser vestibular glands
Greater vestibular glands (bartholin) secrete mucus for vaginal lubrication

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119
Q

Describe bartholinitis

A

From chlamyd or gonn. May cause cyst if obstructed - infection - abcess

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120
Q

Describe innervation to the vagina and external genitalia

A

upper 4/5 uterovaginal plexus
lower 1/5 somatic pudendal
Pain afferents vary on pelvic pain line - inferior thoracic lumbar spinal ganglia, S2-4 spinal ganglia.
Perineum - pudendal and ilioinguinal nerve
Pudendal nerve exits GSF, and enters via LSF through the pudendal canal

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121
Q

Difference between STI and STD

A

STD with symptoms

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122
Q

Discuss the risk factors for STIs

A

Young, socioeconomic group, number of parters, orientation, unsafe activity, ethnic group ect.

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123
Q

Briefly describe the prevalence of STIs

A

Chlamydia most common followed by papillomavirus.

Gonorrhea and Syphilis in men who have sex with men

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124
Q

Describe the pathogen in Chlamydia infections

A

Chlamydia trachomatis - obligate intracellular gram negative bacterium - cocci or rods.
Serotypes D-K

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125
Q

Symptoms of Chlamydia infections

A

Males: Urethritis, epididymitis, prostatitis, proctitis
Females: Urethritis, Salpingitis, cervicitis, perihepatitis.
Eye - conjunctivitis
Neonate - inclusion conjunctivits and pneumonia

126
Q

Diagnosis of chlamydia

A

Endocervical or urethra swab
1st void urine
conjunctiva swab
NAAT - nucleic acid amplification test

127
Q

Treatment of chlamydia

A

Doxycycline or azithromycin. Erythromycin in kids

128
Q

Pathogen in Gonorrhea

A

Neisseria Gonorrhoeae, gram neg diplocci

129
Q

Symptoms of gon

A

Male: Urethritis, prostatitis, epididymitis, proctitis, pharyngitis
Female: Asymptomatic, Endocervitis, PID, urethritis
If diseminated then bacteraemia, skin and joint lesions

130
Q

Diagnosis of Gonorrhea

A

Swab (pharyngeal), urine (NAAT)

131
Q

Treatment of gonorrhea

A

Ceftriaxone and azithromycin (prevent resistance and treat chlamydia)

132
Q

Causitive organism in Herpes

A

Herpes Simplex Virus2.

HSV1 normally associated with cold sores

133
Q

Explain symptoms of herpes infection

A

Primary infection - painful genital ulceration, dysuria, fever, inguinal lymphadenopathy.
Recurrent infection or ma remain latent. Asymptomatic - severe. Virus latent in dorsal root ganglia

134
Q

Treatment of herpes (and prevention)

A

Aciclovir (barrier contraception helps prevent transmission)

135
Q

Describe causes of genital warts

A

HPV (6 & 11). 16 & 18 are oncogenic (verical and anogenital

136
Q

Symptoms of genital warts

A

Benign, painless, verucous epithelial or mucosal outgrowths (cutaneous, mucous or anogenital).
Vaccine for all common/ oncogenic straigns 99% effective

137
Q

Diagnosis of genital warts

A

Clinical, biopsy and genotype analysis, hybrid capture (from cervical swab).
Screening:
Cervical pap smear cytology -cancer
Colposcopy (cervix contains any abnormal cells) + acewhite test

138
Q

Treatment of genital warts

A

None

Cryotherapy, topical podophyllin, interferon, surgery

139
Q

Describe the pathogen in syphilis

A

Treponema pallidum - spirochaete

140
Q

Describe the symtoms of syphilis

A

Primary - indurated (hard) ulcers (chancre) painless.
Secondary -lymphadenopathy, mucosal lesions, fever, rash, malaise
Tertiary - neurosyphilis, GPI (general paralysis of the insane) Tabes dorsalis

141
Q

Diagnosis of syphilis

A

Serology

142
Q

Treatment of syphilis

A

Penicillin

143
Q

Rarer causes of inguinal lymphadenopathy

A

Lymphogranuloma venereum (LGV)-C trepoma
Chancroid- Haemophilus ducreyi, painful genital ulcers
Granuloma inguinale/ Donovanosis (Klebsiella glanulomatis)

144
Q

Describe trichomonas vaginalis

A

Flagellated protozoan
Thin frothy and offensive discharge
Irritation, dysuria and vaginal inflammation
Vaginal wet preparation +/- culture enhancement
Treated with metronidazole

145
Q

Describe vulvovaginal candidiasis

A

Candida species
Profuse, white itchy, curd like discharge
Topical azoles, oral fluconazole or nystatin
Diagnosis - high vaginal smear
Risk factors - antibiotics, DM, oral contraceptives, pregnancy, obesity, steroids

146
Q

Describe scabies and pubic lice

A

Can be transferred sexually

147
Q

Describe bacterial vaginosis

A

Disturbance in normal flora.
More Gardnerella, Mycoplasm and anaerobes
Scanty but offensive fishy discharge
Cervical smear and clinical diagnosis (>5pH).
Metronidazole

148
Q

Lab diagnosis of bacterial vaginosis

A

Clue cells - epithelial scells studded with gram variable coccobacilli.
Less lactobacilli
Absence of pus cells

149
Q

What is pelvic inflammatory disease?

