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MFHD Flashcards

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Biology 101 flashcards
1
Q

What is Asherman syndrome?

A

Rare, acquired condition of uterus. - Scar tissue / adhesions form in uterus due to some form of trauma, In severe cases the entire front + back walls of uterus can fuse together

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2
Q

Oligospermia = ?

A

<15 million/ml

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3
Q

Azoospermia= ?

A

Complete absence of sperm

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4
Q

Asthenospermia = ?

A

Problems with sperm mobility - slow movement, not in straight line

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5
Q

Teratospermia = ?

A

Abnormal sperm morphology

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6
Q

What physiological changes happen to sperm in capacitation?

A

MPH
Membrane (changes to cell membrane)
Proteins (changes in sperm cell surface proteins)
Hyper activation / improved mobility

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7
Q

How is implantation regulated?

A

Uterine + embryo must be synchronised

  • embryo must reach blastocyst stage
  • uterus must attain state of ‘receptivity’
  • Uterus only receptive for 24 h!

*Window of implantation = endocrine control! Preparation of endometrium for implantation - progesterone dominance!

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8
Q

What are the 4 stages of implantation?

A 
HAAI. 
Hatching - shedding of zona pellucida  
Apposition 
Adhesion
Invasion
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9
Q

What is decidual tissue and what process does it undergo?

A

Decidual tissue = stromal cells of endometrial lining

- Undergoes decidualization —> forming maternal component of placenta

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10
Q

What is ectopic pregnancy?

A

Blastocyst implants anywhere other than endometrial lining of uterine cavity
- most common site of ectopic pregnancy: within Fallopian tube, but can be in ovary, abdominally / organs e.g. liver

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11
Q

What are the risk factors for ectopic pregnancy?

A

Surgeries, prior STIs, history of infertility, prior ectopic pregnancy, *smoking, advanced age, Fallopian tube injury e.g. PID / endometriosis

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12
Q

How do you manage ectopic pregnancy?

A

Medical - methotrexate

Surgical - laparoscopic, laparotomy

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13
Q

What are the general symptoms of ectopic pregnancy?

A
  • lower abdominal pain + guarding
  • vaginal bleeding
  • signs of pregnancy: amenorrhoea, nausea, breast tenderness, increased urination
  • enlarged uterus
  • closed cervix
  • cervical motion tenderness (extreme pain with bimanual exam in pelvic exam finding) —> usually associated with PID
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14
Q

What is the function of hCG?

A

Rescues corpus Luteum from luteolysis

hCG - maintains CL function & progesterone output until placenta takes over

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15
Q

When does placenta take over production of progesterone from corpus Luteum?

A

~6 weeks of pregnancy

some say ~8-10 weeks

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16
Q

How does placenta produce oestrogen?

A

Placenta lacks the enzyme to produce oestrogen directly - it cooperates with foetus to make oestrogen

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17
Q

What is pre-eclampsia? (placental pathology)

A

Hypertensive, multisystem disorder characterised by increased BP + proteinuria

  • For foetus - can result in FGR
  • For mum - can cause renal failure, seizures, stroke

*Poorly perfused placenta

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18
Q

What is placental accrete?

A

Abnormally deep attachment of placenta

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19
Q

What is placental incretia?

A

Thru INto deep layers of myometrium

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20
Q

What is placental percreta?

A

Thru uterine serosa - thru wall of uterus

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21
Q

What is placental Previa?

A

Attachment of placenta too close to cervix —> obstructs delivery of baby

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22
Q

What is gestational trophoblastic disorder?

A

Abnormal proliferation of trophoblast with enlarged hydropic chorionic villi
Clinically: high hCG, vaginal bleeding, enlarged uterus, preeclampsia

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23
Q

What is hydatidiform mole? How many different types are there?

A

Voluminous mass of swollen (sometimes cystically dilated) chorionic villi - appearing grossly as grapelike structures

2 subtypes: complete / partial - both result from abnormal fertilisation, both have elevated hCG + absence of foetal heart sounds

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24
Q

What are the differences between complete / partial hydatidiform moles?

A

Complete:

  • NOT compatible with embryogenesis
  • NEVER contain foetal parts
  • ALL chorionic villi abnormal
  • Chorionic epithelial cells DIPLOID
  • Entire genetic content supplied by 2 spermatozoa (or diploid sperm) —> diploid cells containing ONLY PATERNAL chromosomes
  • Hydropic swelling of poorly vascularised chorionic villi with a loose, myxomatosis, oedematous stroma

Partial:

  • Compatible with early embryo formation
  • May contain foetal parts
  • Some normal chorionic villi
  • Chorionic epithelial cells almost always TRIPLOID
  • NORMAL egg fertilised by 2 spermatozoa (or diploid sperm) —> triploid
  • Villi has characteristic irregular, scalloped margin
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25
Q

What is invasive mole?

A

Complete moles that are invasive locally but DO NOT have the aggressive metastatic potential of choriocarcinoma

  • Retains hydropic villi which penetrate uterine wall deeply (possibly causing rupture + sometimes life-threatening haemorrhage)
  • epithelium of villi shows atypical changes + proliferation of both trophoblastic & syncytial components
  • metastases DO NOT occur!
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26
Q

What is gestational choriocarcinoma?

A

Very aggressive malignant tumour

  • Arise from gestational chorionic epithelium / (less frequently) totipotential cells within gonads [as germ cell tumour]
  • ~50% arise from complete hydatidiform moles
  • (In most cases) Manifests with a bloody, brownish discharge + rising b-hCG in urine & blood in the absence of uterine enlargement

*By the time most are discovered - widespread vascular spread has occurred to lungs / vagina / brain liver…

  • Placental choriocarcinoma - remarkably sensitive to chemo —> ~100% affected patients are cured!
  • Gonadal choriocarcinoma - response to chemo poor!
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27
Q

How can infections reach placenta?

A
  1. Ascension thru birth canal (more common)
    - Mycoplasma, candida & numerous bacteria of vaginal flora
  2. Hamatogenous (transplacental) spread
    - Placental villi most frequently affected
    - Can be caused by syphilis, TB, toxoplasmosis, rubella, CMV..
    - transplacental infections can affect foetus —> TORCH (toxoplasmosis, other infections, rubella, CMV infection, herpes) complex
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28
Q

What is a major risk factor for tubal ectopic pregnancy?

A

Chronic salpingitis (inflammation of fallopian)

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29
Q

Why is ectopic pregnancy a concern?

A

Rupture of ectopic pregnancy -may be catastrophic, with sudden onset of intense abdominal pain + signs of an acute abdomen, followed by shock
*Prompt surgical intervention necessary

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30
Q

What is the role of progesterone in pregnancy?

A
  • maternal recognition of pregnancy, implantation, decidualization
  • maintain uterine + placental integrity + synthetic capacity
  • foetal tranquilliser
  • maternal effects: increased appetite, fat deposition, tranquillise , mammary dev
  • modifies immune response
  • **Influences sensitivity of myometrium to uterotonins —> decreases spontaneous activity + response to oxytocin & prostaglandins

*Progesterone —> progesterone receptor —> INHIBIT CAPs (contraction associated proteins) gene expression —> contractile proteins inhibited

  • progesterone withdrawal required for childbirth!
  • Low progesterone —> abortion
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31
Q

What is the role of oestrogen in pregnancy?

A

Oestrogen —> oestrogen receptor —> ACTIVATES CAPs

  • Produced by feto-placental unit (increases towards term)
  • Foetus produces androgens —> androgens converted by placenta to oestrogen
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32
Q

What are the stages of parturition?

A

0 - myometrium quiescence
1 - activation of myometrium + ripening of cervix [*Uterotonins (hormones) —> stimulate contraction by increasing intracellular Ca2+]
2 - expulsion of baby
3 - expulsion of placenta + uterine involution

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33
Q

What is placental CRH important in parturition?

A

Placental CRH (in cytotrophoblast + syncytiotrophoblasts) increases towards term —> circulates in both mother & foetus —> stimulate cortisol synthesis [cortisol has positive feedback —> more CRH gene expression]

*CRH drives androgen production in foetus + acts upon myometrium

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34
Q

How is oestrogen produced for parturition?

A

From cholesterol, placenta produces pregnanolone —> androgen in foetus —> androgen comes back to placenta to be aromatised to oestrogen —> oestrogen drives myometrium contractility (while progesterone inhibits)

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35
Q

What is Ferguson reflex?

A
  • Positive feedback pathway
  • Neuroendocrine reflex comprising self-sustaining cycle of uterine contractions initiated by pressure at cervix / vaginal walls
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36
Q

When does implantation normally occur?

A

Blastocyst normally implants ~day 5-7

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37
Q

What happens after fertilisation?

A

Zygote —> morula —> blastocyst

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38
Q

When is hCG first detectable in maternal blood?

A

On day 8

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39
Q

What is yolk sac?

A

1st layer of interchange with mother & exchange of nutrients + gases by diffusion only!

  • Lasts a few weeks
  • Is the 1st site of foetal hemopoiesis (RBC production)
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40
Q

What’s the 1st foetal organ to develop (after placenta)?

A

Heart! It starts contracting ~day 21

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41
Q

What are the 3 shunts that exist in-utero & close after delivery?

A
  1. Foramen ovale (RA-LA)
  2. Ductus arteriosus (PA-descending thoracic aorta)
  3. Ductus venosus (umbilical vein-IVC)
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42
Q

Why is cortisol important for foetus?

A

Important for maturation of foetal lung (pulmonary surfactant)

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43
Q

Describe foetal lung development.