A

The result of infection ascending from the endocervix causing endometritis, alpingitis, parmetritis, oophoritis, tubo-ovarian absess and/or pelvic peritonitis

150
Q

Describe the epidemiology of PID

A

Gon/ Chlamyd 40% concurrent.
BV also implicated
IUCD increases risk in week 1 of infection.
COCP protective agianst symptoms
Alcohol, drugs and smoking are predicitive

151
Q

Describe the pathophysiology of PID

A

Ascending infection

Inflammation causes fibrosis and adhesions due to damage of epithelium

152
Q

Describe the clinical features of PID

A

Pyrexia, dyspareuina, adnexal tenderness, cervical excitation (chandeliers sign), bilateral lower abdominal tenderness/pain
Abnormal discharge +/- blood
History- STIs

153
Q

Differential diagnoses of PID

A 
Ectopic pregnancy
Endometriosis 
Ovarian cyst (complications of)
Appendicitis
IBS
UTI
Fucntional pain (unknown origin)
154
Q

investigations in PID

A

Triple smear - chlad, gonn endocervix and high vaginal for BV trichomonas and candida

155
Q

Management of PID

A

Analgesia
IM ceftriaxone, PO doxycycline and metronidazole (14 days)
Surgery if severe - US guided, laproscopic
Hospitalised if pregnant, tubo-ovarian abscess or lack of response to oral therapy

156
Q

Risks associated with PID

A

Ectopic regnancy
Infertility
Chronic pelvis pain
Fitz Hugh Curtis syndrome

157
Q

What is Fitz Hugh Curtis syndrome

A

RUQ pain and perihepatitis following chlamydial PID, risk increases with repeat episodes,

158
Q

Describe the covering of the ovaries

A

Simple squamous epitheliam (germative epithelium)- peritoneal covering

159
Q

Describe the cells of the cortex of the ovary

A

Initially primordial follicles, oocyte surrounded by a single layer of squamous follicular/ granulosa cells

160
Q

What changes in the follicles occur in puberty and why? (up to theca folliculi)

A

Squamous to cuboidal graulosa cells, becomes unilaminar primary follicle.
Divides and becomes multilaminar primary follicle (FSH stimulates), ZP forms between oocyte and granulosa. Outer margin stromal cells develop into theca folliculi

161
Q

Describe the formation of a secondary follicle

A

Fluid filled spaces form between the granulosa cells.

Theca folliculi develops into theca interna (oestrogen) and theca externa (vascular CT)

162
Q

Describe the formation of a ternary follicle and graafian follicle

A

Formation of an antrum - fluid filled spaces pushes granulosa to periphary
Expands so it fills encompases the oocyte (apart from cumulus oophorus) known as a graafian follicle (single large fluid filled antrum) (now ready). Corona radiata breaks down prior to ovulation.

163
Q

What is the cumulus oophorus

A

Small number of graulosa cells that hold oocyte

164
Q

What is the corona radiata

A

Single layer of granulosa cells surrounding oocyte

165
Q

How does the follicle change at ovulation

A

Tissue around becomes ischemic, follicle ruptures, oocyte released. GC become granulosa lutein cells (secrete prog) and theca interna becomes theca lutein (oestrogen). Blood clot in the middle

166
Q

What is a corpus albicans

A

Absence of hCG - denerates, fibrosed/ hyalinised to whiteness.
Can become corpus nigricans due to pigmentation from degraded erythrocytes

167
Q

Describe the histology of the fallopian tube

A

Columnar cilliated epithelium and LP (mucosa). PEG cells (secrete mucus and pronounced). SM of varying thickness- less at isthmus

168
Q

Describe the different layers of the uterus

A

Endometrium - stratum functionalis (coiled arteries) and stratum basali (straight arteries)
Myometrium - 4 layers of SM

169
Q

Decribe the stages of the endometrium

A

Early proliferative - SF grows, glands sparse and straight
Late proliferative - glands coiled as they grown quicker than LP
Early sectretory - max thickness - very pronounced coiled glands
Late secretory- stroma becomes odematous and decidual cells develop which help create placenta and secrete prolactin in pregnancy.
If no implantation - lack of prog causes it to shed

170
Q

Describe the histology of the cervix

A

Simple columnar meets stratified squamous at Squamocolumnar junction near external os. many glands on columnar side for vaginal lubrication

171
Q

Describe the histology of the vagina

A

3 layers - mucosa, submucosa and muscular (skeletal and smooth). No glands. Rich in glycoproteins (especially with oestrogen)

172
Q

Describe breasts in new born

A

Duct system and nipple surrounded by aerolar tissue

173
Q

Breast changes at puberty

A

Development of lactiferous ducts and deposition of adipose

174
Q

Histology of the breast

A

lactiferous ducts with cuboidal/columnal/ squamous (in sinuses). Myoepithelial cells

175
Q

Function of o and p in breast development

A

It is believed that oestrogen results in proliferation of the duct system whilst progesterone influences development of the secretory tissues

176
Q

Describe the outer layers of the testes

A 
Tunica albuginosa - tough CT
Tunica vasculosa (vessels)
177
Q

Describe histology of testes

A

Seminiferous tubules surrounded by perilobular CT (collagenous) in between lobules there is CT and islands of leydig cells (testosterone)

178
Q

Briefly describe maturation of spermatogoonia

A

spermatogoonia - spermatocyte - spermatotid

Outside of ST in

179
Q

Histology of a seminiferous tubule

A

Spermato… out to in. Sertoli cells form blood barrier. Speratogoonia cells develop engulfed within. Cytoplasmic bridges to link and facillitate simultaneous development.
Myofibroblasts around the outside which can contract

180
Q

Junction between seminiferous and tubuli recti

A

Plug of sertoli cells then simple cuboidal

181
Q

Epithelium of rete testis

A

Simple cuboidal

182
Q

Describe the histology of the efferent ductules

A

Ducts in LCT.
Pseudostratified cilliated to waft
Simple cudoidal cells to absorb fluids
Contractile cells around outside

183
Q

Describe the histology of the epidydimis

A

Pseudostratified (sterocillia (dont waft)) and basal cells.

outside SM gets thicker towards vas.

184
Q

Describe the histology of the vas

A

Epithelium, LP, 3 layers of SM, out and in are longitudinal middle is circular.
Pseudostat with few stereocilia
folding due to tone of circular muscle

185
Q

Describe the histology of the seminal vesicles

A

Coiled tubliosaccular glands - develop out of ducus deferens. highly folded mucosa, LP. Each gland covered by a muscular coat (sympathetic due ejac).
Secretes fructosa, proteins and prostaglandins
Pseudostat columnar

186
Q

Describe the duct system in the prostate

A

Mucosal, submucosal, main in central middle and peripheral zones. all drain into urethra separately

187
Q

Separation of the prostate glands by what?

A

Fibromuscular capsule divides into lobules

188
Q

Describe the histology of the prostate

A

Hetrogenous epithelium. Copora amylacae in older men

189
Q

What is a primary sexual characteristic

A

Develops before birth

190
Q

List the order of events within puberty for females

A 
Thelarche
Adrenarche
Growth spurt (12)
Menarche (12.5)
Pubic hair adult
Breast adult
191
Q

List the order of events within pubery for males

A 
Genital development
Adrenarche
Speratogenesis
Growth spurt
Adult genitalia
Adult pubic hair
192
Q

What mechanism causes puberty

A

GnRH from hypo, maturation of central systems, weight gain (47kg in females), less sensitive to neg feedback, pineal gland and melatonin?

193
Q

What causes public hair, libido and breast development and male genital development?

A

Public hair and libido = androgens
Breast development = oestrogens
Male genitals = testosterone

194
Q

Define climateric

A

The peiod of life when fertility and sexual activity are in decline. Pre, menopause and post

195
Q

Describe pre menopause

A

Early or absent ovulation, follicular phase shortens. Decrease in oestrogen and inhibin so LH and FSH(++) rise.
Reduced fertility

196
Q

Describe changes in menopause includign vascular changes, bone, genital

A

No more follicles. Oestrogen decreases, LH and FSH rise.
Hot flushes due to absence of oestrogen
Osteoporosis as oestrogen inhibits osteoclasts (2.5% per year)
Involution of breast tissue, loss of vaginal rugae
Skin changes
Bladder changes

197
Q

Describe treatment for problems of menopause

A

Oestrogen, HRT. Oral, topical patch or gel. Not advised for cardioprotection. Not a first line protection for osteoporosis. Prog added to prevent uterus cancers.