A

*Foetal lungs = fluid-filled structures that must transition rapidly to air-breathing at birth

Stages of lung dev:

  1. Embryonic 0-6 weeks
  2. Pseudo glandular 6-16 weeks
  3. Canalicular 16-26 (gas exchange possible but in latter stages)
  4. Saccular 26-term
  5. Alveolar (32 weeks & ongoing after birth into early childhood)

*Foetal breathing movement: begin as early as 12 weeks’ gestation

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44
Q

What happens to the lungs in preterm birth?

A

Pulmonary immaturity - preterm baby’s greatest threat! [due to respiratory distress syndrome (RDS), bronchopulmonary dysplasia (BPD)

  • Major improvement in reducing RDS + improving survival with antenatal administration of corticosteroids prior delivery
  • Surfactant —> given to new born via trachea —> assist ventilation of preterm lung
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45
Q

What are some foetal renal impairment conditions?

A

Bilateral renal agenesis = absence of both kidneys at birth
Multi cystic dysplasia kidney disease = kidneys consisting irregular cysts of varying size that resemble a bunch of grapes

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46
Q

What are the maternal causes of FGR (foetal growth restriction)?

A

HTN, renal disease, diabetes, SLE, chronic disease e.g. CF, drugs (cigarettes, alcohol, cocaine, heroin), meds e.g. beta-blocker, age extremes, malnutrition, previous history

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47
Q

What are the placental causes of FGR (foetal growth restriction)?

A
  1. Primary placental disease - placenta insufficiency
    - Placenta unable to deliver adequate supply of nutrients + O2 to foetus
  2. Placental mosaicism (e.g. trisomy 16,20)
    - Difference between chromosome makeup of cells in placenta + cells in foetus
  3. Placenta praevia - placenta attaches inside the uterus but in abnormal position near / over cervical opening
    - Symptoms: vaginal bleeding in 2nd half of pregnancy
  4. Placental abruption - placenta separates early from uterus (before childbirth)
    - symptoms: vaginal bleeding, lower abdominal pain, dangerously low BP
  5. Placental infarction - interruption of blood supply to a part of placenta —> cell death
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48
Q

What is amniotic fluid a marker of?

A

Foetal hydration.

Also reflects foetal urine output

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49
Q

What are the symptoms of pregnancy complications?

A

Per vaginal (PV) bleeding, abdominal pains (can indicate miscarriage, ectopic pregnancy)

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50
Q

When do most pregnant women feel foetal movements?

A

~22 weeks

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51
Q

Why is BP in pregnant women usually low?

A

Due to vasodilation!

*Always check BP & URINE in 2nd + 3rd trimester! If BP >140/90 mmHg, and there’s protein in urine —> you’d be worried of pre-eclampsia!

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52
Q

What is puerperium?

A

6 weeks from time of delivery of baby + placenta

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53
Q

What are the anatomical + physiological changes in pregnancy / postpartum?

A

CVS:

  • in pregnancy: increased volume + decreased peripheral vascular resistance —> increased CO
  • immediately postpartum: increased CO

*Pregnancy induces a hypercoagulable state —> increase risk of DVT

GIT changes mainly on mobility —> constipation + haemorrhoids

Often complain dry vagina on initial intercourse; resumption of menses delay if breastfeeding

*Those who develop gestational diabetes have 50% lifetime risk of developing DM

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54
Q

What are the early maternal issues?

A

Common:
- ‘afterbirth’ pains, perineal discomfort, constipation / haemorrhoids, voiding, MSK pain, postpartum neuropathy, blues, breast engorgement (occurs 1st week postpartum)

Uncommon:
1. postpartum haemorrhage = excessive bleeding following birth:
—> caused by 4T’s: Tone, Trauma (laceration, rupture, haematoma), Tissue (retained tissue / invasive placenta), Thrombin (coagulopathy)
2. DVT / PE
3. Infection

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55
Q

What are the late maternal issues?

A

Common:
- Voiding function, persisting back pain, exercise ability, sexual dysfunction

Uncommon:
- mastitis, postpartum depression

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56
Q

What are the roles of oestrogen & progesterone in lactation?

A

Oestrogen - responsible for growth of ductal tissue + alveolar budding
Progesterone - required for optimal maturation of alveolar glands

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57
Q

What are the functions of oxytocin + prolactin in lactation?

A

Oxytocin (posterior pituitary)

  • released in response to afferent nerve endings in nipple + areola stimulated during suckling
  • contracts myoepithelial cells around alveoli
  • ejects milk along lactiferous ducts thru nipple pores into baby’s mouth

Prolactin (anterior pituitary)

  • receptor sites on alveoli —> produce milk
  • Prolactin is a necessary hormone for milk production
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58
Q

What are the processes involved in initiation + maintenance of lactation?

A
  1. Mammogenesis
    - ductal sprouting + branching, cellular division + proliferation
  2. Lactogenesis I
    - late pregnancy
  3. Lactogenesis II
    - Onset of copious milk production
    - 30-72h post birth
    - marked decreased progesterone
  4. Lactogenesis III
    - maintenance of lactation
    - autocrine (supply / demand)

**Lactation is not initiated until plasma oestrogen, progesterone + placental lactogen levels decrease after delivery!

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59
Q

What are the breastfeeding challenges?

A
  • painful / traumatised nipples. [tenderness + sensitivity normal BUT PAIN IS NOT]
  • blocked ducts —> can cause pain
  • breast engorgement
  • mastitis
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60
Q

What is breast engorgement?

A
  • bilateral
  • due to vascular congestion + accumulation of milk
  • breasts become firm + painful —> infant likely have difficulty attaching

Management:

  • softening areola
  • breastfeeding more often
  • apply warmth to assist milk ejection reflex
  • apply cold packs after feeding / expressing
  • simple analgesia / anti-inflammatory med
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61
Q

What is mastitis?

A
  • Unilateral!
    inflammation of interstitial cells (due to skin of nipple being vulnerable to dev of fissures)—> cellulitis (can become abscess if untreated)
  • localised tenderness, redness, heat
  • systemic reactions!!! (Fever, malaise, nausea, vomiting)
  • common organisms: S.aureus, E.coli, strep

Management:
- resolves with antibiotics + continued expression of breast milk

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62
Q

What’s the difference between breast engorgement and mastitis?

A

Breast engorgement - bilateral, no systemic symptoms

Mastitis - unilateral, systemic involvement

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63
Q

How do you know if there’s abscess formation in mastitis?

A

Presence of pitting oedema over inflamed area + any degree of fluctuation = abscess formation!

Necessary to incise + open loculated areas & provide wide drainage

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64
Q

What is fecundability & fecundity?

A 
Fecundability = probability of achieving a pregnancy within a single menstrual cycle 
Fecundity = probability of achieving a life birth within a single cycle
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65
Q

What would you ask when taking history from a female who’s suspected of infertility?

A 
Social history 
Age 
Med history
Menstrual history
Age of menarche
Surgical history, obstetric history
Duration of infertility 
Contraceptive + sexual history
Previous contraceptive methods
STIs? 
Fam history
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66
Q

What are some of the factors that could reduce chance of conception?

A

Obesity / underweight
Smoking / alcohol / caffeine
Occupation - heavy metal, pesticide, solvents —> decrease fertility

*Chlamydia - can cause infertility

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67
Q

What are the genes important for testis development?

A

SRY, SOX9

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68
Q

What is the function of AMH and testosterone?

A

Promote regression of paramesonephric duct (Mullerian) & retention of mesonephric (Wolffian duct)

*Wolffian - epididymis, vas deferans, seminal vesicles, ejaculatory ducts

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69
Q

Progesterone production from placenta is most dependant on?

A

Side chain cleavage enzyme expression in placenta!

SCCE expression in placenta –> converts cholesterol to pregnenolone

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70
Q

What does serovars D-K chlamydia trochomatis cause?

A

Genital tract infections

*most common notifiable STI

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71
Q

What causes LGV (lymphogranuloma venerum)?

A

LGV: invasive, associated with genital ulcer in tropical countries

  • Chlamydia trochomatis serovars L1-3
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72
Q

What do you use to treat chlamydia?

A

Doxycycline - contraindicated in pregnancy!

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73
Q

What does Chlamydia trochomatis serovars A,B,Ba,C cause?

A

Trachoma (chronic conjunctivitis, can cause blindness)

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74
Q

What are some examples of microbes that cause STIs?

A
  • Chlamydia
  • Gonorrhoea
  • Syphilis
  • Mycoplasma
  • HSV (herpes)
  • HPV (papilloma)
  • HTLV (human retroviral infection)
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75
Q

What are the consequences of STI caused by gonorrhoea?

A

Males - epididymitis, prostatitis, urethral stricture

Females - cervicitis, endometritis, bartholinitis, salpingitis

Both - urethritis, proctitis (rectum), pharyngitis, disseminated gonococcal infection

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76
Q

What is Neisseria gonorrhoea (gram…shape)?

A

Gram-negative diplococcus

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77
Q

How do we treat gonorrhoea STIs?

A

Use ceftriaxone + azithromycin

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78
Q

Which STIs must we test in pregnancy?

A
  • **SYPHILIS! - congenital transmission —> spontaneous abortion, still birth, neonatal infection
  • can be tested using swab / blood tests
  • HTLV (human retroviral infection) - can also be transmitted from mother-child
  • HSV - can be harmful to baby if acquired during pregnancy
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79
Q

How many stages are there in Syphilis infection?

A

3

  • Primary (resolves in 1-5 weeks, very infectious!)
  • Secondary (palmar rash, lymphadenopathy, condylomata Latum)
  • Tertiary (neurosyphilis, aortitis)
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80
Q

How do you treat Syphilis infections?