198
Q

Neg affects of HRT

A

Headaches, indigestion, depression, Breast cancer, stroke, DVT, PE

199
Q

Define primary amenorrhoea

A

Absence of ovulation by age 14 with secondary sexual characteristics or absence by age 16 with normal SSC

200
Q

Define secondary amenorrhoea

A

Absence of ovulation for 3 months with normal history or cyclic bleeding or 9 months in a women with history of irregular periods (usually 40-55)

201
Q

Desribe problems in the outflow tract that can cause primary amenorrhoea

A

Vaginal atresia, Mallerian agenesis, imperforate hymen

202
Q

Describe problems in the outflow tract that can cause secondary amenorrhoea

A

Intrauterine adhesions (asherman’s syndrome) AA to remember. trauma

203
Q

Describe gonadal problems that can cause amenorrhoea primary

A

Gonadal dysgenesis e.g. turners, hypergonadotrophic amenorrhea. Receptor abnormalities FSH or LH, congential adrenal hyperplasia, adrogen insensitivity syndrome (testicular feminization syndrome)

204
Q

Describe gonadal problems that can cause amenorrhoea secondary

A

Premature menopause. Polycystic ovarian syndrome. Pregnancy, drug induced

205
Q

Hypo/ pit causing primary

A

Kallmann syndrome

206
Q

Hypo/ pit secondary

A

Exercise, stress, weigh loss or gain, sheehan syndrome (vascular necrois of pit) hyperprolacinaemia, haemochromatosis. Hypo or hyper thyroidism.

207
Q

Define menorrhagia

A

> 80ml, >7 days regular.

208
Q

Causes of menorrhagia

A

Distorsion of uterine cavity, organic, iatrogenic, endocrinological, haemostatic

209
Q

Treatment of menorrhagia

A

Hormones/ agonists, USS if structural

210
Q

Define dysfunctional uterine bleeding (DUB)

A

Heavy, frequent or prolonged uterine bleeded with no obvious organic cause. Anovulatory

211
Q

Who normally gets DUB

A

Extremes of life. PCOS

212
Q

Describe pathophysiology of DUB

A

HPO axis.

No prog withdrawal so endometrium builds up and breaksdown erratically

213
Q

DUB management

A

HCG TSH, tamoxifen (block oestrogen), OCP

214
Q

Define dysmenorrhea

A

Painful periods

215
Q

Define oligomenorrhoea

A

Less frequent periods 35 days- 6months

216
Q

Define premenstrual syndrome

A

Physical (bloating, constipation) and emotional (stress, headache, fatigue) symptoms 2 weeks before menstruation (hormones in luteal phase?)

217
Q

What is mastalgia

A

Breast pain

218
Q

List the hormones involved in reproduction produced by the hypo, the ant pit, post pit and the gonads and state which cell types

A

Hypothalamus - GnRH

Anterior pit - Somatotrophs-GH, Corticotrophs- ACTH, thyrotrophs - TSH, Gonadotrophs- LH/FSH

219
Q

Control of gonadotrophin secretion

A

Hypothalamus - pulsatile GnRH trigger by neurones (1 hour).
Into hpophyseal portal circulation (median eminence to ant pit) (axons to ant pit also end in median eminence).
Neg feedback of gonadotrophs, androgens and oestrogens

220
Q

Action of gonadotrophins on the testes

A

FSH - Sertoli to promote spermatogenesis and inulin production (via androgens tho?)
LH - Leydig cells to produce testosterone, promote spermatogenesis and maintain repro

221
Q

Glcopeptides vs polypeptides

A

FSH, LH & TSH vs GH, ACTH and Prolactin

222
Q

Action of gonadotrophins on the ovaries

A

FSH - granulosa cells to stim developmet, secretes inhibin
LH - secretion of oestrogen from theca interna (stim development of follicle). Surge = ovulation. LH maintains corpus luteum

223
Q

List the phases of the menstrial cycles

A

Preparatory/ follicular - growth of follicle, preparation of endometrium. Changes to faciliotate sexual interactions.
Ovulation- Also formation of corpus luteum

224
Q

Oestrogen through the menstrual cycle

A

Slowly increases with follicle - high for Lh surge, small decrease, rise again with CL, decrease with death of CL

225
Q

Progesterone through menstrual cycle

A

Low without CL, produced by CL

226
Q

LH and FSH through the menstrual cycle

A

LH relatively low, increases LH surge, slowly decreases.

FSH, small surge, decreases (inhibin)

227
Q

Describe the effects of oestrogen

A 
Fallopian tube function
Thickening of endometrium
growth and motility of myometrium
Thin alkaline cervical mucus
Ca metabolism
Changes in hair, skin and metabolism
Vaginal changes (thicker, elastic, glycogen)
228
Q

Describe the effects of progesterone

A 
Augment oestrogen but,
Not motility of myometrium
Secretary phase of endometrium
Thick acidic mucus at cervic
Changes in mammary tissue
Metabolic and electrolyte changes
229
Q

Describe the migration of the primordial germ cells

A

Arise in the caudal part of the yolk sac and migrate along the dorsal mesentary into the retro peritoneum/ gonads

230
Q

Describe the control and development of the male testis (not ducts) and female ovary

A

In males SRY region on Y chromosome causes the medullary cords of the primitive gonad to develop. The absence causes the cortical cords to develop. Thick tunica albuginea vs none. Males have no cortical cords. Women medullary cords degenerate

231
Q

Describe the development of the gonadal ducts

A

Wollfian duct - primitive renal function, ends at cloaca. Maintained by testosterone.
Paramesonephric (Mullerian) formed from invaginations of urogenital epithelium. Also end at cloaca but opens into the abdominal cavity. Mullarian inhibiting hormone in males causes duct to degenerate.