A

Benzathine penicillin (long-acting)

  • DO NOT use short acting penicillin!
  • Doxycycline generally should be reserved for non-pregnant!
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81
Q

What do people with Mycoplasma infection (STI) present with?

A

Men: urethritis
Women: cervicitis

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82
Q

How do you treat Mycoplasma infections?

A

Use doxycycline followed by moxifloxacin

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83
Q

Describe HSV infections. (What does it cause, transmission)

A

HSV 1 + 2 —> can cause genital ulceration
Transmission: skin-skin
Can be harmful to baby if acquired during pregnancy

*HSV —> primary + recurrent herpes, neonatal herpes

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84
Q

What do you use to treat HSV infections? (Herpes)

A

Valaciclovir

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85
Q

Describe HPV infections (human papilloma virus) [what does it cause, prevention..]

A

Low risk HPV types —> benign anogenital warts

Males: cancer of penis (some cases)
Females: cervical dysplasia + cancer, vulvar cancer

Prevention: vaccination

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86
Q

What are the treatments for HPV infections?

A

Topical treatment: cryotherapy, podophyllotoxin, imiquimod, laser therapy

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87
Q

How is HTLV infections (human retroviral) transmitted & what’s most commonly affected in HTLV-1 associated inflammatory disease?

A

Transmission: mother-child, sexual intercourse, blood transfusion, organ transplantation, sharing of infecting paraphernalia

*Most commonly affected in HTLV-1 associated inflammatory disease: spinal cord

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88
Q

What is euploidy? How does it occur?

A

Results from + / - of whole sets of chromosomes

Can arise by:

  • 2 sperm nuclei enter ovum
  • ovum fuses with polar body
  • complete non-disjunction in zygote / somatic cells
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89
Q

Is polyploidy lethal ?

A

YES. Either in utero/ neonatally

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90
Q

How did aneuploidy occur?

A

= Changes in chr number not involving whole sets of chr

Arise from: non-disjunction of chromosomes at meiosis

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91
Q

Are all monosomies lethal?

A

ALL monosomy (except 45X) are lethal!!

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92
Q

What are the presentations of Turners syndrome (45XO)?

A
  • often short + webbed neck, short stature, swollen hands + feet at birth
  • AMENORRHOEA, POOR BREAST DEV
  • heart defects, diabetes, LOW TH, VISION + hearing problems
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93
Q

What are the presentations of Klinefelter (47XXY)?

A

Primary feature: sterility!!

  • weaker muscles
  • less body hair
  • smaller genitals
  • breast growth
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94
Q

What is uniparental disomy (UPD)?

A

The individual has 2 copies of a specific chr but they both come from 1 parent!

  • can result from isodisomy (meiosis II error) / heterodisomy (meiosis I error)
  • can —> imprinting disorder
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95
Q

What is multifactorial inheritance? How does it differ from polygenic traits?

A

Multifactorial = phenotypes are produced by a COMBINATION of genetic + environmental factors

Polygenic tracts = determined mostly by GENETICS involving multiple loci but v. Intel environmental factors involved e.g. hair / eye colour

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96
Q

Where is pseudo-autosomal regions (PAR) located?

A

At termini of both X and Y chromosomes

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97
Q

What is Swyer syndrome?

A

XY females.

  • mutations in SRY
  • Hypogonadism (primary amenorrhoea, NO onset of puberty!)
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98
Q

What are some X-linked inherited disorders?

A
  • Haemophilia
  • X-SCID (X-linked severe combined immunodeficiency disorder)
  • R-G colour blindness
  • Muscular dystrophy
  • Fragile X
  • X-linked hypophosphatemia (phex inactivation —> hypophosphatemic Vit D-resistant rickets )
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99
Q

What is erectile dysfunction?

A

Inability to achieve + / maintain erection sufficient for intercourse

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100
Q

How does penile erection occur?

A

PARASYMPATHETIC —> releases cholinergic —> nitric oxide (NO) goes thru guanylyl cyclase —> GTP converted to cGMP —> cGMP activates protein kinase —> reduce Ca2+ in muscle —> less Ca2+ causes smooth muscle RELAXATION —> blood into penis + starts blocking veins when arterial pressure is high => penile erection

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101
Q

Is penile erection para/sympathetic? What about ejaculation?

A

Penile erection - parasympathetic (point)

Ejaculation - sympathetic (shoot)

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102
Q

What are the potential vascular causes of erectile dysfunction?

A

HTN, CVS, atherosclerosis, DM

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103
Q

What are the neurogenic causes of erectile dysfunction?

A

Spinal cord injury, trauma, stroke, Parkinson, MS, epilepsy, DM

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104
Q

What are the endocrine causes of erectile dysfunction?

A

Klinefelter, acquired hypogonadism, thyroid / pituitary disease

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105
Q

What are the iatrogenic causes of erectile dysfunction?

A

Med side effect, post-operative, traumatic

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106
Q

What are the structural causes of erectile dysfunction?

A

Peyronie’s disease - plaques (segments of flat scar tissue) form under skin of penis —> can cause penis to bend / indebted during erections

Congenital chordee - abnormal dev of penis - curves downwards

Hypospadias - abnormal opening of urethra on ventral aspect of penis (anywhere along the shaft)

Old age

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107
Q

What is the 1st line treatment for erectile dysfunction?

A

PDE5 inhibitors!

(In Aus) OD Viagra (sildenafil citrate) / OD Levitra (vardenafil hydrochloride) / OD + OAD Cialis (tadalafil)

  • MOA: dependent on intact nerves!
  • Start maximal dose; de-escalate therapy
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108
Q

What are some other treatment options for erectile dysfunction (not 1st-line)?

A
  1. Vacuum erective device (VED)
    - more cost effective than daily PDE5 inhibitors use
  2. Penile prosthesis implant
    - 3-piece inflatable penis device
    - works on hydraulic principle
    - usually lasts 5-10 years
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109
Q

What are the classic triad of acute prostate cancer emergency ? How do you treat it?

A

Lower back pain, lower limb motor + sensory weakness, urinary + bowel incontinence

  • Diagnosis - MRI (CT) spine
  • Remember to do DRE!!

Treatment: acute spinal stabilisation (if there’s spinal cord compression), steroid, radiation + androgen deprivation therapy

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110
Q

What is priapism?

A

Persistent erections >4 hours

Painful (venous) vs. painless (arterial)

*You need blood flow for erections to occur!

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111
Q

What is penile fracture?

A

Sudden injury to erect penis, usually during sexual intercourse (“pop”)

  • acute pain + penile detumescence followed by penile bruising + deformity
  • Immediate repair associated with faster recovery, better preservation of erectile function + avoids penile curvature
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112
Q

What is Fournier’s gangrene? (Male urological emergency)

A

Rapidly fulminating, gangrenous infection of genitalia

  • usually begins as extension of infection from urinary, perineal, abdominal / retroperitoneal sites // secondary trauma
  • diagnosis: inflammation, necrosis, crepitus
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113
Q

What is emphysematous pyelonephritis? (Male urological emergency)

A

Urosepsis with obstruction + presence of gas in collecting system (seen on CT)

*Gas in kidney —> bad!

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114
Q

What is the most common form of cancer in men?

A

Prostate cancer

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115
Q

What is the morphology of prostate cancer?

A
  • More advanced lesions - appear as firm, grey-white lesions with ill-defined margins that infiltrate the adjacent gland

Histo: glands typically smaller than benign glands, typically lined by a single uniform layer of cuboidal / low columnar epithelium
- Nuclei are enlarged, prominent nucleoli + dark cytoplasm

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116
Q

How is prostate cancer graded?

A

By Gleason system - 5 grades on the basis of glandular patterns of differentiation [Grade 1 = most well-differentiated tumours; grade 5 = no glandular differentiation]

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117
Q

Which zone of prostate does 70-80% of prostate cancer arise from?

A

Peripheral zone!!

- Contains majority of glandular tissue

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118
Q

Why do we do DRE to test prostate cancer?

A

70-80% arise in outer (peripheral) zones - hence may be palpable as irregular hard nodules on DRE

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119
Q

What happens when prostate cancer is locally advanced?

A

Often infiltrate seminal vesicles + periurethral zones of prostate & may invade the adjacent soft tissues, wall of urinary bladder / (less commonly) rectum

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120
Q

What is the most important test used in diagnosis + management of prostatic cancer?

A

PSA (prostate-specific antigen) assay

*Organ-specific BUT not cancer-specific!!!

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121
Q

What is the limitation of PSA (prostate-specific antigen) assay?

A

It’s organ-specific BUT NOT cancer-specific!

*BPH, prostatitis, ejaculation —> also increases serum PSA

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122
Q

What are the most common treatments for clinically localised prostate cancer?

A

Radical prostatectomy + radiotherapy

*Advanced metastatic carcinoma - treated by androgen deprivation

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123
Q

How many zones are there in prostate?

A

3.

Peripheral - contains majority of glandular tissues (70-80% prostate cancer arise here)
Central - surrounds ejaculatory ducts
Transition - surrounds urethra as it enters prostate gland

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124
Q

How many cell layers does a normal prostate gland contain?

A

Two. - Flat basal cell layer + overlying columnar secretory cell layer

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125
Q

What are the clinical features of acute bacterial prostatitis?

A

Fever, chills, dysuria, may be complicated by sepsis

On rectal exam, prostate exquisitely tender + boggy

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126
Q

What are the clinical features of chronic bacterial prostatitis?

A

Low back pain, dysuria, perineal + suprapubic discomfort

*usually associated with recurrent UTI

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127
Q

How do you treat acute & chronic bacterial prostatitis?

A

Antibiotics

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128
Q

What causes BPH? What’s the ultimate mediator of prostatic growth?