232
Q

Describe the dvelopment of vagina and uterus

A 
Urogenital ridge grows outwards around primitve gut and paramesonephric ducts merge forming top 1/3 of vagina, uterus and fallopian tubes.
Stimulates endoderm (urogenital sinus) to develop into lower 2/3
233
Q

Describe the components of the external genitalia in their indifferent stage and what they develop into in the male and female

A

Genital tubercle - Clitorus vs glans
Genital fold - Fuse to form scrotal raphe and spongy urethra vs labia minora
Genital swelling - labia majora vs scrotum
Infuenced by testosterone
Mesoderm?

234
Q

Describe the descent of the ovaries and testes

A

Caudal genital ligamnet (gubernaculum) attches to labiosacral folds. As trunk elongates testes are pulled through inguinal canal into scrotom. Processus vaginalis enters first.
In females this causes descent of the ovaries into the pelvis.

235
Q

Describe common abnormalities of genital development

A 
Hypospadias - incomplete fusion of urethral folds (inferior aspect of penis or scrotal raphe)
Epispadias on dorsum - associated with extrophy of bladder.
Uterus didelphys (no fusion)/ arcuatus/ bicornis (two horms) Uterus bicornis unicollis
Genotype-phenotype mismatch
236
Q

Describe spermatogenesis

A

At puberty - spermoogonia mitose 64 times into spermatocyte. meiosis into spermatids. Remodelled through tubule, rete testis, ducti efferentes, epidydimis to spermatozoa

237
Q

Describe the spermatogenic cycle and wave

A

spermatogenic cycle
duration of the cycle which separates consecutive cell divisions of spermatogonia (pig is 8 days, sheep 10, cattle 14) to produce spermatocytes.

spermatogenic wave
spermatogenesis occurs in sequential waves along the length of the seminiferous tubules so that spermatozoa are produced in waves; the phenomenon which ensures that spermatozoa are produced continuously, except for seasonal pauses when spermatogenesis is initiated and terminated each year.

238
Q

Describe the production of ovum

A

Germ cells colonise gonadal cortex and become oogonia. Proliferate to 7 million. only 2 million at birth.
Meiosis is stimulated but stops at early stage (primary oocytes) until puberty- here they are primordial follicles. Aftery pubery they develpp one at a time.
First division just before released.

239
Q

Define term and pre term labour, spontaneous abortion

A

Labour - expulsion of products of conception after 24 weeks
Spontaneous abortion - expulsion of products of conception at less than 24 weeks.
Pre term - before 37
Term - 37-42

240
Q

Brief stages of pregancy

A

First - creation of birth canal
Second - expulsion of fetus
Third - expulsion of placenta & contraction of uterus

241
Q

Describe the position of the uterus at 12, 20 and 36 weeks

A 
12 = Palpable
20 = Umbilicus
36 = Xiphisternum
242
Q

Describe the lie of the fetus

A

Relationship to long axis of uterus - normally longditudinal and flexed

243
Q

Describe the presentation of the fetus

A

Which part is next to the pelvic inlet - cephalic (vertex/head) or breach (podalic)

244
Q

Normal size of birth canal and of head

A 
Head in normal position = 9.5
Pelvic inlet maximum = 11cm (may increase with softening of ligaments. Expansion of cervic, vagina and perineum to 10cm.
245
Q

Describe cervical ripening

A

Reduction in collagen, increase in GAGs, reduction in aggregation of collagen fibres
Triggered by prostaglandins (pG E2 and F2x)

246
Q

Apart from cervical ripening what else creates the birth canal and describe the process.

A

Contractions of the myometrium smooth muscle triggered by pacemakers. fibres get progressively shorter through repeated contraction and relaxation known as Brachystasis. Pushes fetus into cervix. Cervix thins and flattens (effacement). More oxytocin. Cervix dilates. Rupture of amnion.

247
Q

Describe contractions throughout pregancy

A

Early - low amplitude - every 30 minutes (not felt)

Late - less frequent but higher amplitude = ‘Braxton-Hicks’ contractions

248
Q

Describe contractility control of the myometrium

A

Made more forceful by prostaglandins (more Ca) and oxytocin (positive feedback) (more action potentials due to a lower threshold)

249
Q

Describe prostaglandin production and function

A

Biologically active lipids
Local hormones
Produced by endometrium
Controlled by oestrogen:progesterone. Later in pregancy progesterone production falls resulting in prostaglandins.

250
Q

Describe oxytocin production and function in pregancy

A

Ferguson reflex (afferent implses from vagina and cervix). post pit but controlled by hypothalamus. Acts on SM receptors (more of which if high O:P)

251
Q

Describe the second stage of labour

A

Rapid.
Urge to bear down
Presenting part appears in birth canal.
Head flexes, rotates internally.
Head stretches vagina and perineum (risking tear/ episiotomy).
Delivery involves rotating furthur (now facing mother’s but) and extends.
Shoulders rotate and deliver followed rapidly by the rest.

252
Q

Describe the third stage of labour

A

Uterus contracts down hard, shears off placenta. Expels it from uterus (normally 10mins).
Compresses blood vessels to reduce haemorrhage.

253
Q

How is the third stage of labour artificially enhanced?

A

Giving oxytocic drug

254
Q

Describe the establishment of independent life

A

Neonate takes first breath - trauma and cold stimulate
Reduces pulmonary vascular resistance and increases arterial pO2.
Formen ovale closes, DA contracts due to pO2.

255
Q

Describe the symmetry and polarity of uterine contractions

A

Contractions from two poles (lat to fundus by isthmus)

256
Q

Role of relaxin

A

causes changes in cervix over a period of weeks

257
Q

Difference between effacement and dilation?

A

Effacement is peeling (how long the canal is), dilation is formation of gap

258
Q

Descrbe the types of pelvis

A

Gynecoid - wide
Anthropoid - Narrow transverse, wide inclination of sacrum. Wide AP
Android - narrow forepelvis, forawrs sacrum, narrow pelvic outlet (sub pubic)
Platypeloid - Narrow AP, Wide pelvic outlet.

259
Q

Describe width of different positions of head

A

Vertex -9.5 perfecti
Sinciput - not fully flexed 10cm
Brow - slightly extended - 13.8cm
Face - 9.5cm

260
Q

Describe clin sig of passenge

A 
Number
Weight 
Presentation 
Lie (longditudinal or transverse)
Attidtude (flexion or extension)
261
Q

Describe breach types

A

Frank - feet by head
Full - cros legs
Single footing

262
Q

Two phases in the first stage

A

Latent - slow dilation

Active - faster and contractions

263
Q

Describe the types of instrumental delivery

A

Forceps or Von toux (vacuum)

264
Q

Blood in placenta separation

A

Intervillous space back into veins of spongy layer of decidua basilis, cant brain back into maternal bloodstream as uterus has retracted.
Living ligatures - retract around placenta to seal off blood vessels (interlacing muscle fibres. Blood clotting mechanisms

265
Q

Describe mammary glands

A

Embedded in breasts
15-20 lobulated masses of tissue (Fibrous and adipose tissue in between
Lobes= alveoli, BV and Lactiferous ducts

266
Q

Describe development of mammary glands in puberty and in pregnancy

A

Only a few ducts at birth
At puberty ducts sprout and branch and alveoli begin to develop
With each menstrual cycle there are changes in oestrogen and progesterone
In pregnancy - hypertrophy of ductular-lobular-alveolar system to form prominent lobules. Differentiation of alveolar cells to be capable of milk production from mid gestation. Little milk secreted - high prod:oestrogen favours growth not secretion.

267
Q

Describe the milk secretion soon after birth

A 
Colostrum produced (40ml).
Less water, fat & sugar than later milk so more protein (IgG)
268
Q

Describe 2 week milk secretin

A 
Mature milk - gradual change
90% water
7% sugar (lactose)
2% fat
Proteins (lactalbumin and lactoglobin)
Vit and min
Sweet and semi skimmed
Secreted by alveolar cells
269
Q

Describe the control of milk secretion (briefly) and production

A

Secretion by fall of steroids (high prog: oestrogen in pregnancy falls)
Prolactin (Dopamine) promoted by suckling, neuroendocrine reflex. Promotes production for next feed (turgor).
Also let down reflex.

270
Q

Describe the ‘let down reflex’

A

Myoepitheliual cells arround alveoli contract due to oxytocin to squeeze milk out of breast. Also a neuro-endocrine reflex that becomes conditioned

271
Q

benefits of breast feeding

A

Bonding

Babies have fewer infections

272
Q

What is a TDLU

A

terminal duct lobular unit.
Functional unit - end of branching duct
=acini and intralobular stroma

273
Q

Increasing age and breasts

A

Describe in TDLus and stroma replaced by adipose tissue

274
Q

Most worrying palpable breast mass

A

hard craggy and fixed as may be invasive carcinomas

275
Q

Milky discharge from nipple?