A

Proliferation of stromal + epithelial elements with resultant enlargement of gland, in some cases urinary obstruction

**Ultimate mediator of prostatic growth = DHT (dihydrotestosterone) - synthesised in prostate from circulating testosterone by action of enzyme 5a-reductase type 2

DHT binds to androgen receptors - regulate expression of genes that support growth + survival of prostatic epithelium & stromal cells

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129
Q

Why do people with BPH have urinary obstruction?

A

In BPH, the affected prostate is enlarged and contains many well-circumscribed nodules

Urethra is usually compressed by the hyperplastic nodules —> often to a narrow slit

*in some cases - hyperplastic glandular + stromal elements lying just under the epithelium of proximal prostatic urethra —> may project into bladder lumen as pedunculated mass —> ball-valve type of urethral obstruction

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130
Q

Which zone of prostate does BPH occur in?

A

Inner, TRANSITIONAL zone

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131
Q

Describe the hyperplastic glands in BPH. (Histo…cells…)Lined by?

A

Lined by tall, columnar epithelial cells + peripheral layer of flattened basal cells

*hyperplastic glands are large, with papillary unfolding

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132
Q

What is corpora amylacea?

A

“Starch-like bodies”

Small hyaline masses found in prostate gland. Looks kinda like sliced onions

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133
Q

What is the most common clinical feature of BPH?

A

Lower urinary tract obstruction - often in the form of difficulty in starting stream of urine (hesitancy) + intermittent interruption of urinary stream while voiding

Frequently accompanied by urinary urgency, frequency, nocturia

*Presence of residual urine in bladder due to chronic obstruction —> increases risk of UTI

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134
Q

In men with BPH, there is complete urinary obstruction. What would happen if appropriate treatment is absent?

A

Hydronephrosis (excess fluid in kidney due to back up of urine)

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135
Q

What are the possible initial treatments for BPH?

A

Finestride - inhibit DHT formation
Flomax - relax smooth muscle by blocking alpha adrenergic blockers

*Surgical treatments - reserved for severely symptomatic cases recalcitrant to med therapy

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136
Q

What is orchiectomy?

A

Surgical removal of testis

137
Q

Assays of tumour markers are helpful in diagnosing which of the testicular tumours?

A
  1. Seminoma - 10% have elevated hCG (cz of presence of syncytiotrophoblasts)
  2. Yolk sac tumour - 90% have elevated AFP (alpha feta protein)
  3. Choriocarcinoma - 100% have elevated hCG
  4. Mixed tumour - 90% have elevated hCG + AFP
138
Q

In post-pubertal males, 95% of the tumours that arise from germ cells are malignant or benign?

A

Malignant.

139
Q

How many different types of testicular tumours are there?

A
    • Seminoma, embryonal carcinoma, yolk sac tumour, choriocarcinoma, teratoma, mixed tumour
140
Q

Which testicular tumour form FIRM masses and may occur at any age?

A

Teratoma. (= tumours in which neoplastic germ cells differentiate along somatic cell lines)

141
Q

What is the most frequent clinical presentation of patient with testicular cancer?

A

PAINLESS testicular mass, non-translucent

  • associated with hydrocele (10%), gynaecomastia, back pain
  • hydrocele = fluid-filled sac around testicle
142
Q

What are the differences between Seminomas and non seminomatous tumours?

A

Seminomas - often remain confined to testis
—> metastases most commonly encountered in iliac + paraaortic lymph nodes
—> haematogenous metastases occur late in the course of disease

Nonseminomatous - tend to metastasise earlier (lymphatic / haematogenous route)

143
Q

Which of the primary testicular neoplasm is most common in children <3yo?

A

Yolk sac tumour.

*Very good prognosis

144
Q

What are the morphology, histology + distinctive feature of yolk sac tumour? (Size, cells..)

A
  • often large, may be well-demarcated
  • low cuboidal-columnar epithelial cells forming micro cysts, lace-like (reticular) patterns / sheets / glands / papillae
  • distinctive feature: presence of Schiller-Duvall bodies (resemble primitive glomeruli)

**Tumour has AFP!

145
Q

Describe choriocarcinoma.

A

Tumours in which the pluripotential neoplastic germ cells differentiate along trophoblastic lines

  • small, non palpable lesions
  • composed of sheets of small cuboidal cells irregularly intermingled with / capped by large, eosinophilic synctial cells containing dark, pleomorphic nuclei
  • HCG elevated in serum
  • Haemorrhage + necrosis prominent!
146
Q

Seminomas is extremely radio-sensitive and has the best prognosis. True or false?

A

True.

147
Q

Describe seminoma.

A

SOFT, WELL-demarcated, grey-white tumours that bludge from cut surface of the affected testis.

  • large tumours may contain foci of coagulation necrosis (usually WITHOUT haemorrhage)
  • large, UNIFORM cells with DISTINCT cell borders, CLEAR cytoplasm + round nuclei
  • lymphocytic infiltrate usually present
  • 15% cases syncytiotrophoblasts present - source of HCG
  • Peak age 40-50
148
Q

Describe embryonal carcinoma.

A

Ill-defined, INVASIVE masses containing foci of HAEMORRHAGE + NECROSIS

  • tumours large + primitive looking with basophilic cytoplasm, indistinct cell borders + large nuclei with prominent nuclei
  • poorly differentiated, may contain primitive glandular structures + irregular papillae
149
Q

On microscopy, you found that the cells are large with distinct cell borders and round nuclei. Is this seminoma or embryonal carcinoma?

A

Seminoma!

Embryonal - large cells but with INDISTINCT cell borders and large nuclei!

150
Q

What are the risk factors for penile cancer (uncommon)?

A

Lack of circumcision / premalignant lesions / chronic inflammation / phimosis / *Tobacco use / **HPV

151
Q

What are the premalignant conditions associated with penile cancer?

A
  1. Buschke-Lowenstein tumour (giant condyloma) - usually benign but locally invasive, HPV associated
  2. Bowenoid papulosis - benign, HPV identified
  3. Lichen sclerosis - caused by chronic inflammation, associated with urethral strictures
  4. Leukoplakia - associated with irritation, treatment: complete excision
  5. Cutaneous horn - hyperkeratosis, treatment: complete excision
152
Q

95% of penile cancer arise from?

A

SCC

153
Q

What is the difference between Hypospadias and epispadias?

A

Hypospadias = abnormal opening of urethra on the inferior aspect of penis

Epispadias = abnormal opening of urethra on upper aspect (dorsum) of penis

154
Q

What is balanitis?

A

Inflammation of glans penis

155
Q

What is posthitis?

A

Inflammation of overlying prepuce (foreskin)?

*P—P

156
Q

What is balanoposthitis?

A

Inflammation of both glans penis + prepuce (foreskin)

157
Q

What are the differences between phimosis and paraphimosis?

A

Phimosis = prepuce cannot be retracted easily over glans penis

  • may occur as congenital anomaly
  • 80% boys able to retract their foreskin by 3yo

Paraphimosis = inability to reduce foreskin back to an atomic position
- urologic emergency!!

158
Q

What causes balanoposthitis?

A

Most common agents - Candida albicans, anaerobic bac, Gardnerella, progenic bac
*Most cases occur as consequence of poor local hygiene in uncircumcised males, with accumulations of smegma (desquamated epithelial cells, sweat + debris)

159
Q

What are the characteristics of squamous cell carcinoma in situ of penis (Bowen disease)?

A
  • Appears grossly as a solitary plaque on the shaft of penis
  • histo: NO invasion of underlying stroma
  • occurs in older uncircumcised males
160
Q

What are the characteristics of invasive SCC of penis?

A
  • infiltration of underlying CT —> indurated, ulcerated lesion with irregular margins
    Histo: typical keratinising SCC
161
Q

What are the characteristics of verrucous carcinoma of penis?

A

Variant of SCC characterised by a papillary architecture, virtually no cytology atypia & rounded, pushing deep margins

*locally INVASIVE but DO NOT metastasize!

162
Q

What is the skin of scrotum usually affected by?

A

Inflammatory processes incl. local fungal infections + systemic dermatoses

163
Q

What is hydrocele?

A

Most common cause of scrotal enlargement.

  • caused by accumulation of serous fluid within tunica vaginalis
  • may arise in response to neighbouring infections / tumours / idiopathic
  • collection of pus + lymph + blood (can be seen when light is passed thru!!!) - trans illuminates!
164
Q

What is haematoceles?

A

Accumulation of blood within tunica vaginalis —> testicular enlargement

165
Q

What is chyloceles?

A

Accumulation of lymphatic fluid within tunica vaginalis —> testicular enlargement

166
Q

What is elephantiasis of scrotum?

A

Extreme cases of lymphatic obstruction caused by filariasis —> scrotum + lower extremities enlarge to grotesque sizes

167
Q

What is cryptochordism?

A

Failure of testicular descent into scrotum!

*associated with increased frequency of testicular cancer

168
Q

When does testes normally descend from abdominal cavity into pelvis?

A

By 3rd month of gestation & then thru inguinal canals into scrotum during last 2 months of intrauterine life

169
Q

What are the complications of cryptochidism?

A
  • Because undescended testes become atrophic —> bilateral cryptochidism => sterility!!
  • unilateral cyrptochidism associated with atrophy of contralateral descended gonad —> may also lead to sterility!
  • failure to descent —> infertility! + 3-5increased fold of testicular cancer
170
Q

What is spermatocoele ?

A

Cyst from epididymis that contains spermatozoa

171
Q

What is orchitis?

A

Inflammation of 1/ both testicles

172
Q

What happens to testis when there’s epididymitis + orchitis?

A

Involved testis typically swollen + tender
Histo: predominantly neutrophil is inflammatory infiltrate

*usually begin as primary UTI then spread to testis thru ductus deferens / lymphatic of spermatic cord

173
Q

What happens when mumps is complicated by orchitis?

A

Affected testis oedematous + congested + contain predominantly lymphoplasmacytic inflammatory infiltrate

Severe mumps orchitis —> extensive necrosis / loss of seminiferous epithelium / tubular atrophy / fibrosis / sterility

174
Q

Can TB cause testicular inflammation?

A

Yes. Testicular TB generally begins as epididymitis, with secondary involvement of testis

Histo: granulomatous inflammation + caseous necrosis

175
Q

Is testicular torsion a urologic emergency?

A

Yes

176
Q

What happens in testicular torsion?

A

Torsion (twisting of spermatic cord) —> obstruction of testicular venous drainage while leaving the thick-walled + more resilient arteries patent —> intense vascular engorgement + venous infarction

177
Q

Why is testicular torsion an emergency?

A

Intense vascular engorgement + venous infarction!

Blood supply cut! —> cause sudden pain + swelling

178
Q

A man woke up from sleep because of sudden onset of testicular pain. What is one of the top differential diagnoses?

A

Testicular torsion - sudden onset of testicular pain!!

179
Q

What is bell clapper abnormality?

A

Inappropriately high attachment of tunica vaginalis + abnormal fixation to muscle & fasciae coverings of spermatic cord —> testicle can rotate freely on spermatic cord within tunica vaginalis => intravaginal testicular torsion!

180
Q

What are the classic clinical triad of ectopic pregnancy?

A

Pain + amenorrhoea + vaginal bleeding

181
Q

What are the course of blood vessels in endometrium?

A

Uterine arteries —> arcuate arteries —> radial branches —> straight + spinal arteries

182
Q

What happens after ~8th day of fertilisation?

A

Trophoblast overlying embryoblast forms 2 layers:

  • synctiotrophoblast (outer layer)
  • cyrotrophoblast (inner layer) = simple cuboidal cells
183
Q

What are the 2 waves hypoblasts send out to line blastocyst activity?

A

1st: Heuser’s membrane / exocoelomic membrane converts blastocyst cavity —> primary yolk sac
2nd: converts primary yolk sac —> secondary yolk sac

184
Q

What is allantois?

A

Out-pouching of yolk sac, extends into connecting stalk.

Helps form umbilical arteries in cord

185
Q

Describe formation of extra-placental membrane.

A

As embryo grows, decidua capsularis & parietalis will touch each other —> capsularis then degenerate —> amniotic cavity will grow & push amnion against chorion —> obliterate chorion cavity

*extra-placental membrane = fusion of amnion + chorion + decidua

186
Q

Describe the formation of chorionic villi.

A

Cytotrophoblastic cells grow into projections of syncytiotrophoblast = primary villi (~11-13days)

Cytotrophoblastic cells grow out to form a “shell” around trophoblast

Mesenchyme grows into villi = secondary villi (~day16)

Capillaries develop within the villi = tertiary villi (week 3)

187
Q

What is difference between chorion laeve and chorion frondosum?

A

Chorion laeve = Smooth part of the chorion

Chorion frondosum = bushy/leafy part - when villi on the embryonic pole continue growing

188
Q

What is the decidual cells that form under implanting embryo?

A

Decidua basalis

189
Q

What form placenta?

A

Chorion frondosum (foetally-derived) + decidua basalis (maternally-derived)

190
Q

What is the placental membrane consist of?

A
  • synctiotrophoblast (with microvilli)
  • synctiotrophoblast basement membrane
  • mesenchyme
  • capillary basement membrane
  • capillary endothelial cells
191
Q

What is the function of stereocilia in the lining of epididymis and ductus deferens?

A

Absorb large volumes of fluid that carries new sperm into epididymis, + reabsorbing defective / expired / dead sperm

192
Q

Blood tested barrier is formed by?

A

Basal tight junctions between adjacent sertoli cells

193
Q

What innervates blood vessels that fill erectile tissue during erection?

A

Pelvic splanchnic nerves (parasympathetic)

194
Q

Which virus infects variety of skin and mucosal surfaces to produce wart-like lesions?

A

HPV (DNA virus)

195
Q

Testicular lymphatics drain directly to which lymph nodes?

A

Para-aortic lymph nodes

196
Q

Pelvic pain is pain below ___ ?

A

Umbilicus

197
Q

What is pelvis innervates by?

A

Somatic (sacral + coccygeal nerves) & pelvic part of autonomic NS

198
Q

Where are the visceral pain receptors located?

A

Serosal surfaces / within mesenteric / within walls of hollow viscera

199
Q

What are the sources of visceral pain?

A
  • distension / obstruction of viscous or organ capsule
  • spasms of intestinal muscularis fibres
  • inflammation / infection
  • ischaemia from vascular disturbances
  • haemorrhage
  • neoplasm
200
Q

What are the common causes in the pelvis that can present with visceral pain?

A
  • obstruction of ureter by calculus
  • distension of ovarian cyst due to haemorrhage
  • ischaemia of uterine leiomyoma (fibroid)
  • Inflammation of appendix
201
Q

What are the characteristic of visceral pain?

A
  • DEEP
  • DULL
  • vague
  • poorly defined sensation
  • colicky + cramping
  • accompanied by malaise + discomfort with autonomic phenomena e.g. pallor / sweating / nausea / vomiting / fever
202
Q

What are the sources of somatic pain?

A
  • abdominal + pelvic muscles
  • fascia
  • parietal peritoneum
  • subcutaneous tissue
  • skeletal system
203
Q

What can cause patient to present with somatic pelvic pain?

A
  • myofascial trigger points (hyperirritable spots in skeletal muscle)
  • hernia
  • haematoma
  • muscle strain / injury
  • inflammation
  • trauma
204
Q

What is the mechanism of somatic pain?

A
  • Often related to inflammation of parietal peritoneum
  • somatic nerves innervate parietal peritoneum so the pain is located directly over inflamed area
  • pain due to inflammation of parietal peritoneum —> usually constant + aching with episodes of sharp exacerbation
  • Well localised abdominal tenderness + involuntary guarding + rebound tenderness
205
Q

What is neurogenic pain?

A

Pelvic pain due to disease that injure sensory nerves!

206
Q

What normally cause neurogenic pain?

A
  • Herpes zoster
  • impingement by arthritis
  • herniated nucleus pulposus
  • MS
  • syphilis
207
Q

What are the differences between acute / chronic / cyclic pain?

A

Acute - intense, sudden onset, sharp, short course [reflects tissue damage]

Chronic - pain>6 months, maybe due to nerve damage following surgery, trauma, inflammation / infection

*pain as a result of changes in the nerve itself = neuropathic pain

Cyclic (both acute + chronic) = pain that occurs with a definite association to menstrual cycle

208
Q

A patient comes in with acute pelvic pain. What are the differential diagnoses?

A

Gynaecological:

  • complication fo pregnancy e.g. ectopic pregnancy / abortion / placental abruption / uterine rupture
  • acute infections: PID / Tubo-ovarian abscess
  • adnexal disorder: haemorrhagic functional ovarian cyst / torsion of adnexa / rupture of ovarian cysts
  • vaginal foreign bodies e.g. “lost” IUDs, condoms, tampons
  • chemical irritants

Recurrent pelvic pain (cyclic):

  • Mittelschmerz (mid-cycle pain)
  • Primary dysmenorrhea (painful menstruation)
  • Secondary dysmenorrhea

GI:
- Gastroenteritis / appendicitis / bowel obstruction / diverticulitis / IBD / IBS

Genitourinary:

  • interstitial cystitis / painful bladder
  • pyelonephritis

MSK:
- abdominal wall haematoma / hernia

Other:
- abdominal wall haematoma / aortic aneurysm

209
Q

What is Mittelschmerz pain?

A

Rupture of ovarian follicle at ovulation - pain is self-limiting

210
Q

What is adnexa?

A

Region adjoining uterus that contains ovary + Fallopian tube + vessels, ligaments, CT

211
Q

What happens in torsion of adnexa?

A

Twisting of a vascular pedicle of an ovary / Fallopian tube / paratubal cyst —> ISCHEMIA + acute pain

212
Q

If a girl comes to you presenting with severe and constant pelvic pain, nausea, and told you that she started feeling that after exercising, after examination you found that she has tender abdomen and rebound tenderness as well as a large pelvic mass in the lower quadrants. What could she have?

A

Torsion of adnexa

  • Diagnosis usually by ultrasound
  • Surgical management - untwist adnexa + either cystectomy / oophorectomy (surgical procedure to move 1 / both ovaries)
213
Q

What is pelvic inflammatory disease (PID)?

A

Acute onset of bilateral lower abdominal pain that increases with movement + fever + pure lent vaginal discharge

  • direct + rebound tenderness
  • cervical motion tenderness
  • bilateral adnexal tenderness

*Can progress to Tubo-ovarian abscess if pain + fever present >1week before treatment

214
Q

Why do we need surgical drainage for Tubo-ovarian abscess?

A

To prevent rupture!

Life-threatening surgical emergency because gram-ve endotoxic shock can develop rapidly!

215
Q

What are the differences between primary and secondary dysmenorrhea?

A

Primary = menstrual pain w/o pelvic pathology
- caused by INCREASED ENDOMETRIAL PROSTAGLANDIN PRODUCTION during secretory phase —> increased uterine tone with high-amplitude contractions

Secondary = menstrual pain with underlying pathology

  • excess prostaglandin production / hypertonic uterine contractions secondary to cervical obstruction / intrauterine mass / presence of foreign body
  • differentials: endometriosis, Asherman, endometrial polyp, fibroid, adenomyosis
216
Q

What conditions are associated with chronic pelvic pain?