A

Endocrine disorder e.g. pit adenoma or medication

276
Q

Causes of densities and calcification in the breast

A

Densities - invasive carcinomas, fibroadenomas and cysts

Calcification - DCIS and benign changes

277
Q

Describe benign stromal tumours types

A 
Fibroadenomas (most common) - any age by often older
Phyllodes tumour (60s)
278
Q

Eoidemiology of breast cancer

A

Rare before 25 (unless genetic). Incidence increases with age. 1% in men

279
Q

Describe disorders of breast development

A

Milk line remnants (polythelia- accessory nipples)

Accessory axillary breast tissue

280
Q

Describe inflammatory conditions of breast

A 
Acute mastitis - Staph aureus
during lactation
Erythematous, painful, pyrexia
May result in breast abscess
Antibiotics and express mil.

Duct ectasia - 50/60 idiopathic, mass or discharge, duct dilation and inflam. mimic carncinoma

Fat necrosis - mass, skin changes, mammographic abnormality, history of trauma

281
Q

Describe fibrocystic change (benign epithelial lesion)

A

Common
Mass
Disappears after fine needle aspiration
Histology - cyst formation, fibrosis and apocrine metaplaia (wider acini)

282
Q

Descrube epithelial hyperplasia (benign epithelial lesion)

A

Incidentall often
More epithelial cells which fill and distend ducts and lobules
Slight increased risk of carcinoma

283
Q

Describe breast papilloma (benign epithelial lesion)

A

Large ones near lactiferous ducts near nipple, small are often multile and deeper, slight increased risk of carcinoma.
Possible nipple discharge, small palpable mass or abnormality
May be bloody
Looks like a leaf

284
Q

Describe fibroadenoma

A

Mass, usually mobile and elusive
Can be multiple or bilateral
Can replace most of breat
Macroscopcally - well circumscribed, rubbery, white
Histology - Mixture of stomal and epithelial elements

285
Q

Describe phyllodes tumours

A

Rare before 40
Benign, malignant or boarderline. Most are benign.
Can involve entire breast.
Nodules of proliferating stroma covered by epithelium (phullon = leaf)
Stroma more cellular and atypical than fibroadenomas

286
Q

Describe gynaecomastia

A

Unilateral or bilateral
Puberty or elderly
Relative decrease in androgen effect or increase in oestrogen effect
Can mimic male BC if unilateral
No increased risk of BC,
Occurs in neonates due to placental hormones.
Klinefelter’s sydrome
Oestrogen excess in liver cirrhosis
Testicular tumour
Drug related e.g. spironolactone, heroin, alcohol

287
Q

Describe risk factors for breast cancer

A 
Age
Age of menarche and menopause (longer time period of oestrogen)
Breast feeding - protective
Age of pregancy (breast up oestrogen)
Obesity and fat
HRT
geography
atypical changes on previous biopsy 
previous BC
Radiation
Hereditary e.g. RAC1/2, p53
288
Q

Briefly describe classification of breast carcinoma

A

Either in situ or invasive and be ductal or lobar

289
Q

Describe in situ carcinomas

A

Limited by basement membrane so only in ducts.
Does not invade vessels and therefore cannot metastasise
DCIS. can calcify, can spread through ducts and lobules and be very extensive.
Central necrosis and calcification

290
Q

What is Paget’s disease

A

Cell extend to nipple skin without crossing BM
Unilateral red and crusting nipple
Eczematous or inflammatory conditions should be suspected of being Pagets
May lead to/ be malignant

291
Q

Describe invasive carcinomas

A

Invaded beyond BM
No link to DCIS.
Metastasise
More have lymphatic involvement by the time its palpable.
Peau d’oragne due to loss of lymph drainage.
May be ductal (70-80%) or Lobular (single file cellular invasion) both with similar prognosis.

292
Q

Describe common mets sites of BC

A 
Lymph - axilla
Bones
Lungs
Liver Brain
Invasive lobular can be peritoneum, leptomeninges, GI tract, ovaies uterus
293
Q

Desribe the triple approach to the investigation and diagnosis of BC

A

Clinical - history, family, exam
Radiograph imaging - mammorgraphy and US
Pathology - FNAC and core biopsy

294
Q

Describe treatmetn of BC

A

Breast surgery, axillary surgery, post op radiotherapy to axillae
Sentinal lymph node biopsy.
Chemo - may be neoadjuvant
Hormones e.g. tamoxifen is oestogen receptor positive
Herceptin - HER 2

295
Q

Describe the pathogenesis of the cervic

A

Mainly HPV16 &18 infect metaplastic squamous cells in transformation zone. Increase proliferation of cells and inhibit repair.
Although most infections are transient

296
Q

Risk factors for cervical cancer

A

Sex related
immunosuppressed
Smoking
OCP

297
Q

Describe cervical screening

A

Easy to examine (colposcopy)
Pap test detects low stage lesions (scaped, stained and microscope)
25 years old, every 3 years then every 5 after 50.
If abnormal then colposcopy and biopsy.
Also test for HPV