A

Gynaecological:

  • endometriosis
  • chronic pelvic inflammatory disease
  • pelvic adhesions
  • pelvic congestion
  • adenomyosis
  • leiomyoma

Urinary tract:

  • interstitial cystitis
  • recurrent UTI

GI:
- IBD / IBS / colitis / chronic intermittent bowel obstruction / chronic constipation

MSK:

  • pelvic floor myalgia
  • hernia
  • fibromyalgia
  • myofascial pain (tigger points)

Neurologic:
- neuralgia esp. of pudendal nerves / ilioinguinal, genitofemoral..

217
Q

What is endometriosis?

A

Abnormal implantation of endometrial glands + stroma in a location outside endomyometrium

  • *Endometriotic tissue is not just MISPLACED but is also ABNORMAL!!!
  • endometriotic tissue —> exhibits increased levels of PROSTAGLANDIN E2 + increased oestrogen production due to high aromatase activity of stromal cells
218
Q

What are the characteristics of endometriosis when it involves ovaries?

A

When ovaries involved - lesions may form large, blood-filled cysts that turn BROWN as blood ages [CHOCOLATE CYSTS]

219
Q

What are the clinical features of endometriosis?

A

Depends on the distribution of lesions!

  • Extensive scarring of oviducts + ovaries —> discomfort in lower abdominal quadrants + eventual sterility
  • rectal wall involvement —> pain on defecation
  • involvements of uterine —> dyspareunia (painful intercourse)
  • involvement of bladder serosa —> dysuria
  • ALMOST all cases —> severe DYSMENORRHOEA (painful menstruation) + pelvic pain resulting from intrapelvic bleeding + periuterine adhesions
220
Q

What is adenomyosis?

A

= growth of the basal layer of endometrium down into myometrium

  • Aberrant presence of endometrial tissue —> induces reactive hypertrophy of myometrium —> enlarged, globular uterus (often with thickened uterine wall)
  • May produce menorrhagia (prolonged/heavy vaginal bleeding with menstrual cycle) + dysmenorrhoea + pelvic pain before onset of menstruation
221
Q

Is chronic PID a major cause of infertility?

A

Yes.

222
Q

What is pelvic congestion syndrome?

A

Occurs when varicose veins develop around ovaries —> valves no longer function normally —> blood back-up —> veins become engorged / “congested” - can be very painful!

*chronic pelvic pain!

223
Q

What is endometritis?

A

Inflammation of endometrium

*Often a consequence of PID
May be due to retained products of conception, subsequent to miscarriage / delivery, presence of foreign body e.g. IUD

Clinical features:

  • fever, abdominal pain, menstrual abnormalities
  • increased risk of infertility + ectopic pregnancy (as a consequence of damage + scarring of Fallopian tubes)
224
Q

Why is there an increased risk of infertility + ectopic pregnancy in endometritis

A

Endometritis = inflammation of uterus

  • as a consequence of damage + scarring of Fallopian tubes
225
Q

What are the skin findings in breast cancer?

A

Erythema, thickening, dimpling of overlying skin

226
Q

What are the known risk factors for cancers in females?

A

Smoking, alcohol, obesity, chronic infections (HPV), fam history

227
Q

90% of women with endometrial cancer present with abnormal uterine bleeding. True or false?

A

True

228
Q

What bleeding patterns should prompt endometrial evaluation?

A
  • ANY bleeding in POSTmenopausal women
  • in women 45-menopause: frequent / heavy / prolonged intermenstrual bleeding; also amenorrhoea > 6 months
  • <45 with persistent abnormal bleeding in the setting of unopposed oestrogen exposure (obesity) / with fam history
229
Q

Fam history of Lynch syndrome significantly increase risk for which cancers?

A

Colorectal + endometrial cancer

230
Q

Endometrial thickness of ___ mm in postmenopausal women requires further investigation using Transvaginal ultrasound?

A

> 4mm

231
Q

What are the clinical features of ovarian cancer?

A

Abdominal pain + distension, bloating, “feeling full quickly”, new onset constipation, weight loss

Acute presentations: tense ascites, pleural effusion, bowel obstruction, unprovoked DVT

**No screening

**Most commonly derived from epithelial cells (90%)

232
Q

What are the risk factors for cervical cancer?

A 
HPV infection 
Early sexual activity 
Multiple sexual partners
Previous STI
**Smoking 
Lack of regular Pap smear screening

*Pap smear screening - look for cell changes in cervix

**New cervical screening test - looks for HPV which can lead to cell changes in cervix

233
Q

What are the short & long-term complications of PID?

A

Short term:

  • pelvic peritonitis
  • Fitz-Hugh-Curtis syndrome - inflammation of liver capsule which classically presents with R upper quadrant abdominal pain

Ling term:

  • Tubo-ovarian abscess — may spread to adjacent organs
  • Infertility
  • ectopic pregnancy
234
Q

What is condyloma?

A

Any warty lesion of vulva

235
Q

What is condylomata acuminata?

A

Warty lesion of vulva.

  • can be papillary + distinctly elevated / somewhat flat + rugose
  • can occur anywhere on anogenital surface
  • **Koilocytosis - perinuclear cytoplasmic vacuolisation + wrinkled nuclear contours that’s a hallmark of HPV infection

*strongly associated with HPV subtypes

236
Q

What are the 2 distinct forms of vulvar squamous cell carcinoma?

A

*~90% of carcinoma of vulva is SCC!

Less common form: related to high-risk HPV strains (esp. HPV subtypes 16,18)
- onset of carcinoma often preceded by precancerous changes in epithelium = vulvar intraepithelial neoplasia (VIN)

2nd form: older women, NOT associated with HPV but often preceded by years of reactive epithelial changes

237
Q

What is cervicitis?

A

Inflammatory conditions of cervix - extremely common, associated with purulent vaginal discharge

238
Q

What are the normal vaginal flora?

A

Streptococci, staphylococci, E.coli

239
Q

Most tumours of cervix are of ___ origin and caused by oncogenic strains of ___ ?

A

Epithelial origin

Strains of HPV

240
Q

What is the pathogenesis of cervical carcinomas?

A

A subset of infection persists —> progress to cervical intraepithelial neoplasia (CIN), a precursor lesions from which most invasive cervical carcinomas develop

241
Q

What is the important risk factor for the development of CIN (cervical intraepithelial neoplasia)?

A

HPV exposure**, early age at 1st intercourse, multiple sex partners, male partner with multiple previous sexual partners

242
Q

You have a patient with HPV-related cervical carcinoma. Describe the “events” leading to it.

A

HPV-related carcinogenesis: begins with precancerous epithelial change, CIN

Usually starts at low-grade dysplasia (CIN I) —> progresses to moderate (CIN II) —> severe dysplasia (CN III) over time

243
Q

What are the differences (characteristics) between cervical intraepithelial neoplasia (CIN) I, CIN II, and CIN III?

A

CIN I - dysplastic changes in the lower third of squamous epithelium + koilocytosis change in superficial layers of epithelium

CIN II - dysplasia extends to middle third of epithelium + takes the form of delayed keratinocytes maturation

CIN III - almost complete loss of maturation, even greater variation in cell + nuclear size, chromatin heterogeneity, disorderly orientation of cells
- koilocytotic change usually absent

244
Q

ALL invasive carcinoma of cervix are caused by HPV. True or false?

A

True!!!

245
Q

What is the most common form of invasive carcinoma of cervix?

A

Squamous cell carcinoma

246
Q

What are the risk factors for progression of CIN (cervical intraepithelial neoplasia) to invasive carcinoma?

A

Smoking, HIV infection

247
Q

Where does invasive carcinoma of cervix develop in?

A

Transformation zone (the exposed columnar cells of cervix —> undergo squamous metaplasia to become squamous epithelium… transformation zone has 2 types of epithelial coexisting)

248
Q

What leads to a barrel cervix?

A

Invasive tumour of cervix encircling cervix + penetrate into underlying stroma —> barrel cervix

249
Q

What is the inflammation fo Fallopian tube?

A

Salpingitis

250
Q

Salpingitis is almost always microbial in origin. Is that true?

A

Yes, e.g. chlamydia, mycoplasma hominids, strep, staph

251
Q

What does all forms of salpingitis produce?

A
  • Fever
  • lower abdominal pain / pelvic pain + pelvic masses (as a result of distension of the tubes with exudate / inflammatory debris)
252
Q

What can cause tuboovarian abscess?

A

Adherence fo inflamed tube to ovary + adjacent ligamentous tissues

253
Q

What are adhesions of tubal plicae associated with ?

A

Increased risk of tubal ectopic pregnancy

254
Q

What does damage to / obstruction of tubal lumina lead to?

A

Sterility

255
Q

A sexually active 26 year old girl comes to you with 8 week history of amenorrhea. Which hormones would you be most interested in checking in the first instance?

A

Human chorionic gonadotropin (hCG)!!!

Pregnant is the most important explanation to rule out in ANY sexually active woman of reproductive age presenting with amenorrhea, bleeding / pain

256
Q

What are the classic clinical features of endometriosis?

A

Infertility
Dysmenorrhoea
Pelvic pain
Dyspareunia

257
Q

At what point in menstrual cycle do oestrogen levels peak?

A

Just prior to ovulation

258
Q

What are typical symptoms of ovarian cancer?