298
Q

Describe CIN and its progression and treatment

A 
Cervical intraepithelial neoplasia.
Dysplasia induced by infection.
CIN I - resolves spontaneously
CIN II
CIN III - Carcinoma insitu, 10% progress to invasive carcinoma 
CIN I-CIN III to 7 years
CIN I- follow up or cryotherapy
CIN II-III superficial excision
299
Q

Describe cervical carcinoma (everything)

A

45 years
80% SCC
15% adenocarcinoma
Exophytic (outward) or infiltrative
Spreads locally, Bladder, rectum, vagina, lymph/.
Bleeding
Treatment - cervical cone excision if microinvasive (7mm wide 1mm in then 100%)
Hysterectomy, lymoh dissection and radio and chemo if invasive

300
Q

Describe Endometrial Hyperplasia

A

Increase gland:stroma, precursor to carcinoma
Prolonged oestrogen exposure .
If complex and atypical then hysterectomy

301
Q

Describe endometrial adenocarcinoma

A

Common
Older
Irregular post menopausal bleeding - good survival as detected earlier.
Can be endometriod or carcinoma.
Endometrioid is more common, from hyperplasia, spread via myometrial invasion.
Serous - poorly differentiated, agressive, exfoliates so spreads to peritoneum.

302
Q

Describe tumours of the myometrium

A

Mostly benign (Leiomyoma). Results in fibroids. Very common. Multiple, tiny to massive.
Asymptomatic, heavy/painful periods, urinary frequency, infertility.
Not malignant.
Resembles SM, well circumscribed, firm, white
(can get uterine leiomyoma)

303
Q

Symptoms of ovarian cancer

A

Asymptomatic (detected late)
Most symptoms due to mets.
Mass effect: abdominal pain, distension, urinary and GI symtoms, ascites
Hormonal problems - menstrual disturbances, ianppropriate sex hormones.

304
Q

Descrube 4 types of ovarian tumours

A

1) mullarian epithelium (including endometriosis)
2) Germ cells (pluripotent)
3) Sex cord-stromal cells (endocrine apparatus of the ovary
4) mets?

305
Q

Describe ovarian epithelial tumours including types, risk factors

A

Can be serous mucinous or endometriod (all may be benign, borderline or malignant) many are cystic.
Risk factors - low parity, mutations, Smoking, endometriosis
Serous - often peritoneal spread so commonly ascites
Mucinous - large, cystic, benign, pseudomyxoma peritonei, ascites, peritoneal mets, GI
Endometrioid - Can arise from endometriosis, associated with edometrial carcinoma

306
Q

Describe Germ cell ovarian tumours

A

15-20% of ovarian neoplasms
tetratomas, usually benign, may be neoplastic e.g. cjoriocarcinoma or yolk sac (HCG and a-fetoprotein).
tetratomas may be mature (benign), immature (malignant and rare) or monodermal (highly specialised).
Mature are cystic, loads of different tissues.
Monodermal may be stomal ( benign and thyroid) or carcinoid (malignant and carcinoid syndrome)

307
Q

Describe ovarian sex cord stromal tumours

A

Sertoli, leydig/ granulosa and theca cells from sex cord.
May be feminising or masculising respectively.
Post menopasal - large amounts of oestrogen (risk factor).
In children can cause precocious or impair depending if M or F cells.

308
Q

Describe ovarian mets

A

Normally from other mullerian structures.
Also GI or breast.
Often bilateral

309
Q

Describe the types of vulval tumours

A

SCC - HPV, age, inflam e.g. lichen sclerosis. From vulvar intraepithelial neoplasia (VIN) (no invasion). Spreads to lymph, lungs and liver
Extramammary paget’s disease - Pruritic, red, crusted on labia majora, single or clustered malignant cells along basal layer, wide local excision required
BCC
Malignant melanoma

310
Q

Describe tumours of gestation

A

Proliferation of placental tissue- villous or trophoblastic.

Hydatifiform mole (complete or partial) - Associated with other types, cystic swelling of chorionic villi (thin walled grapes_ and trophoblastic prolif, diagnosed with USS, causes miscarriage. Treatment with curettage, monitor HCG - if it doesnt fall then invasive mole.

Invasive mole- perforates uterine wall. locally destructive, vaginal bleeding and uterine enlargement, high HCG, chemo

Choriocarcinoma - malignant trophoblast derived, no vili, rapidly invasive but responds well to chemo. Often with moles, abortions but also normal. Vaginal bleeding (spotting), high HCG, uterine evacuation and chemo

311
Q

Difference between complete and partial moles

A

Complete = Lost female chromosomes. embryos die, high HCG. assoc with choriocarcinoma
Partial mole = 2 sperm - foetus present. not assoc with choriocarcionoma. less chance its invasive

Esa 4 (3 decks)

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