A 
Bloating 
Abdominal discomfort + distension
Early satiety
Fatigue 
Unintentional weight loss

*Most likely tumour marker to monitor disease progression in this case - CA125

259
Q

What hormone is elevated in polycystic ovary syndrome?

A

Luteinizing hormone (LH)

260
Q

A 29 yo woman noted a nodularity in her R breast. On exam there’s a well circumscribed mass 2cm in size. There were no changes in the overlying skin & no axillary lymphadenopathy. Microscopic shows proliferative mass with stromal + epithelial components. What is the most likely diagnosis?

A

Fibroadenoma.

A biphasic tumour composed of stroma + epithelial proliferation
*Most common benign neoplasm of the breast!

261
Q

The mid-cycle LH surge is a key reproductive event. If the amplitude of LH surge was significantly reduced, what physiological changes would occur?

A

Reduced progesterone in the luteal phase.

The LH surge is necessary for full differentiation of thecal + granulosa cells into the corpus luteum. A fully functional CL will not occur with an attenuated (reduced) LH surge and therefore will be reduced progesterone!!

262
Q

What is the practice of narrowing vaginal opening thru creation of a covering seal by cutting & repositioning labia minora / majora with or without removal of clitoris called?

A

Infibulation

263
Q

What is the medication that’s used to treat erectile dysfunction and pulmonary arterial HTN?

A

Sildenafil

264
Q

What is menorrhagia?

A

Profuse / prolonged bleeding at the time of period

265
Q

What is metrorrhagia?

A

Irregular bleeding between periods

266
Q

What are the common cause of abnormal uterine bleeding?

A 
Endometrial polyps 
Leiomyoma 
Endometrial hyperplasia 
Endometrial carcinoma
Endometritis
267
Q

What is an important precursor of endometrial carcinoma?

A

Endometrial hyperplasia

268
Q

How does endometrial hyperplasia happen?

A

EXCESS OESTROGEN relative to progestin —> induce exaggerated endometrial proliferation (hyperplasia)

269
Q

What are the potential causes of oestrogen excess?

A
  • failure of ovulation
  • prolonged administration of oestrogen is steroids w/o counterbalancing progestin
  • oestrogen-producing ovary lesions (e.g. PCOS)
  • obesity (adipose tissue converts steroid precursor —> oestrogen)
270
Q

In endometrial hyperplasia, what is the risk of developing carcinoma related to?

A

Presence of cellular atypia!

271
Q

How many different types of endometrial carcinoma are there?

A

2 types. - endometrioid and serous

272
Q

What are the major differences between endometrioid and serous type of endometrial carcinoma?

A

Endometrioid: (80%)

  • arise in association with OESTROGEN EXCESS + ENDOMETRIAL HYPERPLASIA in PERImenopausal women
  • mutations in mismatch repair genes + PTEN tumour suppressor genes
  • histo: closely resemble normal endometrium

Serous (15%)

  • arise in setting of ENDOMETRIAL ATROPHY in older POSTmenopausal women
  • mutations in TP53 tumour suppressor gene
  • form small tufts + papillae (rather than glands seen in endometrioid)
  • exhibit much greater atypia
  • behave aggressively!
273
Q

What are the risk factors for endometrioid type of endometrial carcinoma?

A

Obesity, DM, HTN, infertility, exposure to unopposed oestrogen

*prolonged oestrogen replacement therapy & oestrogen secreting ovary tumours —> increase risk

274
Q

What is the clinical significance of endometrial polyps?

A

A cause of abnormal uterine bleeding!

275
Q

What is the most common benign tumours in females that arise from the SMOOTH MUSCLE CELLS in MYOMETRIUM?

A

Leiomyoma (fibroids)

276
Q

What is the most frequent presenting sign of leiomyoma?

A

Menorrhagia (abnormally heavy bleeding at menstruation)

277
Q

What would you see histologically, in leiomyoma?

A

Tumours (benign) are characterised by bundles of SMOOTH MUSCLE CELLS mimicking appearance of normal myometrium

278
Q

Does leiomyosarcoma arise from pre-existing leiomyoma?

A

NO. Leiomyosarcoma arise de novo from mesenchymal cells of myometrium!

279
Q

What are the major differences between leiomyoma and leiomyosarcoma?

A

Leiomyoma - frequently multiple & arise premenopausally

Leiomyosarcoma - almost always SOLITARY & in postmenopausal women

280
Q

What are the diagnostic features of overt leiomyosarcoma?

A

Tumour necrosis, cytology atypia, mitotic activity

*the tumour typically: soft, haemorrhage, necrotic

281
Q

What biochemical abnormalities would we observe in polycystic ovarian disease in most patients?

A

Excess androgen production, excess oestrogen**, high LH, low FSH

282
Q

How many different types of ovary tumours are there? Which of them is the most common?

A

Surface epithelial tumours - most common
Germ-cell tumour
Sex-chord stroma cell tumour
Metastases

283
Q

What happens, leading to surface epithelial tumours of ovary?

A

Repeated ovulation + scarring —> surface epithelium becomes entrapped in cortex of ovary —> forming epithelial CYSTS —> can become metaplastic / undergo neoplastic transformation —> diff epithelial tumours

284
Q

What is the most common ovarian epithelial tumours, and is also the most common ovary malignancies?

A

Serous tumour

285
Q

What are the morphology and histology of benign serous tumours?

A
  • serosal covering is smooth + glistening
  • surface of cystadenocarcinoma has nodular irregularities representing areas in which the tumour has penetrated into serosa
  • cystic spaces usually filled with clear serous fluid
  • contain single layer of tall COLUMNAR epithelial cells (often ciliated)
  • PSAMMOMA bodies common in tips of papillae
286
Q

What is mucinous tumour of ovary?

A

Similar to serous tumour, the essential difference being that the neoplastic epithelium consist of MUCIN-SECRETING CELLS!

287
Q

What are the similarities and differences between serous and mucinous tumour of ovary?

A

Both produce cystic masses.

Mucinous tumour produce cystic masses that are similar to serous tumours except by the MUCINOUS nature of cystic contents!

Mucinous tumour larger + multicystic

Mucinous tumours much less likely to be bilateral!

288
Q

What are the characteristics of malignant mucinous tumour of ovary?

A
  • Solid ares of growth
  • cellular stratification
  • cytology atypia
  • stromal invasion
  • serosal penetrations
289
Q

How do we differentiate Krukenberg tumour from mucinous tumour of ovary?

A

Krukenberg tumour = metastatic mucinous adenocarcinoma from GI tract which often produces BILATERAL OVARIAN MASSES

Compared to

Mucinous tumour of ovary - less likely to be bilateral!

290
Q

What is pseudomyxoma peritonei?

A

Rare malignant growth characterized by the progressive accumulation of mucus-secreting (mucinous) tumor cells within the abdomen and pelvis

291
Q

Describe the endometrioid tumours of OVARY (“under” surface epithelial tumours of ovary).

A

May be solid / cystic

Formation of tubular glands, similar to those of endometrium

Usually malignant

292
Q

What is Brenner tumour?

A

Uncommon, solid, usually unilateral OVARIAN tumour

  • consist of ABUNDANT STROMA containing nests of TRANSITIONAL-TYPE epithelium (resembling urinary tract)
  • generally smoothly encapsulated!!
293
Q

How common is teratoma (germ cell tumour) among ovarian malignancies?

A

Constitute 15-20% of ovarian tumours

294
Q

Benign (mature) cystic teratoma is often associated with ___ cyst.

A

Dermoid cyst

295
Q

What are the features of benign (mature) cystic teratoma?

A

Often fillies with sebaceous secretion + matted hair
- sometimes nodular projection from which teeth protrude

  • sometimes produce infertility + prone to undergo torsion
  • (rare) paraneoplastic complication - limbic encephalitis —> may develop in women with teratoma containing mature neural tissue + remits with tumour resection
296
Q

What is the mean age for immature malignant teratoma?

A

Found early in life! Mean age 18yo

297
Q

What is the difference between mature (cystic teratoma) and immature (malignant teratoma)?

A

Immature - often bulky, predominantly solid + punctuated by areas of NECROSIS

298
Q

What is a specialised teratoma?

A

Rare. Composed entirely of specialised tissue!

E.g. struma ovarii - composed entirely of mature thyroid tissue that may actually produce hyperthyroidism

299
Q

What are some of the non-neoplastic inflammatory diseases of breast?

A
  • acute mastitis
  • duct ectasia : nonbacterial chronic inflammation of breast associated with inspissation of breast secretions in main excretory duct. (Ductal dilation)
  • fat necrosis : central focus of necrotic fat cells surrounded by neutrophils + lipid-laden macrophages
  • lymphocytic mastopathy : may cause palpable nodules in breast, associated with autoimmune thyroid disease & T1D [prominent lymphocytic infiltrate around lobules + fibrosis of stroma]
  • granulomatous mastitis : non-specific reaction pattern to systemic disease / chronic infection / foreign materials
300
Q

What do fibrocystic changes of breast predominantly consist of ?

A

Cyst formation + fibrosis!

301
Q

What is the most common type of fibrocystic lesion (of breast)?

A

Non-proliferation changes (cysts + fibrosis)

302
Q

What are the characteristics of cysts + fibrosis (nonproliferative fibrocystic changes) of the breast?

A

Characterised by an INCREASE in FIBROUS STROMA associated with DILATION of ducts + formation of variably sized CYSTS

  • blue-dome cysts = unopened, brown to blue, filled with watery, turbid fluid
  • Apocrine metaplasia - lining cells are large + polygonal with abundant granular, eosinophilic cytoplasms & small, round, deeply chromatic nuclei
303
Q

Breast has __ cells and __ cells?

A

Luminal cells + myoepithelial cells

*most cancers arise from inner epithelial (luminal) cell layer!

304
Q

What are the 2 proliferative changes (fibrocystic) in breast?

A

Epithelial hyperplasia

Sclerosing adenosis

305
Q

Describe epithelial hyperplasia (proliferative fibrocystic change of breast)

A
  • presence of >2 cell layers
  • Duct lumen: filled with a heterogenous population of cells of differing morphology. Irregular slit-like fenestrations prominent at periphery

*Sometimes proliferating epithelium projects as multiple small papillary excrescences (growth / lump) into ductal lumen = ductal papillomatosis

306
Q

What is atypical ductal hyperplasia (breast)?

A

Hyperplastic cells have features bearing some resemblance to ductal carcinoma in situ!

***increase risk of invasive carcinoma of breast

307
Q

What is atypical lobular hyperplasia (breast)?

A

Describe hyperplasia that exhibit changes that approach but do not meet diagnostic criteria for lobular carcinoma in situ

308
Q

Atypical ductal & atypical lobular hyperplasia - associated with increased risk of invasive carcinoma. True or false?

A

True!!!

309
Q

What are the characteristics of sclerosing adenosis (breast)?

A
  • lesions contain marked intraocular fibrosis + proliferation of small ductules & acini
  • proliferation of luminal spaces (adenosis) lined by epithelial cells + myoepithelial cells
  • acini arranged in swirling pattern + well-circumscribed outer border (unlike in breast carcinoma)
  • marked stromal fibrosis, may compress + distort proliferating epithelium
310
Q

What are the benign tumours of breast?

A
  • fibroadenoma (most common benign neoplasm of female breast!!)
  • Phyllodes tumour
  • intraductal papilloma
311
Q

What are the characteristics of fibroadenoma (benign breast tumour)?

A
  • biphasic tumour composed of FIBROBLASTIC STROMA + EPITHELIUM_LINED GLANDS
  • solitary, discrete, mobile masses
  • firm
  • histo: loos fibroblastic stroma containing ductlike, epithelium-lined spaces of various shapes + sizes
312
Q

What are the characteristics of Phyllode tumour (benign breast tumour)?

*phyllode = leaf-like

A
  • biphasic : composed of NEOPLASTIC STROMAL CELLS + EPITHELIUM-LINED LEAFLIKE PROJECTIONS
313
Q

What are the characteristics of intraductal papilloma? (Benign breast)

A
  • benign neoplastic papillary growth
  • solitary, found within principal lactiferous ducts / sinuses
  • serous / bloody nipple discharge
  • double-layered epithelium!**
    —> outer luminal layer overlying a myoepithelial layer
314
Q

What are the general characteristic of breast carcinomas?

A
  • overexpression of HER2 / NEU proto-oncogen
  • hereditary breast cancer: mutations in BRCA1/BRCA2
  • most common location of tumours within breast - upper outer quadrant
  • classified according to whether or not penetrated liming basement membrane
    —> in situ carcinomas = remain within boundary
    —> invasive / infiltrating carcinomas = have spread beyond it
315
Q

What are the 2 non-invasive (in situ) breast carcinoma?

A

Ductal carcinoma in situ (DCIS)

Lobule carcinoma in situ (LCIS)

  • both usually arise from cells in terminal duct lobular unit
  • both confined by basement membrane
  • both DO NOT invade stroma / lymphovascular channels
  • 1/3 of both will eventually develop invasive carcinoma!!
316
Q

What are the characteristics of ductal carcinoma in situ (DCIS)?

A
  • tends to fill + distort ductlike spaces
  • architectural patterns often mixed
  • comedo = cells with high-grade nuclei with EXTENSIVE CENTRAL NECROSIS
  • frequent associated with CALCIFICATIONS
  • excellent prognosis

Treatment:

  • surgery + irradiation
  • antioestrogenic agents e.g. tamoxifen, aromatase
317
Q

What is the Paget disease of nipple?

A
  • caused by extension of ductal carcinoma in situ (DCIS) up the lactiferous ducts + into contiguous skin of nipple —> producing unilateral crusting EXUDATE over nipple + areolar skin
  • in almost all causes, an underlying carcinoma is present (~50% invasive)
318
Q

What are the characteristics of Lobular carcinoma in situ (LCIS)?

A
  • usually expands but X alter acini of lobules
  • uniform appearance
  • cells MONOMORPHIC with bland + round nuclei
  • loosely cohesive cells
  • intracellular mucin vacuoles sometimes forming signet ring cells

Treatment:
- chemoprevention + tamoxifen

319
Q

What are the invasive (infiltrating) breast carcinoma?

A
  • Invasive ductal carcinoma
  • invasive lobular carcinoma
  • inflammatory carcinoma
  • medullary carcinoma
  • colloid carcinoma (mucinous)
  • tubular carcinoma
320
Q

What are the characteristics of invasive ductal carcinoma of breast?

A
  • hard, palpable mass
  • tumours range from well-developed tubule formation + low-grade nuclei to consisting of sheets of anaplastic cells (with numerous mitotic figures + areas of necrosis)
  • tumour margins typically irregular
  • invasion of lymphovascular spaces
321
Q

What are the characteristics of invasive lobular breast carcinoma?

A
  • consists of cells morphologically identical to cells of LCIS
  • cells invade individually to STROMA
  • cells often aligned in “single-file” strand / chains
  • presence of mutations that overrule function of e-Cadherin (contributes to cohesion of normal breast epithelial cells)
  • unique pattern of metastases among breast cancers —> most commonly to CSF, serosal surfaces, GI tract, ovary, uterus, bone marrow
  • almost ALL express hormone receptors!
322
Q

What are the characteristics of inflammatory breast carcinoma (invasive)?

A
  • enlarged, swollen, erythematous breast
  • usually w/o palpable mass
  • underlying carcinoma generally poorly differentiated + diffusely infiltration

**Poor prognosis!!

323
Q

What is the “triple-negative” in medullary breast carcinoma (invasive)?

A

NO oestrogen receptors
NO progesterone receptors
DO NOT over express HER2/NEU

324
Q

What are the characteristic of medullary (invasive) breast carcinoma?

A

Rare

  • consists of sheets of large ANAPLASTIC cells with well-circumscribed, “pushing” borders
  • highly pleomorphic tumour cells grow in cohesive sheets, associated with prominent reactive infiltrate of lymphocytes + plasma cells
  • clinically can be Isabel for fibroadenoma!
  • BRCA1 mutations!
325
Q

Why do medullary carcinoma (invasive) and colloid carcinoma (invasive) often can be mistaken for fibroadenoma (benign breast tumour)?

A

They both often present as well-circumscribed masses

326
Q

What are the characteristics of colloid (mucinous) breast carcinoma [invasive]?

A
  • tumour cells produce abundant quantities of extracellular MUCIN
  • usually SOFT + gelatinous
327
Q

What are the characteristics of tubular breast carcinoma (invasive)?

A
  • consists of well-formed tubules with low-grade nuclei
  • lymph node metastases rare
  • prognosis excellent
328
Q

Which of the invasive breast carcinomas almost all express hormone receptors?

A
  • invasive lobular carcinoma
  • colloid (mucinous) carcinoma
  • tubular carcinoma
329
Q

What are the common features of invasive breast cancers?

A
  • tend to become adherent + fixed to pectoral muscles / deep fascia of chest wall + overlying skin
  • with consequent RETRACTION / DIMPLING of skin or nipple —> important sign because may be the 1st indication of malignancy!!!
  • involvement of lymphatic pathways —> localised lymphadema :
  • ***Skin becomes thickened around exaggerated hair follicles —> ORANGE PEEL appearance!!
330
Q

Breast cancer is often discovered as ______ mass? (Pain? Movable?)

A

Discrete, solitary, PAINLESS, MOVABLE mass!

**At the time of clinical detection typically involvement of regional lymph nodes (most often axillary) already present in ~50% patients!

331
Q

What are the ways breast cancer spread?

A

Thru lymphatic + haematogenous channels

  • outer quadrant + centrally located lesions —> typically spread 1st to axillary nodes
  • in medial quadrant —> often travel 1st to lymph nodes along internal mammary arteries
  • more distant dissemination —> can involve virtually any organ / tissue!
332
Q

Describe gynecomastia

A
  • disease of male breast due to OESTROGEN EXCESS
  • morphology: increase in CT + epithelial hyperplasia of ducts
  • button-like, subareolar swelling
333
Q

What is Important in promoting prostate dev, growth, differentiation?

A

DHT

334
Q

What are the 1st and 2nd line of treatments for BPH?

A

1st line:
5AR inhibitors (-sterides)
- inhibit 5AR and decrease plasma DHT —> reduce prostate size & reduce pressure on urethra + bladder

2nd line:
Alpha1-adrenergic antagonists (-sins_
- decrease degree of smooth muscle contraction in prostate —> decrease pressure on urethra, increase urinary flow

335
Q

How do varicoceles cause male infertility?

A

By increasing testicular temperature

Varicoceles - Can result in the pampiniform plexus being unable to cool arterial blood

Varicoceles = abnormal dilation of pampiniform venous Plexus. Majority occur on the left side

336
Q

Where do lymphatic drainage of scrotum / testes go to?

A

Scrotum - to superficial inguinal lymph nodes

Testes - to para-aortic lymph nodes

337
Q

Where does right & left ovarian vein drain into?

A

Right ovarian vein drains into inferior vena cava

Left ovarian vein usually drains into left renal vein

338
Q

When considering a breast lump, a history of trauma to the area would particularly raise suspicion for which non-neoplastic inflammatory disease of breast?

A

Fat necrosis

Clinical Science (8 decks)

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